Home Remedies for Hyperglycemia

Blood Sugar Miracle

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Blood Sugar Miracle Overview


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Models For Hyperglycemia And Stroke

Clinical studies clearly show that admission hyperglycemia is related to the outcome after stroke (Chapter 9). It is less clear, however, if this relation is causal, i.e., high admission glucose causes poor outcome. Issues that need to be resolved are as follows (i) whether stroke-related hyperglycemia reflects pre-existent metabolic abnormalities, such as impaired glucose tolerance, (ii) whether such pre-existent metabolic abnormalities already compromise the brain, which might explain the relatively poorer functional outcome in relation to hyperglycemia, (iii) if hyperglycemia in the days after the initial event is still harmful to the brain or may even represent a compensatory event for reductions in energy supply to the ischemic area, and (iv) if correction of hyperglycemia improves outcome. Studies in animal models can help to clarify these issues. The timing and severity of hyperglycemia in relation to stroke can be readily manipulated in rodent models. A range of rodent models...

Strokeand Hyperglycemia

Hyperglycemia is a frequent finding in various medical emergencies, and it has clearly been associated with poor outcome. Hyperglycemia is potentially modifiable, and in the past decade a number of trials have been Also after stroke, hyperglycemia is frequent and is independently associated with poor outcome. Although this is already known for a few decades, the 1994 guidelines for the treatment of ischemic stroke from the American Heart Association (AHA) did not make any recommendation for the treatment of hyperglycemia in these patients. More recent (2007) consensus papers recommended treating glucose levels more strictly, despite the lack of apparent evidence of a clinical benefit (4-6). In this chapter, focusing on ischemic stroke, we will first outline the incidence and the natural course of post-stroke hyperglycemia, next we will discuss the etiology of post-stroke hyperglycemia and the various mechanisms that could explain how acute hyperglycemia can be detrimental after...

Adjusting for Hyperglycemia

Insulin doses will be adjusted upward when a pattern demonstrating hyperglycemia at a given time of day is present for 2 to 3 days in a row at the same time of day and the hyperglycemia is unexplained by increased food intake, inactivity, or the somogyi phenomenon (rebound hyperglycemia). If the hyperglycemia is explained by an increased food intake or a decline in physical activity, it is preferable to correct the underlying lifestyle indiscretion rather than to raise the insulin dose(s). If fasting hyperglycemia is present, and particularly if fasting hyperglycemia is seen in association with wide variation in BG values, including the presence of normal and or lower values, one must exclude the possibility that the highs represent rebound in response to nocturnal hypoglycemia. This distinction is accomplished by asking the patient to check a BG reading between 2 and 3 AM to see if it is normal. If the overnight BG is high, then it is appropriate to adjust the basal insulin dose...

Hyperglycemia Induced Tissue Damage Pathways and Causes

Since the initial findings from the Diabetes Control and Complications Trial (DCCT) were published in 1993 (1), the intensification of diabetes management to prevent or slow the onset of the complications associated with type 1 diabetes (T1D) has been a hallmark of diabetes treatment. The DCCT findings confirmed the strong link between hyperglycemia and the complications and put to rest a debate about the necessity of tight glycemic control see (2) and (3) for the history of this debate . During the past two decades, much attention has been paid to the mechanisms that promote hyperglycemia-induced tissue damage and to the potential ways to modify this process (4-6). The targeted population for intensified diabetes management may well be 2 million adults with T1D in the United States based on the estimate of 10 of the 20.6 million diabetes patients (7). Further, the incidence of T1D appears to be increasing with a tendency toward younger age at onset (8-10). Taken together, there is a...

Pathways Of Hyperglycemiainduced Damage

As glucose is metabolized, both intra- and extracellular environments are affected by hyperglycemia and endothelial damage can occur. There is a debate (4,6,44) over the pathways through which these hyperglycemia-induced changes in cellular conditions lead to complications. We focus on four major pathways that have been implicated in the process leading to microvascular complications (i) increased polyol pathway flux, (ii) increased advanced glycation end product (AGE) formation, (iii) activation of protein kinase C (PKC) isoforms, and (iv) increased hexosamine pathway flux. While we will focus on these pathways and their association with microvascular complications, these pathways may be implicated in macrovascular complications as well. Further, these pathways are not mutually exclusive. One or more of the pathways may be operating at a given time, and the progression toward complications may require an interaction among them. (ii) AGEs cause tissue damage and have been used to...

Pathogenesis of hyperglycemia in type diabetes

Type 2 diabetes is a heterogeneous disease manifested by hyperglycemia that results from multiple dysregulated biologic pathways. Each of these pathways represents a potential target for therapy (see Figure 3.2). The two major metabolic abnormalities are 1) insulin resistance in skeletal muscle, liver, and adipocytes, and 2) a progressive decline in insulin production by pancreatic p-cells 6 . Insulin resistance results from both environmental factors (predominantly obesity and physical inactivity) and genetic factors that have yet to be fully identified. Early in the natural history of type 2 diabetes, insulin-resistant individuals who are prediabetic compensate by secreting increased amounts of insulin. Hyperglycemia results as the capacity of the pancreas to secrete insulin deteriorates and endogenous insulin production is insufficient to overcome insulin resistance. Because p-cell failure is progressive, treatment interventions must be continuously monitored and advanced. The...

Treatment Of Hyperglycemia

Although the association between hyperglycemia and poor outcome is well established in stroke patients, it remains unclear if patients benefit from tight glycemic control. In experimental stroke reduction in blood, glucose with insulin to the lower physiological range (3-4 mmol L) reduced infarction size (118, 119). In human studies, treatment of hyperglycemia in patients with stroke remains the subject of debate. (possibly > 7.8-10.3 mmol L) should probably trigger the administration of insulin. This recommendation is based on two observations first, the increased risk of poor outcome associated with hyperglycemia second, the accumulating evidence from trials in other medical emergencies than stroke which demonstrates that tight glycemic control improves outcome such as in patients admitted to the ICU (3,120), patients with myocardial infarction (2, 121), or patients undergoing coronary artery bypass grafting (CABG) (122, 123). These results, however, cannot directly be...

Treating Hyperglycemia

The other diabetic emergency is hyperglycemia, or too much blood sugar. It is unpredictable, possibly deadly, and happens from time to time to all people with diabetes. This is more rare than hypoglycemia but still very dangerous. People with types 1 and 2 can suffer from it but react differently. Someone who is hyperglycemic must have an injection of quick-acting insulin and drink lots of sugar-free liquids. If the condition does not improve rapidly, the person must seek emergency medical help. Sometimes, people who do not yet know they have type 2 diabetes can develop hyperglycemia. They and people already diagnosed with type 2 who experience this condition can have it for a long time without realizing it. Their glucose level can zoom to extremely high levels, which can lead to coma and death. Hyperglycemia leads to a condition called HHS. It can happen to people who do not use insulin but take oral medicines. HHS symptoms are sleepiness or mental confusion, extreme thirst, no...

Hyperglycemia and Adverse Pregnancy Outcome HAPO Study

Existed, making the decision regarding cutoffs difficult. The risk of macrosomia increased approximately fivefold as fasting glucose increased above 75 mg dl, 1-h glucose increased above 105 mg dl, or 2-h glucose increased above 90 mg dl. In other words, a fasting glucose greater than or equal to 100 mg dl was associated with a risk of macrosomia five times that of a fasting glucose less than 75 mg dl, with absolute macrosomia rates of 25 vs. 5 . Correlation with other outcomes was less marked, although still significant. HAPO excluded women with severe hyperglycemia from the analysis (fasting glucose greater than 105 mg dl or 2-h glucose greater than 200 mg dl), so the association actually underestimated the strength of the correlation by excluding women with extremely elevated glucose. An initial recommendation for screening cutoffs incorporating the HAPO results is expected later in 2009. Following the publication of the consensus opinion, it is likely that medical organizations...

The Effect of PPARy Ligands on the Enhancement of Insulin Sensitizing Action Via Improving Hyperglycemia

The Diabetes Control and Complications Trial and the United Kingdom Prospective Diabetes Study reported that the strict maintenance of euglycemia by intensive insulin treatment can delay the onset and slow the progression of DN in patients with type 1 and type 2 diabetes mellitus (57,58). These studies suggested that the adverse effects of hyperglycemia are the main cause for the development of long-term complications in diabetes such as kidney disease. TZDs as PPAR-y ligands are a new class of oral antidiabetic agents that are used widely and improve insulin resistance, hyperinsulinemia, and hyperglycemia in patients with type 2 diabetes (59-62). Because amelioration of hyperglycemia can prevent the development and progression of DN, TZDs could be renoprotective in patients with type 2 diabetes and in the corresponding animal models of the disease by their insulin sensitizing ability (63). In fa fa rats, one of type 2 diabetic models, treatment with TZDs reduced albuminuria, improved...

Hyperglycemiainduced Process

Effect of agents that alter mitochondrial metabolism on hyperglycemia-induced ROS formation in bovine aortic endothelial cells. Cells were incubated in 5 mM glucose, 30 mM glucose alone, and 30 mM glucose plus either rotenone, thenoyltrifluoroacetone (TTFA), carbonyl cyanide m-chlorophenylhydrazone (CCCP), antisense, uncoupling protein-1 (UCP-1), or manganese superoxide dismutase (Mn-SOD) hemagglutinating virus of Japan (HVJ)-liposomes, and ROS were quantitated. (Reproduced with permission from ref. 111.) Fig. 6. Effect of agents that alter mitochondrial metabolism on hyperglycemia-induced ROS formation in bovine aortic endothelial cells. Cells were incubated in 5 mM glucose, 30 mM glucose alone, and 30 mM glucose plus either rotenone, thenoyltrifluoroacetone (TTFA), carbonyl cyanide m-chlorophenylhydrazone (CCCP), antisense, uncoupling protein-1 (UCP-1), or manganese superoxide dismutase (Mn-SOD) hemagglutinating virus of Japan (HVJ)-liposomes, and ROS were quantitated....

Control of Hyperglycemia

Several studies demonstrate the importance of intensive glycemic control in preventing or reducing microvascular complications of DM. The effect of intensive glycemic control on macrovascular complications in type 1 and type 2 DM is not as convincing. The Diabetes Control and Complications Trial (DCCT) demonstrated compelling evidence in support of a major reduction in chronic micro-vascular complications among type 1 diabetics under tight glycemic control. In the same study, tight glycemic control was associated with a reduction in major macrovascular events by approximately 50 compared with that in those in whom glycemic control was conventional or less stringent. This difference did not achieve statistical significance. Similarly, the United Kingdom Prospective Diabetes Study (UKPDS) has shown that during 10 years of follow-up intensive glycemic control with either insulin or sulfonylureas decreased the risk of micro-vascular complications by 25 in non-insulin-requiring diabetics....

Can hypoglycaemia be avoided by constant high blood glucose levels

Having persistently high blood glucose levels will avoid hypoglycaemia, but unfortunately it dramatically increases the risk ofdeveloping the long-term complications of diabetes. Maintaining the balance between risky hyperglycaemia and troublesome hypoglycaemia can be very difficult for patients on insulin, but is much easier these days with the different preparations and injection devices available. If you are having troublesome hypo attacks, followed by high blood glucose levels, please

What you need to know about high blood glucose

If your blood glucose stays over 180, it may be too high. (See the chart on page 11.) It means you don't have enough insulin in your body. High blood glucose can happen if you miss taking your diabetes medicine, eat too much, or don't get enough exercise. Sometimes, the medicines you take for other problems cause high blood glucose. Be sure to tell your doctor about other medicines you take. If you're very thirsty and tired, have blurry vision, and have to go to the bathroom often, your blood glucose may be too high. Very high blood glucose may also make you feel sick to your stomach. If your blood glucose is high much of the time or if you have symptoms of high blood glucose, call your doctor.

Dealing with Very High Blood Glucose Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a severe diabetic complication that has to be managed in a hospital. It's characterized by high blood glucose (though it need not be very high) associated with an acid condition of the blood due to the production of ketones, which are the products of fat breakdown. The root of the illness is a lack of insulin. Without enough insulin, glucose can't get into insulin-dependent cells like muscle and the liver, so glucose accumulates in the blood, and the body turns to fat for energy.

Preliminary findings from the largestever study of treatments for diabetes provide no evidence that intensive treatment

Interim results from the ADVANCE Study, involving 11,140 high-risk patients with type 2 diabetes, provide no evidence of an increased risk of death among those patients receiving intensive treatment to lower blood glucose (sugar). ADVANCE was designed to answer two questions in patients with type 2 diabetes first, does intensive treatment to lower blood pressure improve outcome and second, does intensive treatment to reduce blood glucose improve outcome. In September 2007, the ADVANCE Collaborative Group published evidence in The Lancet showing that the blood pressure lowering treatment had reduced the death rate among participants. In January 2008, the part of the study designed to assess the effects of the intensive treatment to reduce blood glucose was completed. As in ACCORD, this intensive treatment program was designed to lower blood glucose to levels below those usually recommended by clinical guidelines.

Impaired Glucose Tolerance IGT and Impaired Fasting Glycemia IFG Nondiabetic Fasting Hyperglycemia

Impaired glucose tolerance (IGT) was considered a class in the previous WHO classification but is now categorized as a stage in the natural history of disordered carbohydrate metabolism. A stage called 'impaired fasting hyperglycemia' or impaired fasting glycemia (IFG) or 'non-diabetic fasting hyperglycemia' is now recognized as these people also appear to be at greater risk for progression to diabetes and macrovascular disease, although prospective data are sparse and early data suggest a lower risk of progression than IGT (21). IFG refers to fasting glucose concentrations which are lower than those required to diagnose diabetes mellitus but higher than the 'normal' reference range.

Fetal Complications Secondary to Maternal Hyperglycemia

If the mother has hyperglycemia, the fetus will be exposed to either sustained hyperglycemia or intermittent periods of hyperglycemia. Both situations prematurely stimulate fetal insulin secretion. The Pedersen hypothesis links maternal hyperglycemia-induced fetal hyperinsulinemia to morbidity of the infant (2). Fetal hyperinsulinemia may cause increased fetal body fat (macrosomia) and, therefore, a difficult delivery, or cause inhibition of pulmonary maturation of surfactant and, therefore, respiratory distress of the neonate. The fetus may also have decreased serum potassium levels caused by the elevated insulin and glucose levels and may, therefore, have cardiac arrhythmias. Neonatal hypoglycemia may cause permanent neurological damage. The maternal postprandial glucose level has been shown to be the most important variable to impact the subsequent risk of neonatal macrosomia (5). When the postprandial glucose levels are maintained below 120 mg dL 1 h after beginning the meal, the...

Requirement for Intracellular Hyperglycemia

Clinical and animal model data indicate that chronic hyperglycemia is the central initiating factor for all types of diabetic microvascular disease. Duration and magnitude of hyperglycemia are both strongly correlated with the extent and rate of progression of diabetic microvascular disease. In the Diabetes Control and Complications Trial (DCCT), for example, type 1 diabetic patients whose intensive insulin therapy resulted in HbA1c levels 2 lower than those receiving conventional insulin therapy had a 76 lower incidence of retinopathy, a 54 lower incidence of nephropathy, and a 60 reduction in neuropathy (3). Similarly, several studies have shown that glycohemoglobin A1 is an independent risk factor for cardiovascular disease (6,7) in type 1 diabetes. Intimal-medial thickness (IMT) of the carotid artery, which is strongly correlated with coronary heart disease (CHD), was demonstrated to be increased in type 1 diabetes (8,9). Although all cells in a person with diabetes are exposed to...

Hyperglycemia in Acute Stroke

Background Stroke Stroke and Hyperglycemia Hyperglycemia After Stroke Etiology of Hyperglycemia in Acute (Ischemic) Stroke Admission Hyperglycemia and Clinical Outcome After Stroke Glucose Levels and Lesion Volume How Does Hyperglycemia Affect the Ischemic Brain Treatment of Hyperglycemia Conclusions Recommendations References Hyperglycemia is frequently found (40-60 ) after all kinds of stroke and it has been related to increased lesion size and poor clinical outcome. In this chapter, we will primarily focus on ischemic stroke we will outline the incidence and natural course of post-stroke hyperglycemia and discuss the possible etiologies of post-stroke hyperglycemia. Subsequently, we will present an overview of various mechanisms that could explain how hyperglycemia is detrimental after ischemic stroke. Finally, we will address the question whether inhospital hyperglycemia should be treated in stroke patients, and if so decided, the glucose levels that should be targeted and the...

Hyperglycemia And Proteinuria

The onset of microalbuminuria in patients with type 2 diabetes may be transient and related to increases in glomerular filtration rate in association with hyperglycemia. Albuminuria has been shown to decrease with decreases in glucose levels in patients with newly diagnosed type 1 or type 2 diabetes 4547 . However, other researchers reported no decline in albumin excretion with control of hyperglycemia in patients with newly diagnosed type 2 diabetes 48 . The United Kingdom Prospective Diabetes Study showed that the risk for microalbuminuria was proportional to the level and duration of glucose elevation 49 . Furthermore, in type 1 diabetes the level of glycosylated

Cgm Trend Data Used To Minimize Postprandial Hyperglycemia And Avoid Hypoglycemia

Insulin Pump Catheter

However, patients given real-time access to CGM glucose sensor information have quickly learned to utilize the trend data to minimize postprandial hyperglycemia and avoid hypoglycemia. Most patients have not required extensive education to utilize the real-time BG data safely and effectively (22-24). In a randomized, prospective clinical trial using the Algorithms currently being tested in the research setting, utilize glucose trend data and insulin delivery data to minimize hyperglycemia following consumption of a meal. The CGM system algorithms often consider time since last meal, onset time of current meal, meal size, meal composition, estimated time of gastric emptying intestinal absorption, time dose of previously delivered insulin, time intensity of previous exercise and an estimate of insulin sensitivity (19,20,28-30). Postprandial hyperglycemia can be minimized by injecting rapid-acting insulin into the subcutaneous (sc) tissue 0 to 20 min before a meal. Moderate hyperglycemia...

Riddle Mc Hart J. Hyperglycemia Recognised And Unrecognised As A Risk Factor For Stroke And Transient Ischemic Attacks.

Allport L, Butcher K, Baird T etal. (2004). Insular cortical ischemia is independently associated with acute stress hyperglycemia. Stroke 35 1886-91. Baird TA, Parsons MW, Phanh T etal. (2003). Persistent poststroke hyperglycemia is independently associated with infarct expansion and worse clinical outcome. Stroke 34 2208-14. Gray CS, Hildreth AJ, Alberti KGMM, O'Connell JE on behalf of the GIST Collaboration (2004b). Post stroke hyperglycemia natural history and immediate management. Stroke 35 122-6. Riddle MC, Hart J (1982). Hyperglycemia, recognised and unrecognised, as a risk factor for stroke and transient ischemic attacks. Stroke 13 356-9. Song EC, Chu K, Jeong SW et al. (2003). Hyperglycemia exacerbates brain edema and perihematomal cell death after intracerebral hemorrhage. Stroke 34 2215-20. Woo E, Ma JTC, Robinson JD, Yu YL (1988). Hyperglycemia is a stress response in acute stroke. Stroke 19 1359-64.

Hyperglycemia Causing Cardiac Conduction Defect

Hypoglycemia Schematic Diagram

Chronic exposure to hyperglycemia has long been recognized to be the major cause of vascular disease in diabetes and the severity of microangio-pathic complications is directly related to the quality of glycemic control (14). Conversely, recurrent exposure to hypoglycemia of any severity causes syndromes that are both hypoglycemia-related and impair the capacity of the individual to respond to this metabolic stress, further increasing the risk of severe hypoglycemia and effectively creating a vicious circle that is difficult to break. These syndromes of counterregulatory hormonal deficiencies and impaired awareness of hypoglycemia (IAH) develop over a period of years and ultimately affect a substantial proportion of people with type 1 diabetes and a lesser number with insulin-treated type 2 diabetes. They are considered to be components of hypoglycemia-associated autonomic failure (HAAF), through down-regulation of the central mechanisms within the brain that would normally activate...

Approach To The Surgical Patient With Hyperglycemia

Diabetic and non-diabetic patients develop hyperglycemia during surgery and medical illness due to enhanced hepatic gluconeogenesis, relative insulin deficiency, and decreased sensitivity of the liver, skeletal muscle, and adipose tissue to the actions of insulin (1-3). While clinical evidence suggests a direct association between hyperglycemia and adverse outcome in patients undergoing vascular and cardiac surgery, there is little prospective data available to indicate that glucose control improves outcome in the average hyperglycemic patient undergoing other types of surgical procedures (4-13). The adverse effects of hyperglycemia are mediated in large part by enhanced oxidative stress, which is not counter-balanced by endogenous antioxidants. The optimal range of blood glucose (BG) control in a specific patient population remains controversial. The fear of hypoglycemia (change in mental status, seizure, coma, myocardial ischemia, arrhythmia, and death) dictates the psychology of...

Hyperglycemia Introduction

The current classification of diabetes in different subtypes is based on the defect(s) that causes hyperglycemia, namely, aberrant or deficient insulin secretion or insufficient insulin action (1). Type 1 diabetes (T1D) originates from autoimmune-mediated destruction of the pancreatic P-cells that normally produce insulin, thus resulting in absolute insulin deficiency. Other types of pancreatic disease involving destruction of the P-cells, such as alcoholic pancreatitis, are classified otherwise. Previously, T1D was also known as juvenile-onset diabetes or insulin-dependent diabetes mellitus (IDDM). However, these expressions may result in misclassification and indistinct prognosis and therapeutic options. Criteria to diagnose T1D are shown in Table 1 (1). Note that diagnostic criteria do not include HbA1c levels, which are exclusively used to follow glycemic control, but not diagnosis.

How Does Hyperglycemia Affect The Ischemic Brain

Although an accumulating number of studies have convincingly demonstrated an association between hyperglycemia and poor outcome after stroke, it remains controversial whether this association is causal, i.e., hyper-glycemia is actually causing poor outcome. Hyperglycemia could also be epiphenomenal to a more pronounced stress reaction with higher levels of blood glucose in more severe stroke. Indeed, higher levels of glucose have been associated with more severe stroke (7, 7375). On the other hand, most but not all (30, 76, 77) studies showed that the deleterious effect of hyperglycemia is independent of clinical severity (7, 13, 53, 75, 76). Several (mainly experimental) studies and observations from imaging studies have provided clues as to how impaired glucose metabolism resulting in hyperglycemia and insulin resistance could be detrimental to the ischemic brain. In this context, it is important to realize that the sequence of reactions that occur after arterial occlusion, leading...

Hyperglycemia the Common Factor

The epidemiological attempt to study the natural history and pathogenesis of diabetes as a whole can only rely on one common and stable factor, high blood glucose, despite the wide variation in clinical manifestations and various contributing factors. However, high blood glucose alone does not answer all the questions. Over the past 30 years, evidence has accumulated that numerous and etiologically different mechanisms (genetic, environmental or immunologic processes) may play an important role in the pathogenesis, the clinical course and the emergence of complications of the 'diabetic state' (9,14). Does correction of hyperglycemia prevent all of the various pathologic changes observed with diabetes There is some evidence that people with diabetes who are not treated develop more complications than well-controlled patients (9,15,16). However, there are few instances in which characteristic complications of diabetes have been described before hyper-glycemia was observed. This...


Hyperglycemia has been shown to be the main cause of microvascular complications in the DCCT (11) and UKPDS study (12). For cardiovascular complications, the contribution of hyperglycemia is probably also significant. Several biochemical mechanisms appear to explain the adverse effects of hyperglycemia on vascular cells (Table 3). This is not surprising because the metabolism of glucose and its metabolites can affect multiple cellular pathways. Glucose is transported into the vascular cells mostly by GLUT-1 transporters, which can be regulated by extracellular glucose concentration and other physiological stimulators, such as hypoxia (40). Once glucose is transported, it is metabolized to alter signal transduction pathways, such as the activation of diacylglycerol (DAG) and protein kinase C (PKC), or to increase flux through the mitochondria to change the redox potential (41-44). Lastly, another metabolic pathway (such as that of aldose reductase), which is normally inactive, can be...

Risk Factors For Stroke In Diabetic Subjects

Traditional risk factors for stroke such as arterial hypertension, dyslipi-demia, atrial fibrillation, heart failure, and previous myocardial infarction are more common in people with DM (3, 36). However, the impact of DM on stroke is not just due to the higher prevalence of these risk factors, as the risk of mortality and morbidity remains over twofold increased after correcting for these factors (4, 37). Risk factors for stroke in diabetic patients identified in previous studies are summarized in Table 2. It is informative to distinguish between factors that are non-specific and specific to DM. DM-specific factors, including chronic hyperglycemia, DM duration, DM type and complications, and insulin resistance, may contribute to an elevated stroke risk either by amplification of the harmful effect of other classical non-specific risk factors, such as hypertension, or by acting independently. Age, male sex, arterial hypertension, atrial fibrillation Prior cerebrovascular disorders,...

Diabetes And Dementia

Impairment and Alzheimer's disease (15). Autopsy studies have not confirmed this relationship between Alzheimer's disease and T2DM (23). Therefore, diabetes may increase the risk for serious memory loss, presenting very much like Alzheimer's disease with a different pathophysi-ology than typical Alzheimer's disease. Convergent evidence supports the notion that insulin plays a role in both the beneficial effects of acute hyper-glycemia and the detrimental effects of chronic hyperglycemia on cognition. As we previously noted, an acute rise in plasma glucose is rapidly followed by a rise in plasma insulin. Therefore, the beneficial effects attributed to increased plasma glucose levels may, in part, reflect effects of increased plasma insulin levels. (We will present evidence supporting this possibility in the following section.) However, detrimental effects may follow chronic glucose and insulin elevations. In T2DM, hyperglycemia is produced by two deficits insulin resistance and...

Diabetic Ketoacidosis Definition And Epidemiology

In the absence of insulin, diabetic ketoacidosis (DKA) complicates type 1 diabetes mellitus (T1DM). DKA is defined by a triad of hyperglycemia, ketosis, and acidemia and occurs in the absolute or near-absolute absence of insulin. Acidosis is defined as venous pH < 7.3 or serum bicarbonate concentrations < 18mmol l. Glucosuria, ketonuria, and ketonemia are typically present. Serum glucose concentrations are typically > 13.8mmol l (250 mg dl), but may be normal in select cases of partial treatment or pregnancy (1). DKA predominantly affects those with T1DM, but can occur in type 2 diabetes mellitus (T2DM), especially in African-Americans and other minorities who are newly diagnosed (2-4).

Determinants And Mechanisms

Possible risk factors for changes in cognitive functioning and brain structure in patients with type 2 diabetes include diabetes-specific factors (e.g., hyperglycemia, glucose-lowering therapy, microvascular complications), factors that are linked to diabetes but are not specific to the disease (e.g., hypertension, stroke, depression), genetic factors and demographic, socio-economic, and lifestyle factors (Fig. 2). All of these risk factors may affect cognitive functioning at different times during life span, but there are still relatively few studies that have specifically addressed these risk factors in relation to cognition in patients with type 2 diabetes. Fig. 2. Relation between type 2 diabetes, related risk factors and cognitive decline. It shows a putative course of development for cognitive dysfunction in type 2 diabetes. In our view, impaired cognitive functioning in patients with type 2 diabetes develops against a background of genetic predisposition and socio-economic and...

Relationship Between Depression And Vascular Disease

Chronic pro-inflammatory cytokine activation is also associated with coronary artery syndromes and thought to mediate the relationship between depression and cardiovascular disease, as well as that between cardiovascular disease and diabetes (70, 71). Specifically, interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) increase hyperglycemia and interfere with lipid metabolism. They are important in the pathogenesis of atherosclerosis. As symptoms of stress increase, so does systemic inflammation, increasing cardiovascular risk (72).

Complications Cerebral Dysfunction In

Cerebral abnormalities may occur in the setting of hyperglycemia and ketoacidosis. When compared to those with T1DM and normoglycemia, patients with diabetic ketoacidosis demonstrate increased levels of tryptophan and 5-hydroxyindoleacetic acid in the cerebrospinal fluid (CSF) (21). Plasma tyrosine and CSF tyrosine and homovanillic acid concentrations are typically normal. Similar findings are demonstrated in those with uremia and hepatic encephalopathy, as well as in rodents with diabetes and DKA secondary to streptozotocin administration. Magnetic resonance (MR) spec-troscopy studies in children with DKA have demonstrated possible neuronal injury and or dysfunction. In one study, 29 children underwent MR spectroscopy and were evaluated with brain ratios of N-acetylaspartate (NAA) to creatinine (Cr) during therapy and after recovery from DKA (22). NAA Cr levels were significantly lower during DKA therapy in the basal ganglia suggesting compromised neuronal function.

Identifying Neurocognitive Phenotypes

A very large neuroimaging literature indicates that adults with either type 1 or type 2 diabetes manifest structural changes in a number of brain regions for comprehensive critical reviews see (73, 74) , but until very recently, there had been little pediatric research on this topic. In what may be the largest study to date, MRI scans were acquired from 108 diabetic and 51 age-matched nondiabetic children, 7-17 years of age, and voxel-based mor-phometry techniques were used to quantify between-group differences in gray- and white-matter volumes, and to correlate those values with measures of recurrent severe hypoglycemia and chronic hyperglycemia (75). Although brain volumes were found to be comparable in the two groups, analyses restricted to the diabetic sample showed statistically reliable relationships between metabolic variables and specific brain regions. Compared to those children with no past history of severe hypoglycemia, those who experienced 1 or more episodes of severe...

Methodological Considerations

When studying children with any type of chronic disorder, it is critically important to be able to identify and document, for each child, the nature and extent of their disease process from both a biomedical and a psychosocial perspective. For the diabetic child, we ought to - but hardly ever - have medical, metabolic, and psychosocial data from diagnosis onward. Did the child experience ketoacidosis and or cerebral edema around the time of diagnosis or anytime thereafter Since diagnosis, how often and for what duration did the child experience excessively low - and excessively high - glucose values, and how were these episodes of hypoglycemia and hyperglycemia operationalized When did the child begin to show evidence of microvascular complications and other comorbid conditions like blood pressure elevations, and how did these progress over time How did the child cope psychologically with the diagnosis of diabetes and with diabetes-related events, like the occurrence of a hypoglycemic...

Longterm Complications

The pathogenesis of diabetic complications is multifactorial, complicated, and not yet fully elucidated. In brief, focusing on the role of hyperglycemia, so-called advanced glycation end products (AGEs) and sorbitol are considered to contribute to tissue damage. In addition there may be more tissue-specific factors that contribute to tissue damage, like protein kinase C in the kidney. An overview of current insights into the pathogenesis of long-term diabetic complications is supplied by Michael Brownlee (23).

Prevention Of Stroke In Patients With Dm

Regarding prevention of stroke in patients with DM, it may be less relevant than in non-DM subjects to distinguish between primary and secondary prevention as all patients with DM are considered to be high-risk subjects regardless of the history of cerebrovascular accidents or the presence of clinical and subclinical vascular lesions. However, the aggressiveness of the preventive measures should be most pronounced in those who have DM and history of stroke or TIA. Obvious targets for the prevention of stroke in patients with DM are the correction of DM-specific risk factors, mainly hyperglycemia, and other diabetes non-specific factors, such as arterial hypertension or dyslipidemia. While in most trials addressing the correction of these latter factors the relative risk reduction was similar between patients with or without DM, the absolute risk reduction of stroke was usually higher in those with DM due to significantly higher risk in this subgroup of subjects.

Take other tests for your diabetes Urine tests

You may need to check your urine if you're sick or if your blood glucose is over 240. A urine test will tell you if you have ketones in your urine. Your body makes ketones when there isn't enough insulin in your blood. Ketones can make you very sick. Call your doctor right away if you find moderate or large amounts of ketones, along with high blood glucose levels, when you do a urine test. You may have a serious condition called ketoacidosis. If it isn't treated, it can cause death. Signs of ketoacidosis are vomiting, weakness, fast breathing, and a sweet smell on the breath. Ketoacidosis is more likely to develop in people with type 1 diabetes.

Blood pressure results

High blood glucose can make the blood vessels in the eyes bleed. This bleeding can lead to blindness. You can help prevent eye damage by keeping your blood glucose as close to normal as possible. If your eyes are already damaged, an eye doctor may be able to save your sight with laser treatments or surgery. Too much glucose in your blood is very hard on your kidneys. After a number of years, high blood glucose can cause the kidneys to stop working. This condition is called kidney failure. If your kidneys stop working, you'll need dialysis (using a machine or special fluids to clean your blood) or a kidney transplant.

Pathophysiological Models Are We There

Based on this critical review of the pediatric literature, it should be obvious that we are not yet in a position to make strong statements about the etiology of neurocognitive dysfunction in the child with diabetes. Indeed, only one attempt has been made to address some of those findings, with the diathesis or vulnerability model (50) offering an explanation for why it is that children with an early onset of diabetes seem to be especially likely to manifest significant brain abnormalities. According to this model, in the very young child diagnosed with diabetes, chronically elevated blood glucose levels interfere with normal brain maturation at a time when those neurodevelopmental processes are particularly labile, as they are during the first 5-7 years of life (128-131). The resulting alterations in brain organization that occur during this sensitive period will not only lead to delayed cognitive development and lasting cognitive dysfunction, but may also induce a predisposition or...

Prevention Or Delay Of Type Diabetes

Three recent trials in older adults with T2D have assessed the effect of lowering blood glucose to near-normal levels on cardiovascular risk. First, patients in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial (n 10,251) had a mean age of 62.2 years at entry and 10 years of diabetes duration. Sixty-two percent were men, and 30 had prior macrovascular disease and a baseline median HbA1c level of 8.1 (48). Study patients were assigned to receive intensive therapy (median HbA1c level achieved of 6.4 ) or standard therapy (median HbA1c level achieved of 7.5 ). After a median follow-up of 3.4 years, compared to the standard-therapy group, those in the intensive-therapy group had higher overall mortality (4 vs. 5 ) and cardiovascular mortality (1.8 vs. 2.6 ) and greater-number of hypoglycemic events (1 vs. 3.1 ). Second, patients in the Action in Diabetes and Vascular Disease Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) Study (n 11,140) had a...

Hyperglycemic Hyperosmolar State Definition and Epidemiology

The hyperosmolar hyperglycemic state (HHS) is also an acute complication that may occur in patients with diabetes mellitus. It is seen primarily in patients with T2DM and has previously been referred to as hyperglycemic hyperosmolar non-ketotic coma or hyperglycemic hyperosmolar non-ketotic state (13). HHS is marked by profound dehydration and hyper-glycemia and often by some degree of neurological impairment.

Abduljalil Et Al. 2008 Eur J Pharmacol

Effects of prior hypoglycemia and hyperglycemia on cognition in children with type 1 diabetes mellitus. Pediatric Diabetes 2008 9 87-95. 75. Perantie DC, Wu J, Koller JM, et al. Regional brain volume differences associated with hyperglycemia and severe hypoglycemia in youth with type 1 diabetes. Diabetes Care 2007 30 2331-2337. 115. Malone JI, Hanna S, Saporta S, et al. Hyperglycemia NOT hypoglycemia alters neuronal dendrites and impairs spatial memory. Pediatric Diabetes 2008 9 531-539.

Neurological Complications In

Been at least 12 cases of homonymous hemianopsia reported in patients with hyperosmolar hyperglycemia (64, 71-75). In addition to hemianop-sia, these patients have noted other visual disturbances including blurred or fragmented vision, visual-field hallucinations, and flashing lights (64, 74). MRI findings such as decreased T2 signal of the white matter, subtle gyral swelling, and enhancement of the overlying meninges have been observed in these patients (64). Other studies have reported transient hemianopsia without MRI changes (74). Case reports range from mild improvement to total resolution in visual disturbances after treatment of the underlying hyper-glycemic state (64, 74). In cases of hemianopsia, it is important to consider HHS as the cause when no lesion is detected on MRI. Other visual phenomena reported in patients with HHS include polyopia, flashing and flickering lights, hallucinations, and a persistence and transposition of objects in the visual fields (74).

Esther van den Berg Yael D Reijmer and Geert Jan Biessels

This chapter addresses the effects of type 2 diabetes mellitus on cognitive functioning. It covers the nature and severity of cognitive decrements in relation to diabetes and pre-diabetic stages. Possible risk factors and pathophysiological mechanisms, such as vascular risk factors, hypoglycemia and hyperglycemia, microvascular and macrovascular complications, depression, genetic factors, and lifestyle, will be examined. Moreover, the chapter provides a description of structural changes in the brain, such as infarcts, white-matter hyperintensities, and brain atrophy in relation to diabetes and cognitive

Need For Improving Diabetes Care References

Type 2 diabetes (T2D) is the most common form of diabetes, a metabolic disorder characterized by hyperglycemia resulting from defects in insulin action, insulin secretion, or both. Early diagnosis of T2D and the high-risk category of pre-diabetes may help reduce the associated public health and clinical burden. Available diagnostic strategies include fasting plasma glucose, oral glucose tolerance test, and casual plasma glucose in the presence of symptoms of hyper-glycemia. Potential use of hemoglobin A1c as part of the strategy for screening and diagnosis has been recently proposed. Those with risk factors for T2D should be targeted including patients with overweight obesity, those with family history of T2D, those aged 45 years and older, race ethnic minorities (such as Native Americans, African Americans, Latinos, and Asian Americans), women with history of gestational diabetes, and those with metabolic syndrome abnormalities (high blood pressure, low HDL cholesterol, and high...

Cerebral Edema In Dka Risk Factors

Hyponatremia, hyperkalemia, and uremia have also been associated with cerebral edema in DKA (37). Uremia and hyperkalemia may be reflective of longer illness duration, severity of insulin deficiency, and pre-renal failure states. Glaser et al. found an association with higher initial serum urea nitrogen levels (for each increase of 9 mg dl, RR 1.7, 95 CI 1.2-2.5) and cerebral edema (28). There was no association with the degree of hyperglycemia. Mahoney et al. and Edge et al. also found no association with degree of hyperglycemia (36, 37). In a recently published study, MR diffusion-weight imaging was used to quantify cerebral edema (38). The apparent diffusion coefficients (ADCs) of brain water during and after DKA treatment were compared in 26 children and correlated with clinical and biochemical variables. Serum urea nitrogen levels and initial respiratory rates were elevated. ADC was not correlated with initial serum glucose or sodium abnormalities. Although initial reports...

Biomedical Risk Factors

Three types of diabetes-related biomedical variables have been linked to the appearance of neurocognitive anomalies in children with diabetes moderately severe episodes of hypoglycemia, ketoacidosis, and chronic hyperglycemia. our understanding of these associations remains imperfect, unfortunately, because so few studies have adequately ascertained those biomedical variables in pediatric samples. Rather than capturing most, or even a representative number, of those events over the course of the diabetic child's disease, the best investigators have been able to do is to estimate metabolic control from one or a handful of glycosylated hemoglobin values, count severe hypoglycemic episodes retrospectively (missing virtually all episodes of nocturnal hypoglycemia), and rely on often incomplete medical records or parents' delayed recall to quantify the number, duration, and severity of episodes of ketoacidosis. Diabetic ketoacidosis (DKA) results from an absolute or relative deficiency in...

Glucose Levels And Lesion Volume

Stroke Hyperglycemia

If hyperglycemia is indeed casually related to poor outcome after stroke, one would expect a relation between higher levels of blood glucose and an increased lesion volume. In hemorrhagic stroke, only little is known about the association between glucose levels and the size of the hemorrhage or its evolution during the clinical course. The evidence is limited to experimental settings where it has been shown that hyperglycemia exacerbates brain edema and peri-hematomal cell death after hemorrhagic stroke (56). In patients with ischemic stroke treated with rt-PA, hyperglycemia has been associated with an increased risk of hemorrhagic complications (57-59). In contrast to hemorrhagic stroke, research concerning hyperglycemia and lesion volume after ischemic stroke is much more extensive. Central in the pathophysiology of ischemic stroke is the concept of the ischemic penumbra (Fig. 1C). The penumbra is a rim of tissue surrounding the infarct core that consists of potentially salvageable...

Etiology And Precipitating Factors

Glucose levels rise in the setting of relative insulin deficiency. The low levels of circulating insulin prevent lipolysis, ketogenesis, and ketoacidosis (62) but are unable to suppress hyperglycemia, glucosuria, and water losses. Levels of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone are elevated, increasing gluconeogenic substrates, gluconeogenesis, and glycogenolysis. Meanwhile, glucose utilization is decreased. Glucose levels rise, leading to glucosuria, osmotic diuresis, and dehydration (14). Those patients who are unable to maintain an adequate fluid intake to compensate for the urinary losses, for example, elderly patients, will develop marked hyperglycemia and a hyperosmolar state. Mental status changes are more common in HHS than in DKA because of the greater degrees of hyperosmolarity in HHS (63). HHS typically presents with one or more precipitating factors, similar to DKA. Precipitating factors may include infection,...

Prediabetes And Cognition Prediabetic Stages

Global Atrophy The Brain

Acute rises of peripheral blood glucose and insulin, after, for example, glucose ingestion, may directly influence cognitive performance (see Chapter 18). Indeed, acute improvement of cognitive performance has been reported after ingestion of glucose (39). However, these changes are temporary. The consequences of long-term exposure to elevated blood glucose or insulin levels, which are considered in this chapter, may be quite different.

Medical Complications

Hyperglycemia In the first 12 h after stroke onset, plasma glucose concentrations are elevated in up to 68 of patients, of whom more than half are not known to have diabetes mellitus (53). An initially high blood glucose concentration in patients with acute stroke is a predictor of poor outcome (53, 54). Lowering blood glucose in the acute stage of ischemic stroke has been in only one phase III clinical trial that was terminated prematurely. This trial did not show a benefit on long-term functional outcome of early administration of insulin, but the reduction in serum glucose achieved was only small (55). For more information on hyperglycemia in the acute phase of stroke, the reader is referred to Treatment of Hyperglycemia, Chapter 9.

Depression Treatment Considerations For Diabetic Patients

These agents act by increasing serotonergic functioning, which in turn increases insulin sensitivity and reduces plasma glucose. Most studies have investigated fluoxetine (doses up to 60mg day) and sertraline. Patients' depressive symptoms responded, and they experienced weight loss, decreased fasting plasma glucose, and lowered HgbA1c levels. Cat-echolamines, on the other hand, are associated with insulin resistance and hyperglycemia. Depressed diabetic patients who were administered nor-triptyline, a norepinephrine-reuptake inhibitor, had poorer glycemic control. Other tricyclic antidepressants can increase food cravings, increase weight, and raise serum glucose levels. Because both catecholamines and serotonin have been implicated in diabetic neuropathy, dual-action antidepressants may be the preferred agents, particularly in non-depressed subjects.

After Stroke

A retrospective study by Melamed (7, 15) showed in 1976 that hyper-glycemia after stroke is frequent and relates to the severity of the stroke and in-hospital mortality. Since then many studies have reported similar associations and showed that this association is more pronounced if hyperglycemia persists during the first 24 h (18) or week (50, 51). Fig. 2. Unadjusted relative risk (RR) of in-hospital or 30-day mortality after stroke in patients with stress hyperglycemia compared with those without stress hyperglycemia. In patients without known diabetes the pooled relative risk for ischemic stroke is 3.3 (95 confidence intervals (CI) 2.3-4.6) for hemorrhagic stroke 2.4 (95 CI 0.7-8.73). (From Capes et al. (8). Reprinted with permission from Lippincott Williams & Wilkins.) Fig. 2. Unadjusted relative risk (RR) of in-hospital or 30-day mortality after stroke in patients with stress hyperglycemia compared with those without stress hyperglycemia. In patients without known diabetes the...


There are multiple factors that promote disturbances in carbohydrate, protein, and lipid metabolism that ultimately lead to hyperglycemia and ketosis, the hallmark of DKA. In the absence of insulin, hepatic glucose production increases while glucose utilization in muscle and adipose tissue decreases. increased counter-regulatory hormone concentrations promote further hepatic gluconeogenesis and glycogenolysis. These metabolic processes combined lead to hyperglycemia. Hyperglycemia saturates the renal threshold for glucose reabsorption, causing glucosuria which causes osmotic diuresis, leading to dehydration and electrolyte loss. Hyperosmolarity and impaired renal function (pre-renal failure) may sometimes occur. Insulin deficiency and increased counter-regulatory hormones promote lipolysis, resulting in free fatty acid and glycerol production. Glycerol is used as precursor for glucose production in the process of gluconeogenesis, whereas free fatty acids are used for ketone production...

Background Stroke

Therefore, it remains of major importance to improve the treatment options for patients suffering from a stroke. Modifiable factors, associated with poor outcome after stroke, such as hyperglycemia, have the potential for being new treatment targets. One of the drawbacks when reviewing the literature on hyperglycemia in acute stroke is that the distinction between stroke subtypes is not always clearly defined. Moreover, the definition of hyperglycemia varies substantially from study to study. In this chapter we will mainly focus on hyper-glycemia after ischemic stroke and just briefly discuss about other stroke subtypes. Concerning the definition of hyperglycemia, we adopted the definition used in each separate study.

Subject Index

Acute stroke, hyperglycemia, see Hyperglycemia, in acute stroke ADA, see American Diabetes Association AD Assessment Scale-Cognitive Syndrome (BADS), 86 Behavioral Inattention Test (BIT), 86 Benton Test of Facial Matching, 89 Biomedical risk factors, of diabetic children and adolescents chronic hyperglycemia, 265-266 ketoacidosis, 264-265 psychological stress and mood disorder, 267 (BAEPs), 398, 399 Brain structure and cognitive functioning, in type 2 diabetic patients demographics and lifestyle, 305-306 depression, 309 genetic factors, 304-305 hyperglycemia and hypoglycemia, chronic hyperglycemia, 265-266 ketoacidosis, 264-265 psychological stress and mood 267-268 school performance, 254-256 See also Adults cognitive impairments, T1D Type 1 diabetes (T1D), in children and adolescents Cholecystokinin (CCK), 401 Cholinesterase inhibitors, in dementia treatment, 121, 438 See also Dementia Chronic hyperglycemia, in diabetic children and adolescents, 265-266 See also Type 1 diabetes...


The American Diabetes Association (ADA) diagnostic criteria for diabetes and the two high-risk categories of pre-diabetes, impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), updated in 2003 are defined in Table 1 (1). There are three ways to diagnose diabetes. Because of simplicity of use, acceptability to patients, and low cost, the fasting plasma glucose (PG) is the preferred diagnostic test. In the presence of symptoms of diabetes (polyuria, polydipsia, weight loss, etc.), a casual plasma glucose of greater or equal than 200mg dl is diagnostic. The 75-g oral glucose tolerance test (OGTT) is more sensitive and modestly more specific than fasting PG, but it is less reproducible and less frequently performed in clinical settings. In the absence of unequivocal hyperglycemia, any test used to diagnose diabetes must be confirmed on a subsequent day by a PG measured either in the fasting state or 2 h after an oral glucose load.

Glucose And Memory

In contrast to acute hyperglycemia, chronic hyperglycemia exerts detrimental effects on cognition. T2DM and its precursor, impaired glucose tolerance, are common among aging adults. Adults above age 60 run a one in five chance of having T2DM (8) and a one in three chance of having either impaired glucose tolerance or T2DM (9). Most, though not all, studies have detected cognitive changes associated with T2DM (10-13). In older adults with T2DM, the most common cognitive deficit is a decline in list learning (12) other areas affected by diabetes may include attention, manual dexterity, reasoning, and psychomotor speed (10-13). Furthermore, there is evidence from rodents and humans that abnormal glucoregulation in the absence of diabetes can impair memory and global cognitive functioning (14-16). It is important to note that cognitive deficits associated with diabetes may, in part, be reversible with treatment for diabetes (11,17-19).

Type Diabetes

The two rodent models most commonly used for this kind of study include streptozotocin-induced diabetes in rodents and the spontaneously diabetic BB Wor-rat. The first model develops incomplete insulin deficiency and severe hyperglycemia and is sustained without insulin supplementation. The second model develops acutely an immune-mediated -cell destruction with complete insulin (and C-peptide) deficiency and requires daily insulin supplementation for its survival (see Chapter 16) (36). Hence, the overriding metabolic abnormalities in these type 1 diabetic models are hyperglycemia and insulin deficiency.

And Depression

One view is that depressive symptoms are triggered by the existence of diabetes. Depressive symptoms are associated with biochemical changes related to the diabetes (i.e., hyperglycemia, inflammation, activation of the hypothalamic-pituitary-adrenal axis, stress) and may be important factors in disrupting overall metabolic control (7, 32, 33). Further, the presence of depression and depressive symptoms may present as a result of lifestyle choices (i.e., poor diet, no physical activity) and psychological stress associated with managing the illness that are frequently associated with the presence of diabetes. Treated type II diabetes has been associated with a significantly higher chance of developing depressive symptoms, even after controlling for BMI and co-morbidities (30), and well-functioning older adults with diabetes are at nearly twice the risk of developing depressive symptoms than those without diabetes (34). depression can cause abnormalities in the...


Inhibiting the enzymes that catalyze this process, thereby delaying carbohydrate absorption. Sitagliptin, a dipeptidyl-peptidase (DPP)-IV inhibitor, is an agent that reduces blood glucose with less risk of hypoglycemia. Met-formin is recommended as first choice for pharmacologic treatment and has good efficacy to lower HbA1c by approximately 1-1.5 as monotherapy (57). However, most patients will eventually require treatment with combinations of oral medications with different mechanisms of action simultaneously in order to attain adequate glycemic control. Table 3 lists the available classes of oral antidiabetic medications, their mechanisms of action, and side effects. In addition to hyperglycemia, individuals with T2D often have a constellation of other metabolic abnormalities which increase their CVD risk (60-64). Risk determinants of CVD include the presence or absence of coronary heart disease (CHD), other clinical forms of atherosclerotic disease, and the major risk factors high...

If you smoke quit

Over time, high blood glucose can harm the nerves in your body. Nerve damage can cause you to lose the feeling in your feet or to have painful, burning feet. It can also cause pain in your legs, arms, or hands or cause problems with digesting food, going to the bathroom, or having sex.

Choreiform Movements

Chorea or ballismus has been observed in the hyperosmolar hyperglycemic state (76). In a report of HHS patients presenting with chorea, the mean age was 71.1 years and had a 2 1 ratio of women to men (76). In patients with HHS, choreiform movements are often but not always unilateral and occur concurrent with or shortly after the episode of hyperglycemia (77). Diabetes is usually newly diagnosed in these patients and develops subacutely over days to months (77). In states of hyperglycemia, potential pathological causes of choreiform movements include decreased GABA-enkephalin inhibitory neurons, intracellular acidosis, accumulation of extracellular glutamate, brain edema formation, disruption of the blood-brain barrier, and global decrease in cerebral blood flow (78, 79). Resolution of hyperglycemia and increases in GAB A levels do not always reverse chorea (77, 78). Chronic arteriolar disease and lacunar infarctions have been proposed as a mechanism, but subacute development of...

Inder Nagra 4 Chorea

Cerebral edema in diabetic comas. II. Effects of hyperosmolal-ity, hyperglycemia and insulin in diabetic rabbits. J Clin Endocrinol Metabol 1974 38(6) 1057-1067. 64. Lavin PJ. Hyperglycemic hemianopia a reversible complication of non-ketotic hyper-glycemia. Neurol 2005 65(4) 616-619. 70. Maccario M. Neurological dysfunction associated with nonketotic hyperglycemia. Arch Neu-rol 1968 19(5) 525-534. 71. Harden CL, Rosenbaum DH, Daras M. Hyperglycemia presenting with occipital seizures. Epilepsia 1991 32(2) 215-220. 72. Duncan MB, Jabbari B, Rosenberg ML. Gaze-evoked visual seizures in nonketotic hyper-glycemia. Epilepsia 1991 32(2) 221-224. 75. Seo DW, Na DG, Na DL, Moon SY, Hong SB. Subcortical hypointensity in partial status epilepticus associated with nonketotic hyperglycemia. J Neuroimaging 2003 13(3) 259-263. 76. Oh SH, Lee KY, Im JH, Lee MS. Chorea associated with non-ketotic hyperglycemia and hyperintensity basal ganglia lesion on T1-weighted brain MRI...

Type l Diabetes

Type 1 diabetes is a life long metabolic disorder that is characterized by absolute insulin deficiency resulting in hyperglycemia and lipolysis. Type 1 diabetes accounts for 5-10 of the total diabetes population, the majority of the other patients has type 2 diabetes. Insulin deficiency originates with autoimmune mediated P-cell destruction. Without insulin treatment, type 1 diabetes leads to dehydration and ketoacidosis and can ultimately be fatal. Prolonged exposure to hyperglycemia is responsible for microvascular damage in the eye, kidneys and nervous system and contributes to macrovascular disease of the coronary, cerebral and peripheral arteries. Limited joint mobility and the diabetic foot are other complications related to chronic hyperglycemia. currently, the corner stone of the treatment of type 1 diabetes is exogenous insulin substitution aiming to restore near-normal glycemia in order to prevent or delay long-term complications. Recurrent hypoglycemia is a frequent...

Nicotinic Acid and Niacin

Traditionally, diabetes has been regarded as a relative contraindication to the use of niacin secondary to its worsening effect on glucose homeostasis. There are case reports of severe hyperglycemia resulting from use of niacin (41). Most recent studies have shown that hyperglycemic effect of niacin is dose-dependent (42). Severe hyperglycemia with niacin use is seen mostly in patients with established glucose intolerance or with a diagnosis of diabetes (43). The higher use of niacin in non-insulin-dependent diabetic patients has resulted in 16 increase in plasma glucose levels and a 21 increase in glycosylated hemoglobin levels (44). Mechanism of niacin-induced hyperglycemia appears to be an increased hepatic glucose output due to enhanced gluconeogensis, secondary to rebound increase in the flow of free fatty acids (FFA) to the liver (45).

Possible mechanisms of impaired endotheliumdependent vasodilation

Although the data are conflicting, overwhelming evidence presently suggests that DM is associated with an impairment of endothelial vasodilation. The mechanism(s) for this impairment is even less well understood. The most likely initial insult is hyperglycemia. Tesfamarian and colleagues took normal rabbit aortic rings and exposed them to high concentrations of glucose (up to 800 mg dL for 3 hours), resulting in a decrease in endothelium-dependent relaxation, in response to acetylcholine and ADP (52,53). This effect appears to be both concentration and time dependent. As stated earlier, this effect does not appear to be a result of the hyperosmolar effects of glucose because mannitol did not cause any such endothelium-dependent vasodilation (53). Bohlen and Lash (73) demonstrated that hyperglycemia at 300 and 500 mg dL suppressed the vasodilatory response to acetylcholine but not to nitroprusside. Similarly, Williams and colleagues (68) found that acute hyperglycemia attenuated...

Protein Kinase C Inhibitors

Hyperglycemia can activate PKC, which in turn increases oxidative stress. Inhibitors of PKC can restore vascular function and also increase mRNA expression of eNOS in aortic endothelial cells (143). Recently, an inhibitor of PKC, LY333531, has been developed it normalizes retinal blood flow and glomerular filtration rate in parallel with inhibition of PKC activity (169). LY333531 is discussed in detail in Chapter 2. Beckman and colleagues (170) found that this inhibitor of PKCP attenuated the impairment of endothelial-dependent vasodilation on healthy human subjects exposed to hyperglycemia.

Selected Metabolic Aspects Of Diabetesg

Most medical students and physicians. However, hyperglycemia is simply the tip of if not decades, before hyperglycemia becomes evident. As compensatory pancreatic subsequently absolute insulin deficiency occurs resulting in clinical hyperglycemia. Consequently, the signs and symptoms of polyuria and polydipsia become apparent associated with elevated HbAlc and exacerbation of hyperlipidemia. Acetyl CoA is an allosteric inhibitor of pyruvate dehydrogenase. Thus, glucose oxidation diminishes when FFA oxidation is excessive. The decreased glucose oxidation leads to accumulation of citrate, an inhibitor of a rate-limiting enzyme in the glycolytic pathway, fructose 1, 6, phosphatase. Glucose-6-phos-phate concentrations consequently increase. This, in turn, diminishes the uptake of glucose contributing to hyperglycemia as does the decreased glycogen synthe-tase activity in skeletal muscle and decreased glucose transport in the same tissue. Beta-cell exhaustion is known to be potentiated by...

Microvascular complications

Microvascular complications are specific for diabetes and are almost certainly related to hyperglycemia (see Figure 5.1). Hyperglycemia leads to multiple biochemical changes, some of which are listed in Figure 5.2, that cause tissue damage 1, 2 . These lead to changes in various organs as summarized in Figure 5.1. Most of these changes can be prevented by good glycemic control which prevents the development of the complications and slows their progression 3 . Hyperglycemia Kidney

Rationale For Control Of Blood Glucose

Normal metabolism should be mimicked as closely as possible. Therapeutic goals include the avoidance of hypoglycemia, hyperglycemia, lipolysis, ketogenesis, proteolysis, dehydration, and electrolyte imbalance. Type 1 diabetic patients should receive a continuous supply of insulin to avoid ketosis. Sufficient insulin should be supplied to counterbalance the hyperglycemic effects epinephrine, norepinephrine, cortisol, glucagon, and growth hormone (1,4,7). High rates of glucose infusion often exceed the body's ability to utilize glucose and cause hyperglycemia in both diabetic and non-diabetic surgical patients.

Prevention Of Tissue Damage And Complications

There appear to be several approaches to preventing or slowing the progression of complications associated with T1D. In this chapter, we have highlighted the research on hy-perglycemia as the number one culprit in the development of long-term complications. However, as we have demonstrated, the etiology of hyperglycemia is multifactorial. In addition, once hyperglycemia is present, the molecular pathways that ultimately lead to complications are varied and may or may not rest on a unifying link. Taken together, our chapter highlights that multiple methods are necessary in order to prevent the long-term complications commonly associated with T1D. One method concerns a focus on stopping hyperglycemia before it happens by identifying the risk across multiple factors (e.g., genetics, lifestyle, and emotional factors) and intervening early, before these factors can cause prolonged hyperglycemia. A second method is aimed at attacking hyperglycemia on the molecular level through novel...

When Does Endothelial Dysfunction Occur In Diabetes

In type 1 diabetes, ED precedes and may cause diabetic microangiopathy, but it is not clear whether hyperglycemia is a sufficient cause of ED (30-36). In our view, it is more likely that hyperglycemia predisposes to the development of ED and that other factors, genetic or environmental, play a role in determining who among type 1 diabetic patients goes on to develop ED, nephropathy and aggressive angiopathy, and who does not. In type 2 diabetes, ED is present from the onset of the disease and is strongly related to adverse outcomes (4,16). Type 2 diabetes mostly occurs in the setting of the metabolic syndrome, but ED in type 2 diabetes is not explained by hypertension, obesity, or dyslip-idemia (37). It is not clear whether this diabetes-specific ED is caused by hyperglycemia or other factors. An important potential determinant is increased inflammatory activity (Fig. 1). In addition, part of the ED in type 2 diabetes may be primary, i.e., cause of diabetes rather than caused by...

Different Pathogenic Mechanisms Reflect A Single

Although specific inhibitors of aldose reductase activity, AGE formation, and PKC activation each ameliorate various diabetes-induced abnormalities in animal models, there has been no apparent common element linking the four mechanisms of hyper-glycemia-induced damage discussed in the preceding section (88,107-110). This issue has now been resolved by the recent discovery that each of the four different pathogenic mechanisms reflects a single hyperglycemia-induced process overproduction of superoxide by the mitochondrial electron transport chain (111,112). Hyperglycemia increases reactive oxygen species (ROS) production inside cultured bovine aortic endothelial cells (113). To understand how this occurs, a brief overview

Diabetes treatment options

Diabetes physicians have traditionally focused on treatments to reduce hyperglycemia. Good evidence from randomized, controlled trials now indicates that reducing hyperglycemia reduces the risk of microvascular complications of diabetes.4655 Subjects with diabetes also carry at least a doubling of risk of cardiovascular disease.56 Whether lowering glucose improves cardiovascular risk is currently uncertain, but the effect, if present, is likely to be modest.4656-59 Potential treatments for lowering glucose in diabetes mellitus will be considered here in a rather theoretical way because this may illuminate the mechanisms by which some of the evaluated plant treatments have an effect (Table 1.3).

Prevention And Treatment Strategies

Significant progress has been made in recent years in understanding the pathophysiology, prevention, and treatment of diabetic nephropathy. Median survival after the onset of nephropathy has increased from 6 to 15 years (56). The basis for the prevention of diabetic nephropathy is the treatment of its known risk factors hyperglycemia, hypertension, smoking, high protein diet, and dyslipidemia (Table 1).

Relationship of Depression to Medical Outcomes

Of further concern is the relationship between comorbid depression and medical outcomes among those with DM1. Several studies have investigated the influence of depression on glycemic control and other adherence measures. Studies have found that individuals with DM and a history of depression showed significantly worse glycemic control as measured by glycosylated hemoglobin (18,27,28). Additionally, afew meta-analytic studies now exist and have shown a significant relationship between depression and poorer metabolic control among those with both DM1 and DM2 (29,30). Not surprisingly, depression has also shown a relationship to greater complications of persistent hyperglycemia (31). Inquiry continues regarding the exact nature of this relationship between depression and hyperglycemia. One study sought to determine whether depression induced a decrease in diabetes self-care and whether changes in self-management mediated the relationship between depression and hyperglycemia. Although...

Impact On Cardiovascular Disease The Dcct And Ukpds Studies

Clinical atherosclerosis results largely from acute embolic or thrombotic events that arise from long-term changes in the arterial wall. The pathogenesis of the arterial wall changes in relation to the metabolic abnormalities that attend poorly controlled diabetes are not well known in humans. Epidemiological studies indicate that both hyperglycemia and hyperinsulinemia increase the risk of atherosclerosis and of the acute clinical complications of that condition. The high triglyceride and low HDL cholesterol concentrations that frequently attend hyperglycemia may contribute as well. Animal studies suggest that good blood glucose control can mitigate the effects of diabetes on the arterial wall. Cross-sectionally, worsening glycemia is associated with thickening of the intima and media layers of the common carotid arteries. Intervention studies to test the impact of improved glycemic control on this or other measures of atherosclerosis are lacking. However, there is mounting evidence...

Cardiovascular Disease in Women with Diabetes

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in women in the USA. Women with diabetes are at a greater risk of CVD than men with diabetes. In this chapter we review the various mechanisms by which hyperglycemia potentiates this increased CVD risk, including coagulation abnormalities as well as endothelial dysfunction. Where applicable, sex-specific differences in these mechanisms are highlighted. Finally, the impact and burden of diabetes on CVD as well as screening for CVD in women are discussed. Key words Diabetes mellitus Coagulation abnormalities Hyperglycemia Endothelial dysfunction Insulin resistance Oxidative stress Metabolic syndrome Cardiovascular disease Sex differences.

Therapeutic Potential Of Hgf In Diabetic Nephropathy

Given that a loss in endogenous HGF production by hyperglycemia may be causative for the histological and clinical manifestations of diabetic renal disease, administration of exogenous HGF (or its gene) would inhibit or reverse the progression of diabetic renal injury. Using a model of DN, we obtained evidence that HGF may be a therapeutic factor for inhibiting TGF-P upregulation and renal fibrosis. We will discuss herein the relationship among molecular, histological, and clinical changes to understand the therapeutic effect of HGF in DN.

Higher Weight Gain Between HD Sessions and Volume Overload

Diabetic patients were reported to gain 30-50 more interdialytic weight than nondiabetics (12), and increased interdialytic weight has been independently associated with decreased survival of diabetic ESRD patients treated with HD (37). The underlying mechanism is unclear and it might be correlated with the degree of hyperglycemia (38) or a higher intracellular sodium content producing increased thirst and further water intake (39). The resulting volume overload requires further UF, which results in both hypotensive episodes and painful muscle cramps.

Maturityonset Diabetes Of The Young

Maturity-onset diabetes of the young (MODY) is an early-onset inherited form of diabetes, caused by defects in P-cell function. It was first described in a large family with autosomal dominant inheritance (1), and, subsequently, different genetically defined subgroups have been identified (2). Mildly elevated hyperglycemia may be asymptomatic and patients may be identified during intercurrent illness or on screening during pregnancy (3). The criteria for diagnosis (2) are as follows

Recognizing when you need islet transplantation

The indications for islet transplantation are the same as those for whole pancreas transplantation The patient suffers from debilitating hypoglycemia or hyperglycemia or has significant complications of diabetes. If you want to join a clinical trial, you'll be fully evaluated by a doctor before undergoing the procedure.

Exercise and Appetite

In general, exercise neither stimulates nor suppresses appetite. In uncontrolled patients with diabetes or impaired glucose tolerance, by enhancing insulin activity, particularly in the postprandial period, glycemic excursions are reduced, and these excursions can play a role in stimulating appetite. For those with postprandial hyperglycemia, a brisk walk 1-2 h after eating can enhance glycemic control. In fact, exercising in a fasting state may result in increased eating after the workout, thus these individuals would be better advised to pursue the postprandial exercise approach.

AGlucosidase inhibitors

Acarbose and miglitol are the two agents in the a-glucosidase inhibitor (AGI) class of antihyperglycemic compounds. AGIs reduce the rate of digestion of polysaccharides in the proximal small intestine. When used before meals, they delay the absorption of complex carbohydrates and blunt postprandial hyperglycemia, resulting in modest reductions in A1C. They are not associated with weight changes or hypoglycemia. AGIs are infrequently used in the USA. The main limitations to their widespread use are the need for frequent dosing, poor tolerability due to frequent gastrointestinal side effects, and only modest antihyperglycemic effects.

Defective Insulin Secretion

The b-cell mass may be altered in the offspring of mothers with diabetes, dependent on the severity of the hyperglycemia. From animal studies, moderate maternal hyperglycemia has been demonstrated to increase proliferation of b cells, leading to enhanced b-cell mass. Severe hyperglycemia in sheep, on the other hand, is associated with degranulation of the b cell, decreased insulin content and reduced glucose-stimulated insulin secretion (72). Pancreatic angiogenesis and innervation may also be affected by maternal diabetes in utero. Pancreatic islet development is dependent on a number of growth factors, and vascularization of the islet cells is controlled by vascular endothelial growth factors (VEGFs) expressed by newly differentiated islet cells. Reduced angiogenesis in response to excess maternal fuels is a possible mechanism for reduced b-cell mass, since pancreatic growth is dependent on adequate vascularization. VEGF is regulated by glucose, and there is evidence from animal...

Alpha Glucosidase Inhibitors

Alpha-glucosidase inhibitors (AGI), including miglitol and acarbose, work by inhibiting enzymatic degradation of complex carbohydrates, thus slowing their intestinal absorption. The effect of AGI is essentially limited to reduction of postprandial hyperglycemia, but this may be sufficient for some older patients with mild diabetes. However, many older patients are intolerant to the gastrointestinal side effects (bloating, flatulence), which may limit the drug's usefulness. AGIs have also been reported to reduce the development of diabetes in a middle-aged high-risk population with IGT (60), but effectiveness among older patients has not been reported.

Calcium Channel Blockers CCBs

Insulin release from pancreas depends on an increase in cytosolic calcium in vitro (34) and CCBs have been used in the treatment of insulinoma (35). It appears that induction of glucose intolerance by CCBs is dose-dependent and clinically used dosages do not pose any majorthreat, though few reports implicate therapeutic use of verapamil with marked hyperglycemia (36).

Advanced Glycation Endproducts And Diabetic Renal Disease

Prolonged hyperglycemia and oxidative stress in diabetes result in the production and accumulation of advanced glycation end products (AGEs) 1 . AGEs are formed via the Maillard or 'browning' reaction between reducing sugars and amine residues on proteins, lipids or nucleic acids. Under normal circumstances, this reaction is slow, meaning that AGE-modification predominantly occurs in long-lived molecules such as collagen and lens proteins 1 . The degree of AGE-modification therefore represents one mechanism to judge the 'age' of a molecule allowing the recognition of senescent targets for excretion or catabolism 2 . In addition, as molecular turnover is reduced with increasing chronological age 3 , the amount and variety of AGE-modified tissue increases, contributing to many of the changes recognised as signs of ageing (such as cataracts and stiffness). In diabetes, prolonged hyperglycemia and oxidative stress hasten the formation of AGEs 4 , meaning not only that long-lived proteins...

David J Schneider and Burton E Sobel

Optimal treatment of patients with diabetes requires an understanding of the mechanisms underlying the disease. Treatment must be designed not only to control hyperglycemia but also to prevent or retard complications that result from diverse processes underlying the development of diabetes. This chapter will focus on the therapeutic promise of elucidation of such processes and their cardiovascular consequences. All diabetic subjects exhibit hyperglycemia. Yet hyperglycemia is only the tip of an iceberg of abnormalities in carbohydrate, lipid, and protein metabolism. Although insulin deficiency is the hallmark of type 1 diabetes, 90 of diabetic subjects suffer from type 2 diabetes, a disorder of dysinsulinemia. For decades before its onset, insulin resistance and compensatory increases in the concentration of insulin and its precursors in blood are present, particularly postprandially. Impaired glucose tolerance occurs eventually as compensatory mechanisms fail. Early treatment may...

Drug Therapy for Advanced Diabetics

Some people, however, will not have the benefit of this knowledge before their type-2 diabetes advances to a more dangerous stage. In severe hyperglycemia, the pancreas becomes burned out after producing high levels of insulin for a long time. Insulin levels drop as a result of decreased production, and blood glucose levels are allowed to rise to very high, toxic levels. Although diet and exercise, along with supplementation, are still strongly recommended, a number of prescription drugs might also be necessary. Sulfonylurea drugs stimulate pancreatic secretion of insulin. Unfortunately, they are often prescribed as first-line treatment for mild to moderate type-2 diabetics, even when their use is inappropriate. By increasing levels of insulin, which are already raised, sulfonylurea drugs actually hasten the progression of early type-2 diabetes by exhausting insulin receptors faster, which causes the pancreas to burn out more quickly. Sulfonylurea drugs should really be considered a...

Microvascular Disease

To better understand the rationale for glucose control it is useful to review the role of hyperglycemia in the development of the long-term microvascular complications. After the discovery of insulin it was noted that patients with insulin-dependent diabetes who lived longer tended to develop retinopathy. It was not clear at the time as to whether these were usual changes of the disease or whether they were related to the level of hyperglycemia. Early pathological studies in animals indicated a relationship between elevated blood glucose levels and retinopathy. Currently a number of different mechanisms have been implicated in the pathogenesis of the microvascular disease and this has been studied extensively in diabetic retinopathy and nephropathy. Chronic duration of the disease, a number of metabolic abnormalities including hyperglycemia, and genetic factors all play a role in causing the microangiopathy. Diabetic retinopathy has been most thoroughly studied because it is one of...

Involvement Of Pkc In Renal Hemodynamics

With glomerular hyperfiltration 36, 37 . We have reported that the possible overproduction of glomerular PGE2 in the glomeruli of diabetic rats could be due to an enhanced synthesis of arachidonic acid via the activation of cytosolic phospholipase A2 (cPLA2) by PKC since specific inhibitor of PKC-P isoform was able to decrease PGE2 and arachidonic acid release by hyperglycemia 30 . Haneda et al. have found that the increase in mitogen-activated protein kinase (MAPK) activity, which was dependent on diabetes-induced activation of PKC pathway, was able to enhance cPLA2 activity, resulting in increase in arachidonic acid release in glomerular mesangial cells exposed to elevated glucose levels 38 . Williams et al. have also reported similar findings showing that PKC activation by glucose increased PGE2 production through cPLA2 and it was normalized in the presence of general PKC inhibitors such as H-7 or staurosporine in glomerular mesangial cells 6 . These results strongly support that...

Oxidative and Nitrosative Stress in Diabetes Induced Vascular Dysfunction

Superoxide anion may quench NO, thereby reducing the efficacy of a potent endothe-lium-derived vasodilator system that participates in the homeostatic regulation of the vasculature, and evidence suggests that during hyperglycemia, reduced NO availability exists (64). Hyperglycemia-induced superoxide generation contributes to the increased expression of NAD(P)H oxidase, which in turn generate more superoxide anion. Hyperglycemia also favors, through the activation of NF-kB an increased expression of iNOS, which may increase the generation of NO (65,66). Superoxide anion interacts with NO, forming the strong oxidant peroxynitrite (ONOO-), which attacks various biomolecules, leading to among other processes the production of a modified amino acid, nitrotyrosine (67). Although nitrotyrosine was initially considered a specific marker of peroxynitrite generation, other pathways can also induce tyrosine nitration. Thus, nitrotyrosine is now generally considered a collective index of reactive...

Renal disease microalbuminuria proteinuria and nephropathy Reduced development of coronary collateral vessels

Recent data shown that the prevalence of DM or impaired glucose tolerance (IGT) may be as high as 70 in patients who have AMI 19 . In 181 consecutive nondiabetics who had AMI, more than two thirds of patients were diagnosed with DM or IGT by oral glucose tolerance testing. Previously undiagnosed DM accounted for one half of all patients who had AMI and an abnormal glucose metabolism. Only one third of subjects met criteria for DM based on fasting blood glucose criteria. Although a random blood glucose at the time of admission for AMI may not be reliable in making the diagnosis of DM, concern that the diagnosis of IGT or DM is erroneous in the acute setting because of stress hyperglycemia may be unwarranted the results of glucose tolerance testing that was performed at the time of AMI were similar to those performed 3 months later. Two recent studies in patients who presented for coronary angiography similarly showed that previously undiagnosed DM or IGT was present in up to two thirds...

Features of Diabetic Macrovascular Disease

Unlike microvascular disease, which occurs only in patients with diabetes, macrovascular disease resembles that in subjects without diabetes. However, subjects with diabetes have more rapidly progressive and extensive cardiovascular disease, with a greater incidence of multivessel disease and a greater number of diseased vessel segments than nondiabetic persons (20). In both subjects with and without diabetes, atherosclerosis begins with endothelial dysfunction that results from injury caused by many factors, including hyperglycemia (21). Endothelial injury increases the adhesiveness of the endothelium with respect to leukocytes and platelets, as well as its permeability to lipoproteins and other plasma constituents. A number of studies have shown that elevated glucose levels and or glucose-derived advanced glycation end products (AGEs) induce the expression of monocyte chemotactic protein 1 (MCP-1) (22) and adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and...

Introduction And Background

Type 1 diabetes mellitus (T1DM) is characterized by defects in beta-cell function that eventually result in absolute insulin deficiency, requiring insulin replacement therapies to ensure survival and limit the complications of hyperglycemia. Type 1A or autoimmune diabetes, which accounts for 85 to 90 of T1DM, is characterized by the presence of autoantibodies to several islet cell molecules, including insulin, GAD, and IA-2, as well as by infiltration of the islets and destruction of beta cells by mononuclear cells (insulitis). Although the presence of insulitis requires a tissue specimen for diagnosis, autoantibodies on the other hand can be measured from serum and are detectable years prior to the onset of hyperglycemia. Along with genetic screening and assessment of stimulated insulin secretion, autoantibodies can also be used to predict the development of T1DM in at-risk populations. Although there is a 10- to 15-fold increase in the lifetime risk of developing the disease for...

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