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Section I Oxidative Stress Metabolic Syndrome Obesity Diabetes and Uncoupling Proteins

The Metabolic Syndrome The Metabolic Syndrome The Question of Balance between the Pro-Inflammatory Effect of Macronutrients and the Anti-Inflammatory Effect of Metabolic Syndrome Due to Early Life Nutritional Modifications 47 Obesity, Nutrigenomics, Metabolic Syndrome, and Type 2 Diabetes 107

The Metabolic Syndrome in PCOS

Due to the high prevalence of insulin resistance in PCOS, some recent studies used the NCEP ATP III criteria to assess the prevalence of the metabolic syndrome in PCOS women. Glueck et al. (95) studied 138 PCOS patients and found a prevalence rate of 46 , whereas, more recently, Apridonidze et al. (82) found a prevalence of 43 by retrospectively reviewing the medical charts of 106 PCOS women attending the Endocrine Clinic of Richmond, Virginia. Both these studies, therefore, described a prevalence of the metabolic syndrome in PCOS women nearly twofold higher than that reported in the general population investigated in the cited NHANES III report (96), matched for age and body weight. Apridonidze et al. (82) also described higher free testosterone and lower SHBG levels in those women with the metabolic syndrome compared with those without it, as well as a higher prevalence of acanthosis nigricans and a tendency toward a greater family history for PCOS. These results were in accordance...

Metabolic Syndrome and Risk of Prostate Cancer

MeS was found to predict prostate cancer during 27 years of follow-up, indicating an association between insulin resistance and the incidence of prostate cancer 33 . Features of the MeS, specifically abdominal obesity and hypertension, are also associated with prostate cancer in African-American men 34 , a population which is more prone to developing MeS symptoms.

Why Diabetes and Metabolic Syndrome Matter

The ultimate impact on health of type 2 diabetes and metabolic syndrome is through cardiovascular disease. The cluster of features associated with type 2 diabetes or the metabolic syndrome is a highly potent recipe for heart disease and stroke. People with type 2 diabetes or the metabolic syndrome have at least a two-to fivefold increased risk of cardiovascular disease. The relative risks are even higher in women with diabetes compared with their counterparts who are nondiabetic. In addition, in the United States, type 2 diabetes is the major cause of blindness, kidney failure, amputations, and neurological complications, such as impotence. Type 2 diabetes decreases life span by an average of seven to twelve years.

Metabolic syndrome definitions

In 1998, the WHO proposed a set of criteria11 to define metabolic syndrome. Its definition required the presence of insulin resistance as a component of the diagnosis. Insulin resistance was defined as the diagnosis of type 2 diabetes mellitus, impaired fasting glucose, impaired glucose tolerance or, for those with normal fasting glucose levels (< 100 mg dL), glucose uptake below the lowest quartile for the background population under investigation under hyperinsuline-mic, euglycemic conditions. In addition to the presence of insulin resistance, the WHO criteria require the presence of two additional risk factors that may include hypertension or treatment with antihypertensive medications, hypertriglyceri-demia, low HDL cholesterol, BMI > 30 kg m2, and urinary albumin excretion rate > 20 ag min (Table 1.1). In 2001, the National Cholesterol Education Program (NCEP) introduced definitions of metabolic syndrome, a constellation of major risk factors, life-habit risk factors, and...

Central Visceral Obesity

Central obesity (obesity localized to central visceral fat depots) is the most prevalent precursor of Type 2 diabetes mellitus (Ohlsson et al 1985). Insulin resistance, which is more prominent in visceral obesity than generalized obesity or that localized to peripheral gluteofemoral depots, is considered to be related to this pattern of obesity (Peiris et al 1986). Free fatty acids have been implicated in the pathogenesis of insulin resistance in muscle through their interface with critical steps in glycolysis. Muscle tissue is the main regulator of systemic insulin sensitivity (Bjorntrop and Rosmond 1999). Compared with subcutaneous fat, visceral fat has increased sensitivity to lipolytic stimuli and has decreased antilipolytic effects to insulin. This means that the potential per unit mass of visceral adipose tissue to mobilize free fatty acid is much larger than that of subcutaneous fat (Bjorntrop 1994). Acute reductions in caloric intake has been shown to improve insulin...

Whole body fat distribution subcutaneous and visceral fat

Even though the total fat mass determines the plasma pool of FFA and thereby the FFA flux from adipose to non-adipose tissue (Lewis et al. 2002), there are differences in the relationship of subcutaneous and visceral fat depots to features of peripheral and hepatic insulin sensitivity (Misra et al. 1997). Visceral fat cells are more sensitive than subcutaneous fat cells to the lipolytic effect of catecholemines and less sensitive to the antilipolytic and fatty acid re-esterification effects of insulin (Kahn & Flier 2000). Furthermore, the venous effluent of visceral fat depots leads directly into the portal vein, resulting in greater FFA flux to the liver. This makes the visceral fat depots more efficient than subcutaneous fat in influencing the carbohydrate metabolism in the human body (Kissebah 1996). Whole-body MRI and CT are the methods of choice for the quantitation of visceral fat accumulation and whole-body fat distribution. Their noninvasive nature and easy-to-follow...

The Metabolic Syndrome CardiovASCuLar Risk Factors And Cardiovascular Events In Women

In 1988, Reaven proposed that individuals who displayed the cluster of abnormalities associated with insulin resistance and compensatory hyperinsulinemia were at significant risk for CvDs (10). Over the last 15 years, the concept underlying the common aggregation of major abnormalities associated with an insulin-resistant state has emerged as a unique entity, the so-called metabolic syndrome. Although there is a concept that insulin resistance is ontologically different from the metabolic syndrome, for many years these two expressions have nonetheless often been used more or less synonymously. This issue is, however, a matter of great controversy at the present time. One of the reasons is certainly represented by the difficulty of measuring the insulin resistance state and the need for more reliable parameters defining the risk for CVD. The need to simplify the definition of the metabolic syndrome for epidemiological studies contrasts with the complexity of the geographical and...

How The Definition Of The Metabolic Syndrome Oyerlaps That Of Insulin Resistance

As reported above, the NCEP ATP III report designated a cluster of related CvD risk factors as a definition of the metabolic syndrome, and stated that this syndrome is closely linked to insulin resistance (25). Insulin resistance and or compensatory hyperinsulinemia are undoubtedly CVD risk factors (10). On the other hand, although insulin resistance is believed to be the basic pathophysiological alteration leading to the metabolic syndrome, neither assessment of insulin resistance nor hyperin-sulinemia were among the criteria proposed by the NCEP ATP III report. This omission was justified by the lack of adequate sensitivity and specificity of the different insulin assays used in clinical practice and other potential limitations. This is of importance, because there are patients with the metabolic syndrome who are unlikely to have insulin resistance and vice versa (35). There are several other considerations emphasizing why different definitions of the metabolic syndrome and of the...

Metabolic Syndrome and Risk of Colorectal Adenoma Development

Two Asian-Pacific Epidemiologic Studies showed an increased risk of colorectal adenoma development associated with MeS (1) the Self-Defense Forces Health Study, carried out between 1995 and 2002 at two Self Defense Forces hospitals in Japan 44 and (2) one study carried out at the Center for Health Promotion, Samsung Medical Center, Seoul, Korea, between March 2004 and December 2005 45 . Both studies included subjects who underwent colonoscopy as a screening examination for polyps. Apart from the association of MeS with colorectal adenoma, an increased risk for MeS was more evident for proximal than distal colon, for multiple ( 3), and for advanced adenoma. Abdominal obesity of the individual components of MeS was an important risk factor for colorectal adenoma. Thus, the MeS appears to be a crucial entity with regard to the prevention of colorectal adenoma and consequently colorectal cancer.

The metabolic syndrome and cardiovascular risk

The DECODE study group have undertaken similar studies in the metabolic syndrome in an attempt to clarify its prevalence and also to define its relationship with cardiovascular mortality. Using a modification of the WHO definition of the metabolic syndrome and excluding patients with diabetes, the non-diabetic adult prevalence of metabolic syndrome in Europeans was found to be 15.7 in males and 14.2 in females. Over a median follow-up of 8.8 years the hazard ratio for all-cause and cardiovascular mortality was 1.44 and 2.26 in men and 1.38 and 2.78 in women, respectively, after adjustment for age, cholesterol and smoking status (Hu etal.,2004). Interesting comparisons between the cardiovascular risk associated with the diagnosis of the metabolic syndrome have been made. While there is no doubt that the application of both sets of criteria identifies at-risk individuals, there remains debate about the best method of factoring insulin resistance as a discrete variable. Insulin...

Prevalence of the metabolic syndrome

As is the case for the diagnosis of diabetes, the application of different diagnostic criteria for the metabolic syndrome results in differing figures of prevalence and the identification of different individuals. It is still too early to see how the new IDF definition of the metabolic syndrome will fare, but application of the NCEP ATPIII and WHO diagnostic criteria to individuals aged > 20 years in the National Health and Nutritional Examination Survey (NHANES) cohort resulted in an age-adjusted prevalence of 23.9 and 25.1 , respectively. Particular differences were noted in the prevalence for certain subgroups, such as African-American males, in whom the WHO estimates were higher (Ford and Giles, 2003). An earlier study by the same authors, using the NCEP ATPIII criteria, had estimated similar overall prevalence figures (though as high as 43.5 in the 60-69-year age group), and suggested that this translated to 47 million US residents using the 2000 census data (Ford etal., 2002)....

Metabolic Syndrome as a Link between Insulin Resistance and CVD

Metabolic syndrome refers to a constellation of risk factors that is apparently associated with risk for both CVD and type 2 diabetes (Figure 2.7). Although a clustering of risk factors had been recognized as early as the 1920s, Gerald Reaven's Banting lecture in 1988 (Reaven, 1988) disseminated the concept to a wider audience and stimulated considerable further research. Reaven linked 'upstream' insulin resistance to a 'downstream' clustering of risk factors potentially responsible for the excess vascular risk in diabetes. He included glucose intolerance, hypertriglyceridaemia, low HDL-cholesterol and hypertension in his clustering, which he termed 'syndrome X', but interestingly obesity was not included (Reaven, 1988). The syndrome has since been variably termed the insulin resistance syndrome, Reaven's syndrome and the dysmetabolic syndrome. However, as it is not a discrete entity caused by a single Figure 2.7 Scheme displaying the concept of metabolic syndrome as a link between...

Conclusion inflammation hypothesis of metabolic syndrome

In conclusion, the pro-inflammatory state of obesity and metabolic syndrome originates with excessive caloric intake and is probably due to over-nutrition in a majority of patients in the U.S. The pro-inflammatory state induces insulin resistance leading to clinical and biochemical manifestations of the metabolic syndrome. This resistance to insulin action further promotes inflammation through increases in lipolysis and plasma FFA concentrations on one hand and interference with the anti-inflammatory effect of insulin on the other. While these factors may be the most important ones in a majority of patients with metabolic syndrome, it is possible that genetic factors may also contribute to the inflammatory stress in metabolic syndrome. These factors may be important in ethnic groups such as Asian Indians who may have increased amounts of upper abdominal fat in spite of normal BMI values.82 Since excessive nutritional intake probably accounts for the inflammation at least in...

Metabolic Syndrome see also Chapter

Hypertension is frequently associated with insulin resistance (and concomitant hyperinsulinaemia), central obesity and a characteristic pattern of dislipidaemia (high triglycerides and low HDL-cholesterol) (Reaven etal., 1996 Reaven, 2002). The relation between insulin resistance and hypertension is well established (Modan etal., 1985 Ferrannini etal., 1987 Swislocki etal., 1989 B hler etal., 1990 Ferrari and Weidmann, 1990) but, despite this association, insulin resistance contributes only modestly to the prevalence of hypertension (Hanley etal., 2002). This constellation of risk factors is known as the (cardiovascular) metabolic syndrome. There are various definitions but all agree on the essential components - glucose intolerance, obesity, hypertension and dyslipidaemia. Almost one-quarter of adults in the USA has the metabolic syndrome (Ford etal., 2002). This is likely to rise in the next several years primarily because of the rapid increase in obesity. People with the metabolic...

The Metabolic Syndrome An Overview

A WHO expert committee in 1998 proposed that the metabolic syndrome should be diagnosed in patients who show evidence of glucose intolerance and or insulin resistance together with two other components of the syndrome (Table 14.1). The expert committee decided to define insulin resistance as insulin sensitivity under hyperinsulinemic euglycemia clamp conditions below the lowest quartile for the population under investigation. This definition of insulin resistance matches the degree of insulin sensitivity in patients with Type 2 diabetes mellitus (Beck-Nielsen et al 1999). Epidemiological studies indicate that the metabolic syndrome is prevalent in industrialized countries. When applying the WHO definition of the metabolic syndrome to the European Group for the study of Insulin Resistance (EGIR) database (Ferran-ninni et al 1996), the prevalence of the syndrome was estimated at 15.6 among healthy Caucasians in Europe (Beck-Nielson et al 1999). Data from the Danish Twin Register (Kyvik,...

Endothelial Dysfunction Insulin Resistance And The Metabolic Syndrome

Dyslipidaemia, and that endothelial dysfunction merely represents the impact of hyperglycaemia and other features of the metabolic syndrome. An alternative concept is that endothelial dysfunction is at the heart of the metabolic syndrome. According to this concept, the endothelial dysfunction in large arteries that is an early and prominent event in atherothrombotic disease is parallelled by endothelial dysfunction in resistance vessels and metabolically important capillary beds that contributes to the development of the metabolic syndrome 50 .

Rationale for defining metabolic syndrome

In the past decade, sedentary lifestyles, atherogenic high calorie diets, and weight gains have characterized adolescents and adults in the United States and in many countries across the globe.1,2 Indeed, a recent report2 estimated the prevalences of overweight and obese people in the U.S. above 60 and 30 , respectively. This is not a unique burden for the U.S., but reflects a worldwide trend demonstrating an increased prevalence in metabolic risk factors3,4 including visceral obesity, insulin resistance, dyslipidemia with abnormal values for triglycerides and high density lipoprotein cholesterol (HDL-c), hypertension, and (if measured) pro-thrombotic and inflammatory markers. In addition to the appreciation that weight gain and obesity are increasing global problems and that the location of body fat has both prognostic and therapeutic importance is the recognition of atherogenic risk factor clustering. This concept was noted by Framingham investigators who found it was common in both...

Metabolic Syndrome Diabetes Plus

Metabolic syndrome is a constellation of problems that often includes diabetes or prediabetes. What are the other conditions Being overweight, especially when extra pounds accumulate around the midsection having high or borderline-high blood pressure having high triglyceride levels and having low HDL (good) cholesterol. Specifically, you have metabolic syndrome if you have diabetes or prediabetes and two or more of the following researchers think that the impact of the metabolic syndrome on health is more than the sum of its parts. Over the years, this collection of health risks has gone by many names. Besides the deadly quartet, it has also been called syndrome X, insulinresistance syndrome, diabesity, and the dysmetabolic syndrome. Metabolic syndrome, although not as flashy or memorable as some of the other names, is the term used by most clinicians and researchers today.

Metabolic Syndrome Definition and classification

The association of insulin resistance, dysglycaemia, hypertension, obesity and dyslipidaemia was first described formally by Reaven in 1988 in his Banting lecture (Reaven, 1988). Since then this syndrome has been referred to as the 'insulin resistance syndrome' and the 'metabolic syndrome' as well as 'syndrome X'. More recently there have been attempts to assemble diagnostic criteria for what has become known as the 'metabolic syndrome' and apply these criteria to populations so that prevalence figures may be obtained. The World Health Organization (WHO) (World Health Organization, 1999), the National Cholesterol Education Programme (NCEP) Adult Treatment Panel (ATP) III (NCEP ATPIII, 2001) and the International Diabetes Federation (IDF) (Alberti etal., 2006) have disseminated similar although not identical criteria that are based on the presence of several core metabolic and cardiovascular criteria such as hypertension, dyslipidaemia, obesity and elevation of either fasting insulin...

Metabolic syndrome

The earliest abnormality in type 2 diabetes is insulin resistance, which is found in people even before diabetes can be diagnosed. People with impaired glucose tolerance, and even 25 percent of the population with normal glucose tolerance, have evidence of insulin resistance. The condition, formerly known as the insulin resistance syndrome, is now called the metabolic syndrome. It is particularly worrisome because it is being found in obese children and adolescents, resulting in greater danger of diabetes and an early heart attack in these children. The next twenty years will show us how these risks play out. I C-reactive protein This marker for inflammation in the body (easily obtained by a blood test) rises as the severity of the metabolic syndrome increases. It indicates that inflammation plays an important role in coronary artery disease. The important role of inflammation is confirmed by the presence of inflammatory factors in the blood that come from fat l Increased abdominal...

Recent Developments

Understanding of the nutritional factors that lead to obesity and insulin resistance is increasing rapidly. Nutritional management of the metabolic syndrome is likely to improve as this knowledge base develops and patients are increasingly diagnosed at an earlier stage. The role of vitamins and trace elements is increasingly recognized. Volpi and colleagues5 recently demonstrated an anabolic effect of essential amino acid supplementation in the elderly. The potential to favourably influence body composition and insulin sensitivity without resort to pharmacological agents is becoming a real possibility.

Comprehensive Risk Reduction of Cardiovascular Risk Factors in the Diabetic Patient An Integrated Approach

The excess CV mortality and morbidity in the diabetic population seems to reflect the strong association of diabetes with insulin resistance and with well-established coronary risk factors. During the past 2 decades, significant advances have been made in elucidating the pathophysiologic determinants and consequences of the metabolic perturbations in the diabetic state. The disease is characterized by insulin resistance and is commonly associated with the metabolic syndrome. Sensitivity to insulin is variable in the population at large. Cellular insulin resistance develops as the result of a complex interplay of genetic and environmental factors. Hyperinsulinemia occurs as an adaptive response to the increasing insulin resistance. Type 2 diabetes develops when insulin-resistant individuals cannot maintain the degree of excess insulin secretion needed to overcome insulin resistance. There are two aspects to the type 2 diabetic state hyperglycemia and hyper-insulinemia. Insulin...

Role of Adipocyte Products and Inflammation

While circulating NEFA and several adipokines are increased in visceral obesity, the levels of the adipose-specific protein adiponectin are decreased, reducing its insulin-sensitizing effects in liver and muscle (19,30). Adiponectin signals via AMP kinase, a stress-activated signaling enzyme implicated in a variety of metabolic responses, including suppression of hepatic gluconeogenesis, glucose uptake in exercising skeletal muscle, fatty acid oxidation, and inhibition of lipolysis, which may explain its beneficial metabolic effects (30-34). In addition to their effects on insulin signaling, the circulating adipose tissue factors strongly influence vascular endothelial function, linking the increased vascular risk in the metabolic syndrome with mechanisms of cellular insulin resistance (30,40). Adipose secretory factors also recruit and activate inflammatory cells, which can further perpetuate a systemic inflammatory milieu that can strongly influence vascular function and...

Maturity Onset Diabetes of the Young

MODY3 and MODY2 are the two most prevalent forms of MODY. Estimated from a study on 90 MODY families, MODY3 accounts for 63 MODY, and MODY2 accounts for 20 MODY (228). Unlike DM2, patients with MODY are usually nonobese and do not have metabolic syndrome (227). Determining the subtype of MODY is helpful for clinical decision making (229). MODY3 and MODY1 patients are sensitive to sulfonylureas for years before insulin is needed. MODY2 tends to have mild symptoms and often requires only lifestyle interventions. The genetic basis of each subtype of MODY is discussed later (Table 3).

Multifactorial Intervention in Type Diabetes mellitus

Several risk factors for the outcome of type 2 diabetes have been identified in prospective epidemiological studies. However, until recently the treatment of type 2 diabetes has been empirical rather than evidence based from randomized intervention studies. Although the diagnosis of diabetes is based on blood glucose levels, it is important to realize that patients with type 2 diabetes mellitus share many clinical features with the metabolic syndrome such as dyslipidaemia, hypertension, hyperinsulinaemia and an increased risk of cardiovascular disease. In cardiovascular medicine a multifactorial treatment approach of several risk factors for cardiovascular disease is generally accepted. We suggest a similar approach in the treatment of type 2 diabetes mellitus based on the results from several intervention studies in patients with this disease.

Location of Fat Deposition in Pregnancy

The location of fat deposition, visceral or subcutaneous, is important because of regional variation in adipocyte metabolism. However, this has not yet been fully explored in pregnancy. It has been observed that in pregnancy fat accumulates predominantly in the central compartment (36). A study using ultrasound to differentiate abdominal visceral fat (the preperitoneal fat layer) and subcutaneous fat showed that intra-abdominal visceral fat accumulation increases during pregnancy resulting in a change in regional fat distribution (37). However, a magnetic resonance imaging (MRI) study (32) found the majority of additional adipose volume (76 ) to be placed subcutaneously predominantly in the trunk (68 ) and thighs (16 ). Obviously further work is required to resolve these discrepancies. The location of fat deposition is important, as there is some evidence that centrally deposited fat is associated with glucose intolerance gestational diabetes mellitus (38) and gestational hypertension...

Effects of NEFA on hepatic insulin action

Circulating NEFA levels are raised in obese subjects, especially those with increased intra-abdominal fat or visceral obesity. It is well established that visceral adipose tissue is more metabolically active than subcutaneous fat, with high rates of triglyceride turnover and NEFA release. This situation may arise due to the close anatomical location with the liver, the dense vascular network, dense sympathetic innervation and increased levels of the -adrenoceptor that mediates lipolysis (Rosell and Belfrage, 1979). NEFA generated from visceral fat enters the portal circulation and is delivered directly to the liver and is subsequently oxidized to acetyl CoA. Acetyl CoA stimulates pyruvate carboxylase and therefore the gluconeogenic production of glucose from pyruvate. Hepatic glucose production therefore increases. However, with increasing adiposity insulin resistance of visceral fat combined with a number of other metabolic characteristics, such as increase lipolytic response to...

Insulin Resistance And Hyperinsulinemia In Healthy Children And Adolescents

These studies corroborate other investigations of metabolic physiology that suggest that there are differences among racial groups in the anatomical and pathophysiological correlates of glucose intolerance (64). In particular, African-American children with equivalent body fatness to white children have less abdominal fat, higher insulin concentrations, and lower insulin sensitivity (91,96). It is not clear whether these differences influence the clinical presentation of glucose intolerance in the different racial groups, but one would expect African-American children to be more vulnerable than white children to alterations in insulin secretion because of their dependence on elevated secretion to compensate for greater insulin resistance. Likewise, they would be more vulnerable than other groups to further decreases in insulin sensitivity, known to emerge during puberty. Whether this has implications for the etiology of Early 2 remains to be seen.

Dual Energy Xray Absorptiometry DXA

Several studies have shown some correlation between DXA and CT measurements of body compositions and abdominal obesity (Kelley et al. 2000 Park et al. 2002 Snijder et al. 2002). But methodological limitations linked to the effect of hydration on X-ray attenuation (Pietrobelli et al. 1996, 1998 Lohman et al. 2000) and distortions of planar projections when scanning the thicker tissue of obese or overweight patients (Roubenoff et al. 1993 Brownbill & Ilich 2005) (Figure 13.2) make DXA model dependent and less accurate than CT or MRI.

Effects Of Exercise In Diabetics Metabolic Effects

Regular physical activity is associated with changes in body composition with a reduction in body fat, increase in muscle mass, and maximal oxygen uptake in healthy individuals insulin sensitivity is closely correlated to these factors. Corresponding results are obtained in patients with diabetes type 2 who engage in a structured exercise program. Improvements of insulin sensitivity are independently correlated to a reduction in abdominal obesity and an increase in muscle cross-sectional area (10). The benefits of exercise, however, are only maintained for short periods of time they attenuate 3 to 6 days after the last exercise session stressing the importance of persistent lifestyle changes (11-13). By adding resistance training to aerobic exercise muscle mass may be increased, particularly in elderly patients who tend to loose muscle mass as a result of aging (10,14).

Intermediate Syndromes Double Diabetes

Banerji and colleagues conducted additional studies in blacks with Type 2 diabetes contrasting insulin-sensitive vs. insulin-resistant syndromes using the euglycemic clamp technique (48). Differences in visceral fat deposition were reported (49), and varying associations with HLA-DQ polymorphisms were identified among 25 insulinsensitive, 21 insulin-resistant, and 89 normogly-cemic African Americans. The insulin-resistant group had a higher than expected prevalence of the DQw7 allele, and the insulin-sensitive group had a lower frequency of DQw6, when compared with each other and with non-diabetic blacks. No HLA-DR or Class I differences were observed. Joffe et al. (2) reported data from South African black Type 2 diabetes patients suggesting a rapid fall in beta-cell function compared with whites, despite obesity and a relatively mild clinical course. There was no increase in C-peptide after sulfonyurea treatment for hyperglycemia. The beta-cell response to a glucose challenge was...

Pharmacological Management

Some evidence that the use of basal insulin as opposed to meal-time insulin will lessen the weight gain effect (85). Newer agents such as the thiozolidinedione insulin sensitisers remain controversial, as the impact of undesirable subcutaneous weight gain, despite reductions in the more harmful visceral fat, continues to be debated (8).

Is There A Metabolic Insulin Resistance Syndrome In African Americans

Insulin resistance, glucose intolerance, hyper-insulinemia, central obesity, dyslipidemia, hypertension and macrovascular disease are components of the metabolic insulin resistance syndrome (68). If the syndrome exists in a population and the components are causally related, then targeting the primary defect might eliminate the cascade of abnormalities. Selective reporting of the components makes assessment difficult in African Americans the association of hyperinsulinemia and hypertension is weakest (Table 9A.4).

Risk Factors For Type Diabetes

The identification of risk factors is essential for the successful implementation of primary prevention programs. Risk factors for type 2 diabetes can be classified as modifiable and nonmodifiable (Table 4). Subjects who subsequently develop diabetes have multiple adverse changes in risk factor levels. A good example is our study of 892 elderly Finnish subjects followed for 3.5 years (38). As shown in Figure 3 the highest risk of developing diabetes was associated with IGT and hyperinsulinemia. Furthermore, hypertriglyceridemia, central obesity, low high-density lipoprotein (HDL) cholesterol, high body mass index, hypertension, and a family history of diabetes were risk factors for diabetes.

Adipose Tissue Endocrine Functions

Adipose tissue is comprised of lipid-filled cells surrounded by a matrix of collagen fibers, vessels, fibroblasts, and immune cells. Its main function is the storage of triglycerides for times of energy deprivation. However, it secretes hormones and other products and is involved in various aspects of metabolism that directly affect the onset of obesity. It metabolizes sex steroids and glucocorticoids. For example, 17-beta-hydroxysteroid oxidoreductase converts androstene-dione to testosterone and estrone to estradiol. This may be important for fat distribution. Estrogens stimulate fat accumulation in the breast and subcutaneous tissue, while androgens promote central obesity. Alteration of these interconversions may predispose individuals to reproductive disorders and certain cancers (292,293). Alteration of coagulation and complement factors may contribute to the obesity-associated cardiovascular disease. Fibrinogen and plasma activator inhibitor Type-1 (PAI-1) are altered in...

Obesity and type diabetes

The risk of obesity and type 2 diabetes was better defined by a high WHR and waist circumference (Larsson et al., 1984). Additionally, the duration of obesity was directly related to the risk of diabetes (Everhart et al., 1992). The risk of type 2 diabetes from obesity is more prevalent across certain ethnic groups such as South Asians and Afro-Caribbeans (Bhopal, 2002).

Nutritional Advice And Structured Training

All steps in the nutritional management of a person with type 2 diabetes should be documented and the outcome evaluated by means of important markers, such as body weight, waist circumference, blood pressure, HbA1c, fasting, and or postprandial blood glucose (self-) monitoring, serum-lipids, AER and well-being or quality of life.

Communitybased studies of lifestyle change

Over two years, subjects attending the intervention church had no weight gain (compared with +3.1 kg on average in the control group), a decreased waist circumference, and increased knowledge about diabetes and nutrition. Self-reported intake of high-fat foods was lower after the intervention, and the majority of respondents felt it had been useful to them. The intervention church continued the physical activity and nutrition program on a self-sustained basis. It appears that this type of intervention had some success in preventing weight gain (though it did not achieve weight loss).

Conclusions And Therapeutic Implications

Then the primary goal should be to treat to and maintain the fasting and postprandial plasma glucose as close to normal as possible, while minimizing the development of visceral obesity. Such a strategy, if it can be implemented, should maintain atherosclerosis progression at the prediabetic level.

Nonalcoholic Steatohepatosis

Non-alcoholic fatty liver disease, has recently become increasingly recognized and may progress to end-stage liver disease. It is histologically indistinguishable from the liver damage that is secondary to alcohol abuse, but occurs in people with no history of alcohol excess. Non-alcoholic fatty liver disease has a wide spectrum of liver damage ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. The combination of steatosis, infiltration by mononuclear or polymorphonuclear cells (or both), and hepatocyte ballooning and spotty necrosis is known as nonalcoholic steatohepatitis (NASH). Non-alcoholic fatty liver disease is the most common cause of abnormal liver blood results among adults in the USA. It is particularly common in those with combined diabetes and obesity in a group of severely obese patients with diabetes, 100 were found to have mild steatosis, 50 had NASH and 19 had cirrhosis. Insulin resistance seems to be the most reproducible causative...

Lipid Abnormalities and Lipid Lowering in Diabetes

Secretory Pathway Lipoprotein

Lipid abnormalities may be associated with coexisting visceral obesity and insulin resistance. Fasting TG and visceral obesity appear to independently predict mortality from CAD in glucose-intolerant and diabetic subjects. The predominance of small, dense LDL was found to be one of the interrelated risk factors that characterize the insulin resistance syndrome. The trend towards increased VLDL and reduced HDL has been found to be present already in first-degree relatives of type 2 diabetic patients with normal glucose tolerance. These lipid abnormalities therefore may represent early markers of insulin resistance.

Magnetic Resonance Imaging MRI and spectroscopy

Mri Spectroscopy Show Muscle

Figure 13.3 Assessment of Abdominal Fat Storage by Computed Tomography (CT) Representative cross-sectional abdominal CT scans of a lean (A) and an obese (B) research volunteer, demonstrating the fat muscle CT contrast shown with demarcations of visceral (large arrowheads), deep subcutaneous (open arrows) and superficial subcutaneous (closed arrows) adipose tissue (AT) depots. The fascia (small arrowhead) within subcutaneous abdominal AT was used to distinguish superficial from deep depot. In the two CT scans shown, the area of superficial subcutaneous AT was similar (144 vs 141 cm2), whereas areas of deep subcutaneous (126 vs 273 cm2) and visceral (84 vs 153 cm2) AT were quite different. Insulin-stimulated glucose metabolism was 6.1 and 4.0 mg min-1 kg FFM-1 in lean and obese volunteers, respectively (FFM fat-free mass). Reproduced from Kelley D E et al. (2000) Am J Physiol Endocrinol Metab 278 (5) E941-E948. Courtesy of the American Physiological Society. Figure 13.3 Assessment of...

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

IGT), but rather risk categories for future diabetes and or cardiovascular disease (22,23). IGT and IFG represent impaired glucose regulation which refers to a metabolic intermediate between normal glucose homeostasis and diabetes. Individuals who meet criteria for IGT or IFG may be euglycemic in their daily lives as shown by normal or near-normal glycated hemoglobin levels (2). IGT is often associated with the metabolic syndrome (insulin resistance syndrome) (24). An individual with a fasting plasma glucose concentration of 6.1 mmol l (110 mg dl) or greater (whole blood 5.6 mmol l 100 mg dl) but less than 7.0 mmol l (126 mg dl) (whole blood 6.1 mmol l 110 mg dl) is considered to have impaired fasting glycemia (IFG). If an OGTT is performed, some individuals with IFG will have IGT. Some may have diabetes but this cannot be determined without an OGTT. If resources allow, it is recommended that those with IFG have an OGTT to exclude diabetes (2).

Nephropathy and Hypertension in Diabetic Patients

In the past decades there has been a growing interest in the nature of diabetic renal disease, mainly focusing on BP, glomerular pressure and protein leakage as related to structural and biochemical abnormalities. A recently published volume intends to cover almost every aspect of renal disease and hypertension in diabetes. One key point is interesting here in general, two or more risk factors must coincide to provoke fast and serious organ damage. In terms of diabetic nephropathy this means that some degree of poor glycemic control may not always be clinically noxious enough per se, unless some other risk factors, especially elevated BP or possibly poorly defined genetic elements coexists. However, increased glomerular pressure seems to be a decisive factor, whether caused directly by poor glycemic control, dietary proteins or systemic hypertension, in particular with loss of renal vascular autoregulation that may be seen in diabetes. Other risk factors may contribute to renal and...

Considering Heart Disease

Although many of these patients have had a diagnosis of diabetes for a relatively short time, they have actually suffered from the metabolic syndrome for many years. This is the reason for their high frequency of vascular diseases in the heart, brain, and legs. I discuss both the metabolic syndrome and vascular diseases in Chapter 5.

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...

Species of Plants Reported to Be Used Traditionally to Treat Diabetes

Decrease blood glucose and abdominal fat. These effects may be mediated via peroxisome proliferator-activated receptor-y (Nakagawa et al., 2004) Traditionally used to treat diabetes in Ghana but extracts did not have hypoglycemic activity in nondiabetic humans and showed some overt toxicity by lowering the immune status (Sittie and Nyarko, 1998) Used to treat diabetes (Marles and

Computed Tomography CT

Total Body Fat

Signal intensity in the CT images corresponds to the linear attenuation coefficient, which depends on physical properties (including density) of tissue within the volume of interest. Signal intensity is expressed in so-called computed tomography numbers or Hounsfield units (HU), which range from -1,000 to +3,095 (4,096 values). Based on their density and the resulting differences in X-ray attenuation, muscle and fat tissue display different ranges of intensity (-190 to -30 HU for fat and 0 to 100 HU for muscle), resulting in muscle fat contrast on the CT image (Figure 13.3). Recorded fat accumulation (for subcutaneous and visceral fat depots) is thus based on volumetric measurements (Dixon 1983 Tokunaga et al. 1983 Busetto et al. 1992). For ectopic (intrahepatic, intramyocellular) lipid accumulation, measurements are based on comparison of X-ray attenuation in liver tissue and spleen (Figure 13.4) or in muscle and fat tissue (bone marrow or external phantom (Goodpaster et al. 2000a))....

Interaction between angiotensin endothelium and insulin resistance

Insulin resistance is associated with metabolic syndrome, which increases the risk of adverse cardiovascular outcomes. There is definitive evidence that insulin resistance and endothelial dysfunction progress in parallel. As insulin resistance progresses to clinical metabolic syndrome, impaired glucose tolerance, and development of diabetes, there is a parallel track that leads from endothelial dysfunction to inflammation, with increased oxi-dative stress leading to overt atherosclerotic disease. Insulin resistance has been shown to interact with this parallel track of endothelial dysfunction through the accumulation of free fatty acids, proinflammatory adipokines, and TNF alpha 59 . In addition, increased oxidative stress, oxidation of LDL, the reduction of HDL, and the development of hypertension, hyperuricemia, and hy-perglycemia contribute to the mechanisms of underlying endothelial dysfunction in insulin resistance 51 .

Preventing Microalbuminuria in Diabetes

In conclusion, there is now fairly good evidence from clinical trials that treatment with an ACE inhibitor should be started early in patients with type 2 diabetes and nor-moalbuminuria. Treatment should be initiated when systolic BP is more than 130 systolic mm Hg. Systolic BP elevation is very common in patients with type 2 diabetes and metabolic syndrome. This means that most type 2 diabetes mellitus patients would qualify for this type of treatment. These patients also often show sodium retention and therefore a combination with an ACE inhibitor and diuretics seems to be most effective in reducing microalbuminuria and BP (1). Now there seems to be a very good foundation for substantial improvements of the prognosis for patients with type 2 diabetes (1,14) and early treatment of hypertension leads to better prognosis, as does, but maybe to a lesser extent, improved euglycemic control (16). Clearly treatment with statins is also important, as documented in many studies, among others...

Obesity and the Abdominal Phenotype in PCOS

This could be due to a depot-specific inhibition of the expression of hormone-sensitive lipase (HSL) by testosterone and or to a decrease in the amount of b2 adrenergic receptors. This could also be an important pathophysiological factor behind the insulin-resistant phenotype of the upper-body obesity in men and of the hyperandrogenic PCOS (104). In humans, it is demonstrated that testosterone increases visceral fat in women. Female-to-male transsexuals treated with testosterone do in fact have an increase in visceral fat only when oophorec-tomized and thus eliminating the protective effects of estrogens (105). In addition, administration of androgens in postmenopausal women has been documented to increase visceral fat while reducing subcutaneous fat (106). This indicates that an increase in the testosterone to estrogen ratio in women causes accumulation of visceral adipose tissue, consistent with the important role of testosterone in determining the...

Prenatal Androgenization and PCOS

In addition to its impact on the reproductive endocrine axis, prenatal androgenization of female rhesus monkeys may also induce metabolic defects that resemble those of PCOS. Like humans, rhesus monkeys are susceptible to obesity and its glucoregulatory effects. Prenatally androgenized female monkeys tend to deposit fat in the visceral area and exhibit impaired insulin secretion or action, depending on the timing of androgen exposure during gestation. Thus, studies of body composition using CT combined with dual X-ray absorptiometry revealed that females treated early in gestation have increased visceral fat compared with controls, even when corrected for BMI and total body fat (40). On the other hand, monkeys treated late in gestation have increased total body fat and nonvis-ceral abdominal fat compared with control females (40). However, both groups of testosterone-treated females preferentially accumulate visceral fat with increasing BMI, while normal females preferentially...

Peroxisome Proliferatoractivated Receptor Ppary Agonists And Treatment Of Alzheimers Disease

Drugs of the PPAR-y class have been approved by the FDA to treat T2DM for approximately a decade. Members of this class currently in clinical use include rosiglitazone and pioglitazone. They are ligand-activated nuclear transcription factors that improve insulin sensitivity. PPAR-y, expressed in adipocytes, regulates adipogenesis and increases the uptake of fatty acids into adipocytes. Thus, PPAR-y agonists reduce the burden of fatty acid uptake for striated muscles, which likely explains their insulin-sensitizing characteristics. PPAR-y agonists also reduce visceral fat stores, which are relocated to subcutaneous stores, and they reduce the expression of TNF-a (89). Furthermore, these compounds produce anti-inflammatory responses in rats and humans (90,91). An interesting characteristic of PPAR-y agonists is that they have little immediate effect on plasma glucose or insulin levels, since they do not stimulate insulin secretion by the pancreas or glucose production by the liver....

Ectopic fat storage fat content in obesity

Non-alcoholic steatohepatitis (NASH), along with other forms of non-alcoholic fat liver disease, can often present its self as the first clinical indication of insulin resistance, with its complications of high blood pressure, coronary heart disease and type 2 diabetes (Scheen and Luyckx, 2003). NASH is relatively common with at least 20 per cent of obese adults or children with type 2 diabetes and in approximately 5 per cent of those who are overweight (Farrell, 2003). The prevalence and degree of severity of liver steatosis are related to BMI, waist circumference, hyperinsulinaemia, hypertriglyceridaemia and impaired glucose tolerance. The pathophysiology of NASH principally involves two steps first, insulin resistance, which leads to steatosis, and second, oxidative stress, which causes lipid peroxidation and stimulates inflammatory cytokines (Farrell, 2003 Yki-Jarvinen, 2002). Identifying the progression of this two-stage disease is difficult and determining an appropriate therapy...

Pathophysiology Of Macrosomia

Pathophysiology Undernutrition

Prepubertal healthy children with a family history of type 2 diabetes (n 9) matched for age, pubertal status, total body adiposity determined by dual energy X-ray absorptiometry, abdominal obesity determined by computed tomography scan, and physical fitness measured by VO2maxwith those without such history (n 13) had three hour hyperinsulinemic clamp studies to assess insulin sensitivity. Those with a family history of type 2 diabetes had lower insulin stimulated glucose disposal and nonoxidative glucose disposal there were no differences in glucose oxidation, fat oxidation, or FFA suppression (47). These data indicate that family history of type 2 diabetes is a risk factor for insulin resistance. Approximately 55 of the variance in insulin sensitivity can be explained by total adiposity. Obese children have hyperinsulinism and 40 decrease in insulin stimulated glucose metabolism compared to the nonobese (53). There is a direct correlation between the amount of visceral fat in obese...

Screening for gestational diabetes in third world countries do we need ethnic and national specific criteria

Ethnic differences in visceral fat distribution and percent body fat could theoretically impact optimal diagnostic criteria for gestational diabetes. This is the reason that ethnic and nation-specific criteria have been set forth by the International Diabetes Federation for waist circumference for the diagnosis of the metabolic syndrome (41) (Table 5). This has been given all the more relevance as insulin resistance, which has been linked to gesta-tional diabetes via maternal obesity, especially visceral obesity (42-57). It has also been shown that the association of higher body fat, especially visceral fat with BMI is not universal but may be ethnically determined. Obesity is a major contributor to insulin resistance, and amongst Caucasians, most people with DM2 are overweight or obese. However, the body mass index (BMI) defined that prevalence of obesity, an important risk factor in the development of type 2 diabetes, is significantly lower in Asian Indians than in Caucasians (58)....

Molecular Cell Biology Of Endothelial Dysfunction In Diabetes

High Glucose Insulin Pathway

Thus, endothelial cells exposed to high glucose in vitro increase the production of extracellular matrix components, such as collagen and fibronectin, and of procoagulant proteins, such as vWF and tissue factor, and show decreased proliferation, migration and fibrinolytic potential, and increased apoptosis. Secondly, high glucose influences endothelial cell functioning indirectly by the synthesis of growth factors (e.g., transforming growth factor- (TGF-P) and vascular endothelial growth factor (VEGF), cytokines (e.g., TNF-a) and vasoactive agents in other cells. Thirdly, the components of the metabolic syndrome can affect endothelial function. The metabolic syndrome insulin resistance, insulin, hypertension, dyslipidaemia, and obesity Obesity. Obesity, especially visceral obesity, is associated with increased risk Asymmetric dimethylarginine (ADMA). There is some evidence that levels of ADMA, an endogenous inhibitor of nitric oxide, are associated with the metabolic syndrome 88 ,...

Fat Diversion from Adipose to Nonadipose Tissue and Lipotoxicity

In summary, adipose tissue storage and release of fatty acids, and particularly the control of these processes by insulin, is grossly abnormal in insulin resistant states. In the postabsorptive period, basal adipose tissue lipolysis is elevated, and suppression by insulin is diminished. In the postprandial period there is likely to be some diversion of fat away from adipose tissue depots and towards nonadipose tissues owing to less efficient fatty acid uptake and storage by insulin resistant adipocytes. FFA efflux from an enlarged and lipolytically active visceral fat depot may not contribute quantitatively to the majority of circulating FFAs, but because of its anatomical location and intrinsic properties appears to play an extremely important role in the manifestations of insulin resistance and type 2 diabetes. A high capacity for efficient triglyceride accumulation in adipose as well as nonadipose tissue may have presented a survival advantage in the past, during times of...

Contemporary Endocrinology

The Metabolic Syndrome Epidemiology, Clinical Treatment, and Underlying Mechanisms, edited by Barbara Caleen Hansen and George A. Bray, 2008 Genomics in Endocrinology DNA Microarray Analysis in Endocrine Health and Disease, edited by Stuart Handwerger and Bruce Aronow, 2008 Controversies in Treating Diabetes Clinical and Research Seifer And Elizabeth A. Kennard, 1999 The IGF System Molecular Biology, Physiology, and Clinical Applications, edited by Ron G. Rosenfeld and Charles T. Roberts, Jr., 1999 Neurosteroids A New Regulatory Function in the Nervous System, edited by Etienne-Emile Baulieu, Michael Schumacher, Paul Robel, 1999 Autoimmune Endocrinopathies, edited by Robert Volp , 1999 Hormone Resistance Syndromes, edited by J. Larry Jameson, 1999 Hormone Replacement Therapy, edited by A. Wayne Meikle, 1999 Insulin Resistance The Metabolic Syndrome X, edited by GERALD

Renato Pasquali and Alessandra Gambineri

The Biology of Sex Difference in Health and Disease Insulin Resistance in The General Female Population The Metabolic Syndrome, Cardiovascular Risk Factors and Cardiovascular Events in Women How the Definition of the Metabolic Syndrome Overlaps that There are many differences between the sexes in the susceptibility and the development of chronic metabolic and cardiovascular diseases, which may be partly explained by the disparate alterations of androgen balance particularly in the presence of obesity. Notably, available studies support the concept that the prevalence of insulin resistance, the metabolic syndrome, type 2 diabetes, and cardiovascular pathologies is different between the sexes. With respect to women, it is particularly evident from a recent meta-analysis that those with the abdominal phenotype of excess weight or obesity, who are characterized by a condition of relative hyperandrogenic state, are at high risk for a specific morbidity for these diseases. The paradigm of...

Why was metformin recommended for this particular patient

Risk factors for atheromatosis (obesity, smoking, sedentary life-style, hyperlipidaemia) are also taken into consideration, without being specific indications. It appears that metformin acts beneficially on a lot of the metabolic syndrome parameters (insulin-resistance syndrome) apart from glycaemia. More specifically, it decreases fasting hyperinsulinaemia, moderately improves the lipid profile and has some antithrombotic action as well, decreasing the PAI-1, the fibrinogen and the platelet aggregation.

Risk Factors for Maternal Postpartum Diabetes Among Women with GDM

Anthropometric factors reflect adiposity, a step in the causal pathway of insulin resistance (108). While adiposity is generally associated with future glucose intolerance, different anthropometric measures reflect different types of adiposity, which in turn are associated with future diabetes to differing degrees. Greater central or visceral adiposity, as reflected by waist circumference and waist-hip ratio, has stronger risk for GDM than subcutaneous adiposity or traditional measures of body mass (109).

Corsi Minerva Kolesar

Mendoza-Guadarrama LG, Lopez-Alvarenga JC, Castillo-Martinez L, Gallegos J, Portocarrero L, Garcia-Garcia R, Roiz-Simancas M, Gonzalez-Barranco J. Orlistat reduces visceral fat independent of weight changes in obese diabetics type 2. International Journal of Obesity 2000 24((Suppl 1)) S167.

Freed M Et Al. Diabetologia 2000 43 Suppl 1 A267

Dyslipidemia of central obesity and insulin resistance. Diabetes Care 1999 22(Suppl 3) C10-3. 167 Nakamura T, Funahashi T, Yamashita S, Nishida M, Nishida Y, Takahashi M, et al. Thiazolidine-dione derivative improves fat distribution and multiple risk factors in subjects with visceral fat accumulation double-blind placebo-controlled trial. Diabetes Res Clin Pract 2001 54(3) 181-90. 168 Carey DG, Jenkins AB, Campbell LV, Freund J, Chisholm DJ. Abdominal fat and insulin resistance in normal and overweight women Direct measurements reveal a strong relationship in subjects at 171 Miyazaki Y, Mahankali A, Matsuda M, Mahanka-li S, Hardies J, Cusi K, et al. Effect of pioglitazone on abdominal fat distribution and insulin sensitivity in type 2 diabetic patients. J Clin Endocrinol Metab 2002 87(6) 2784-91.

Uwaifo Gi Fallon Em Diabetes Care 2002 25 2081-7

2 Bruning JC, Michael MD, Winnay JN, et al. A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance. Mol Cell 1998 2 559-69. Moraes CT, Ricci E, Bonilla E, et al. The mitochondrial tRNA(Leu(UUR)) mutation in mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS) genetic, biochemical, and morphological correlations in skeletal muscle. Am J Hum Genet 1992 50 934-49. Hegele RA. Monogenic forms of insulin resistance apertures that expose the common metabolic syndrome. Trends Endocrinol Metab 2003 14 371-7. Grundy SM, Brewer Jr HB, Cleeman JI, et al. Definition of metabolic syndrome report of the

The interaction of insulin resistance and Bcell function

Metabolic syndrome The metabolic syndrome, also called the IR syndrome, has become the major health problem of this time. This clinical phenotype is characterized by abdomi- nal obesity, dyslipidemia, elevated blood pressure, IR, and a proinflammatory state and is one of the major risk factors for cardiovascular disease 51,52 . Although some single-gene defects affecting satiety or energy homeostasis have been shown to produce this syndrome, in most cases it is the consequence of the interaction of multiple genes with lifestyle factors of excessive carbohydrate and fat consumption and lack of exercise. IR as an integral part of the syndrome is likely both the cause and consequence of many of the metabolic alterations seen in this syndrome. It is not surprising that the metabolic syndrome is a risk factor for type 2 diabetes, because adding (-cell failure to the prevailing IR leads to loss of glucose homeostasis. Type 2 DM is the most common form of diabetes in adults, and its...

Summary and conclusions

Insulin resistance may vary widely in the general population, as well as between sexes. However, data supporting this are still lacking, and this is partly due to the fact that the majority of the studies did not segregate for sex in their analysis, but sex differences were usually taken into consideration by controlling for sex in the statistical approach. In addition, in studies performed in adult populations, simple mathematical models to define insulin resistance have often been used, although they posses intrinsic limitation in this complex pathophysiological area. Nonetheless, available data strongly support the concept that there is some difference in the prevalence of the metabolic syndrome, DM2, and CvD between the sexes, so the hypothesis that insulin resistance and associated hyperinsulinemia may have a sex trait is not arbitrary, although major determinants are not adequately understood. Interestingly, sex-specific genes may therefore have a demonstrable impact on fetal...

Risk factors of youth type diabetes mellitus

Independent of total body adiposity and ethnicity, abdominal fat deposition (visceral adiposity) is considered a risk factor for insulin resistance in children 77,80,81 and T2DM in adults 82 . Obese children with IGT were found to have peripheral insulin resistance without compensatory insulin secretion 83 and higher visceral and intramuscular fat 83 . Most pediatric patients with T2DM in the United States belong to minority ethnic populations, which encompass Native Americans, Pima Indians, Mexican Americans, and African Americans 1,84,85 . Among the Pima Indians, more than 5 of the 15- to 19-year old children are affected 85 the pathogenesis of T2DM is attributed to a genetic predisposition to insulin resistance modified by lifestyle changes 86 . Epidemiologic and clinical studies indicate that black children are more hyperinsulinemic and insulin resistant than their white peers 87-90 . A study that used genetic admixture analysis suggested a genetic and environmental basis to these...

Prediabetes And Cognition Prediabetic Stages

Global Atrophy The Brain

Insulin resistance and disturbances in glucose metabolism often co-occur with other vascular risk factors such as hypertension, dyslipidemia, and obesity. The co-occurrence of these risk factors is usually referred to as the the metabolic syndrome. Reaven postulated in 1988 (37) that insulin resistance should be regarded as the central driving force in this syndrome and that traditional vascular risk factors such as hypertension, diabetes, dyslipidemia and, later on, also abdominal obesity are all part of it. Since then, multiple definitions of the syndrome have been postulated, including or excluding different risk factors. The ATP-III criteria are currently the most widely applied (Table 1) (38). The metabolic syndrome predisposes to both atherosclerotic cardiovascular disease and type 2 diabetes and may also be considered a pre-diabetic condition (37, 38). In the context of this book, which deals with cerebral complications of diabetes, it is important to address the potential...

Insulin Therapy in Type Diabetes

Insulin resistance and the consequent endogenous hyperinsulinemia are strongly associated with central obesity, hypertension and dyslipidemia, all factors that contribute substantially to cardiovascular (CV) risk and in fact characterize the Metabolic Syndrome (31,32). Epidemiological studies in non-diabetic populations have shown an association between endogenous hyperinsulinemia and atherosclerosis (33) thus physicians have been concerned that initiating insulin therapy would be harmful and may accelerate coronary artery disease. However, the association of hyperinsulinemia and atherosclerosis is mainly an association between endogenous hyperproinsulinemia and atherosclerosis (34). In fact, there is no evidence from animal or human studies that exogenous insulin administration causes accelerated atherosclerosis. The UKPDS actually was very reassuring in demonstrating that the insulin treated patients, who presumably had exogenous hyperinsulinemia, showed no evidence at all of...

Abnormalities in the fibrinolytic system

Another well-recognized contributor to augmented activity of PAI-1 in diabetes is the adipocyte. PAI-1 may be released directly from an increased mass of adipose tissue, particularly visceral fat, and that may account, in part, for the association between obesity and impaired fibrinolysis (293-295). However, abnormal concentrations of cytokines such as TGF-P and TNF-a, may also contribute to augment PAI-1 expression in adipocytes (296). Other cytokines including IL-1 and -6 have also been implicated as agonists for PAI-1 synthesis (297). Another factor likely to influence PAI-1 expression in diabetes is the renin-angiotensin system (RAS) because PAI-1 synthesis is augmented

Clinical studies of renin angiotensin aldosterone system inhibition and outcomes of insulin resistance

Improving insulin sensitivity 118-124 . Several factors make the results of these trials using ACE inhibitors or ARBs less robust overall. Different choice of experimental models, target molecules, doses, and route of administration may all have contributed to the conflicting results. In addition, the measure of insulin resistance itself is fraught with problems because of its sensitivity, specificity, positive and negative predictive values, reproducibility, discrimination, and calibration. The parameters used in evaluating glucose homeostasis are not always equivalent or comparable. Clearly, there is a need to improve the modeling technique by using refined methods of quantifying insulin resistance to predict more accurately the likelihood of developing diabetes and cardiovascular disease 125 . At present, metabolic syndrome variables may well be the best predictors for evaluating the likelihood of coronary artery disease.

Medical Complications

Sensitivity to insulin glucose-mediated disposal may be altered in obese children (35). When insulin secretion cannot maintain the degree of hyperinsuline-mia needed to overcome the resistance, Type 2 diabetes mellitus develops. However even when individuals secrete enough insulin to remain nondiabetic, if they present an altered glucose-mediated disposal with hyperinsulinemia they remain at increased risk to develop a cluster of abnormalities that have been given various names, best described as insulin resistance syndrome (IRS) (Vol. 1 Chap. 11). IRS was first described by Reaven in 1988 (29) and has been referred as syndrome X, metabolic syndrome, and dysmeta-bolic syndrome, the latest being the term used for ICD-9 coding 277.9. However the primary reason to select the term IRS is that the term denotes the central role of hyperinsulinemia in the pathogenesis of the cluster of abnormalities which characterize the syndrome, namely a clinical quartet of hyperinsulinemia,...

Preventing type diabetes

I Central distribution of fat When people with diabetes become fat, they tend to carry the extra weight as centrally distributed fat, also known as visceral fat. You check your visceral fat when you measure your waistline, because this type of fat stays around your midsection. So a person with visceral fat is more apple-shaped than pear-shaped. Visceral fat also happens to be the type of fat that probably comes and goes most easily on your body, and it is relatively easy to lose when you diet. Visceral fat seems to cause more insulin resistance than fat in other areas, and it is also correlated with the occurrence of coronary artery disease. If you have a lot of visceral fat, losing just 5 to 10 percent of your weight may very dramatically reduce your chance of diabetes or a heart attack. Asians tend to develop visceral fat at a lower weight than non-Asians and are therefore more prone to type 2 diabetes at a lower weight. Asian Indians are particularly susceptible, developing...

Is lifestyle modification adequate to prevent onset of diabetes

Metabolic syndrome carries with it the underlying pathophysiologic feature of insulin resistance with tissue resistance to insulin action, compensatory hyperinsulinemia, and excessive circulating free fatty acids 78,79 . In addition, cardiovascular risk factors of low HDL and high triglyceride levels, hypertension, and lack of physical activity have all been shown to be predictors of non-insulin-dependent diabetes 80 . The relationships between metabolic syndrome and cardiovascular mortality as well as chronic complications of type 2 diabetes have been well described 81,82 . Several studies have shown impaired glucose tolerance to be a predictor of progression to type 2 diabetes 8385 . In addition, in one study, adiponectin was an independent predictor of type 2 diabetes 86 . It follows, then, that aggressive intervention in patients with impaired glucose tolerance or metabolic syndrome would translate to diabetes prevention. In addition to the Da Qing study, the Finnish diabetes...

Uma Singh Sridevi Devaraj and Ishwarlal Jialal contents

Metabolic Metabolic Syndrome and Cardiovascular Metabolic Syndrome and Inflammation, Metabolic Syndrome, and Acute Phase Proteins 229 Pro-Inflammatory Cytokines, Monocytes, and Metabolic Syndrome 230 Therapeutic Modulation of Inflammation in Metabolic Syndrome 232 Weight Loss, Hypocaloric Diets, Inflammation, and Metabolic Syndrome 232 Pharmacological Therapies with Potential to Prevent or Treat Metabolic Metabolic syndrome (MetS) is a disorder composed of central adiposity, dyslip-idemia, abnormal glucose tolerance, and hypertension. It confers an increased risk for diabetes and cardiovascular disease (CVD). Inflammation plays a pivotal role in atherosclerosis and is involved in abnormalities associated with MetS such as insulin resistance (IR) and adiposity. The various biomarkers of inflammation such as inflammatory cytokines (TNF-a, IL-6, and IL-1p), chemokines (MCP-1 and IL-8), and C-reactive protein (CRP) are increased in obesity and correlate with IR and CVD. IR is also...

Effects of HRT on Risk of Developing Diabetes

Although this reduction was not seen in all studies (60). In a post hoc analysis of the Heart and Estrogen Progestin Replacement Study (HERS), a large randomized, double-blind placebo-controlled study, the use of CEE and MPA in postmenopausal women with documented coronary artery disease (CAD) was associated with a 35 reduction in the new diagnosis of DM2 over 4.1 years vs. placebo. Of interest, the decrease in risk was primarily due to lower levels of fasting blood glucose as opposed to BMI or waist circumference (35). However, the study was designed to determine whether HRT was of benefit in reducing myocardial infarction and death from CAD, and the study demonstrated no reduction of CV risk. Women in the study on HRT had a significant increase in deep venous thrombosis than those on placebo (61), which makes this regimen undesirable for diabetes prevention. In the Women's Health Initiative (WHI), a large randomized placebo-controlled study of hormone replacement therapy (CEE and...

The Clinical And Molecular Phenotype Of Pcos

Oligo- or anovulation and manifesting with oligo- or amenorrhea. Often women with PCOS have augmented luteinizing hormone (LH) secretion that contributes to hyperandrogenemia (11, 12). The metabolic trait of PCOS is characterized by central adiposity with associated insulin resistance and hyperinsulinemia, which further exacerbates the hyperandrogenism and ovulatory dysfunction. These, together with other features of the metabolic syndrome, impose an increased risk for type 2 diabetes and cardiovascular disease (13, 14). A common feature of PCOS resulting from aberrant folliculogenesis is the accumulation of small follicles in the periphery of a thickened ovarian stroma, yielding the characteristic polycystic ovarian (PCO) morphology on ultrasound (15). In summary, hyperandrogenism appears to be the fundamental manifestation of PCOS, probably driven by an inherent hyperandrogenic activity of the ovarian theca cells and or the androgen producing adrenocortical cells. This is associated...

Pulsatility Of Ffa Release

Because FFAs are released into the circulation by lipolysis of adipose tissue triglycerides in relation to the size of the fat depot, the greater overall fat mass of adipose tissue in obese individuals will result in an elevation of fatty acid flux to nonadipose tissues, even in the absence of a qualitative abnormality in adipose tissue metabolism (62). It is worth noting that not all fat depots make an identical contribution to the plasma pool of FFAs. Upper body fat (ie fat in the visceral and subcutaneous abdominal region), but not lower body fat is strongly associated with insulin resistance and increased risk of cardiovascular events (63-67) although the causal nature of this relationship and the relative importance of visceral versus subcutaneous abdominal fat (68,69) are still debated (70,71). There are differences in lipolysis between visceral and subcutaneous fat, with visceral fat shown to have higher lipolytic activity and lower sensitivity to the antilipolytic action of...

Dietary Modifications

Another important but not well-appreciated dietary change has been the substantial increase in fructose intake (in the form high fructose corn syrup), which appears to be an important causative factor in the metabolic syndrome. Soft drink consumption is, for most people, the largest source of dietary fructose. Fructose is a powerful reducing sugar, and can react with proteins through the Maillard reaction (glycation), which may account for several complications of diabetes mellitus and accelerating aging. Fructose may contribute to development of insulin resistance, weight gain, accelerated LDL oxidation, triglyceride elevation, hypertension, protein glycation.

Repercussions of DM in sexual life

It should be noted that DM can cause hardening and stenosis of the arteries that impede the smooth and sufficient flow of blood into the penis. At the same time, DM can cause damage in the nerves that connect the nervous system with the penis, thus leading, through this additional mechanism, to erectile dysfunction. The presence of other factors, from those already mentioned, can also aggrevate the problem (mainly smoking, hypertension, alcoholic abuse and certain categories of medicines). In rare cases the existence of hypogonadism is also a contributory factor. Overweight or obese diabetic individuals very frequently suffer from this metabolic syndrome and are characterized, among other things, by low levels of sex hormone binding globulin (SHBG). This globulin is connected in plasma with the sex hormones. Decreased levels, although affecting the total levels of testosterone, do not influence the levels of free testosterone, which are the active levels. Thus, the determination only...

Diabetic dyslipidemia

The incidence of recurrent coronary heart disease (CHD) events (CHD death, non-fatal myocardial infarction, coronary artery bypass graft and revascular-ization) by 25 . There were 586 patients with diabetes in this study. In the Veterans Affairs HDL Intervention Trial (VA-HIT), gemfibrozil was used as secondary prevention. Patients had documented CHD with low HDL cholesterol levels and the aim was to study the effect of gemfibrozil on the risk of recurrent CHD events. About half of the patients had either type 2 DM or abdominal obesity and hyperinsuline-mia (insulin resistance metabolic syndrome). Gemfi-brozil reduced the risk of myocardial infarction and CHD-related mortality by 22 without any lowering of LDL cholesterol.

Detecting Prediabetes

A person with prediabetes does not usually develop eye disease, kidney disease, or nerve damage (all potential complications of diabetes, which I discuss in Chapter 5). However, a person with prediabetes has a much greater risk of developing heart disease and brain attacks than someone with entirely normal blood glucose levels. Prediabetes has a lot in common with insulin resistance syndrome, also known as the metabolic syndrome, which I discuss

Treatment for Diabetes Mellitus A Potential Therapy for Breast Cancer

6 Vona-Davis L, Howard-McNatt M, Rose DP Adiposity, type 2 diabetes and the metabolic syndrome in breast cancer. Obes Rev 2007 8 395-408. 18 Efstratiadis G, Tsiaousis G, Athyros VG, Karagianni D, Pavlitou-Tsiontsi A, Giannakou-Darda A, Manes C Total serum insulin-like growth factor-1 and C-reactive protein in metabolic syndrome with or without diabetes. Angiology 2006 57 303-311.

Classification Of Diabetes

IFG and IGT refer to a pathophysiologic state between normality and frank diabetes. Patients with IGT may only manifest as hyperglycemic when challenged with an oral glucose load. Between 10 and 15 of IGT patients will develop type 2 diabetes within 5 years, although some may return to normal glucose tolerance. Although patients with IGT do not normally develop the microvascular complications of diabetes, they commonly display other features of the insulin resistance syndrome (also known as syndrome X, the metabolic syndrome or Reaven's syndrome), e.g. hypertension and dyslipidemia, and IGT is associated with a major increase in cardiovascular risk.

Insulinsensitive and resistant Variants in Type Diabetes in African Americans

Table 9A.4 Association of plasma insulin or insulin resistance to the components of the metabolic syndrome X in black subjects Table 9A.4 Association of plasma insulin or insulin resistance to the components of the metabolic syndrome X in black subjects Central obesity SSST waist WHR Central obesity total visceral fat measured by computed different cardiovascular disease outcomes (72,83). Serum triglyceride is inversely related to insulin mediated glucose disposal levels, visceral fat and liver fat (86). The presence of insulin-resistant and insulin-sensitive diabetic subtypes with differing cardiovascular risk factors is consistent with the lower serum triglyceride levels and higher HDL-cholesterol levels found among African Americans and Afro Caribbeans compared to whites (48,51,56,69) and their lower rates of cardiovascular disease (6,55).

Preoperative Evaluation Of The Diabetic Patient

Diabetes and impaired glucose tolerance are major risk factors for the development of atherosclerotic vascular disease (33-36). Diabetics have a nearly six-fold greater risk for developing a first-time myocardial infarction (20.2 vs. 3.5 ) and a higher rate of re-infarction (45 vs. 18.8 ) when compared to non-diabetics (37). Associated risk factors (hypertension, dyslipidemia, family history, central obesity, and smoking) greatly increase the risk of a diabetic dying from cardiovascular disease (34,35). Myocardial infarction (MI) continues to be the leading cause of mortality in hospitalized patients with diabetes. The incidence of perioperative MI (< 7 days after non-cardiac surgery) in patients without a history of previous MI, has been reported in the range of 0.13 to 0.66 . A higher incidence has been confirmed in patients with diabetes. Patients that have experienced a previous MI have an increased risk of acute MI in the perioperative period (4.3-15.9 ). The incidence of...

The Role of Intensive Glycemic Control in the Management of Patients who have Acute Myocardial Infarction

An alternative explanation for the relationship between glucose levels that are measured upon hospital admission and prognosis is the link between insulin resistance, the metabolic syndrome, and cardiovascular (CV) disease. Metabolic syndrome is characterized by insulin resistance and the association with traditional (the deadly quartet'' of obesity, hypertension, glucose intolerance, atherogenic dyslipidemia) and novel (endothelial dysfunction, proinflamma-tory state, hypercoagulability) risk factors for the development of CV disease and DM 17,18 . The metabolic syndrome is present in approximately 30 of middle-aged men 17 and is associated with a threefold to fourfold increase in CV mortality as compared with controls, even when patients who had known CV disease and DM were excluded from analysis 18 . Patients who have insulin resistance and frank DM also may have a host of associated conditions (Box 1) that may contribute to a poor CV prognosis.

Generalised Endothelial Dysfunction Chronic Lowgrade Inflammation Microalbuminuria And Atherothrombosis

Diabetes is associated with activation of the coagulation cascade (1). Hyperglycaemia, non-enzymatic glycation and oxidative stress increase tissue factor activity and factor VII activity, decrease antithrombin activity and impair heparan sulphate synthesis. Initially, anticoagulant defenses such as the response to activated protein C and the secretion of tissue factor pathway inhibitor may be enhanced. In patients with micro- and macroalbuminuria, i.e. in those with severe endothelial dysfunction, activation of the coagulation cascade increases further and endothelial anticoagulant defenses may be overwhelmed. In addition, patients with the metabolic syndrome have high PAI-1 levels and thus impaired fibrinolysis. Importantly, increased coagulation and impaired fibrinolysis may increase thrombus formation and persistence after plaque rupture, and in part explain the poor prognosis of diabetic patients after myocardial infarction.

Modifiable Risk Factors

Central obesity Visceral adiposity precedes the development of type 2 diabetes. Boyko et al. (40) showed in their study of Japanese Americans that intra-abdominal fat area measured by computed tomography (CT) remained a significant predictor of diabetes incidence even after adjustment for body mass index, total body fat area, and subcutaneous fat area and other risk factors for diabetes. Interestingly, high insulin resistance and low insulin secretion predicted diabetes independently of directly measured visceral adiposity suggesting that visceral adiposity could contribute to the development of diabetes through actions independent of its effect on insulin sensitivity. Van Dam et al. (41) showed that in Dutch subjects the association between abdominal obesity (waist circumference) and hyperglycemia was stronger in the presence of a parental history of diabetes. Physical inactivity is a major risk factor for the development of type 2 diabetes. For example, sedentary lifestyle,...

Why do Obesity TDM and Nafld Cluster The Liver as the Metabolic Sensor of Lipotoxicity

As with obesity and T2DM, there is also considerable concern that NAFLD and NASH are reaching epidemic proportions (287) . However, the true magnitude of the disease is not appreciated by many clinicians because the majority ( 70 ) of patients affected have normal liver enzymes (279, 288-290). It has been recently estimated that fatty liver disease affects 1 3 of the adult population or 80 million Americans, and as many as 2 3 of obese subjects in the United States (278, 279, 288). In a large population-based study (n 2,287 subjects) performed in Dallas, Texas, in which liver fat was evaluated by means of the gold-standard MRS technique, 34 of the population had a fatty liver, being much more common in Hispanics (45 ) compared to whites (33 ) and African-Americans (22 ) (288). That adult Hispanic are affected more than Caucasians and African-Americans has been confirmed by others even after adjusting for major confounding variables (94, 96, 99, 101, 291-294). Recent studies indicate...

What are the risk factors for the development of DM

For Type 2 DM, epidemiologic studies as well as data from its pathophysiology and natural history, have shown various factors that are related to an increased frequency of its appearance. These factors are age > 45 years, obesity (BMI > 25 kg m2), family history of DM, a sedentary life-style, certain racial groups and nationalities (African Americans or Hispanics, Native Americans, Pacific Islanders, etc.), history of gestational DM or birth of a child > 4 kg (8.8 lb), history of hypertension or dyslipidaemia and the polycystic ovary syndrome. Also, a low birth weight and cigarette smoking have been associated epidemiologically with the risk of developing DM. However, the most powerful association has been found with the presence of Impaired Fasting Glucose (IFG) and or Impaired Glucose Tolerance (IGT). IFG is defined as the presence of fasting plasma glucose levels between 110-125 mg dl 6.1-6.9 mmol L for Europe 100-125 mg dl 5.6-6.9 mmol L for America), and IGT is the presence...

Peripheral Arterial Disease

The patient with type 2 diabetes is more prone to atherogenic dyslipidemia and the metabolic syndrome and has a fourfold increased risk of developing peripheral arterial disease, with the symptoms in patients with diabetes not directly correlating with gly-cemic control.

Protease Inhibitors PI

The introduction of highly active antiretroviral therapy (HAART) has significantly improved the survival and quality of life of HIV-infected individuals. However, HARRT-regimen, especially those including PIs have also resulted in increased incidence of metabolic syndrome and diabetes. Eleven PIs are now available in US and at least eight of them are clearly

How Common Is Diabetes

Full-blown adult-onset diabetes affects an estimated 15 million Americans, about half of whom have not been officially diagnosed with the disease. (Juvenile-onset diabetes is an autoimmune disease that is rarely reversible.) However, as many as 70 million Americans have some degree of insulin resistance or Syndrome X. Syndrome X refers to a cluster of insulin resistance, high blood pressure, abdominal obesity, and elevated cholesterol and triglycerides. (For more information see my previous book Syndrome X.) Basically, anyone eating the typical American diet is consuming foods that increase the risk of insulin resistance, Syndrome X, and diabetes.

Lifestyle and Type Diabetes

In addition to advancing age, being overweight or obese, and inactivity, inheritance plays a large role in diabetes. Although all of the specific genes that underlie obesity, the metabolic syndrome, and diabetes have not been identified, it is clear that the risk of developing these conditions and diseases is inherited. But how can we explain the widespread inheritance of diseases, the effects of which are so devastating How would Darwin explain the natural selection process that leads to diabetes The widespread inheritance of risk for obesity, diabetes, and the insulin resistance that underlies much of type 2 diabetes does make sense according to a theory called the thrifty gene hypothesis. Until just a few centuries ago, human beings lived in peril of famine. During times of famine, thrifty genes that decreased energy expenditure were highly advantageous to human survival because the energy people took in was small, and because of difficulty in finding food, burning less energy...

The Insulin Resistance Syndrome

Insulin resistance and hyperinsulinemia are frequently associated with a cluster of clinical and biochemical abnormalities that have been described with increasing detail and given a variety of names including deadly quartet, syndrome X, insulin resistance syndrome, metabolic syndrome, and cardiovascular dysmeta-bolic syndrome (9-13). Many prefer to call it insulin resistance syndrome because insulin resistance and the resulting hyperinsulinemia appear to be the underlying abnormalities from which the other features of the syndrome are derived (see Chap. 7). The hallmarks of insulin resistance syndrome are obesity, particularly central or intra-abdominal obesity, glucose intolerance, or type 2 diabetes mellitus, hypertension, a dyslipidemia characterized by elevated triglycerides, low HDL cholesterol and small dense LDL cholesterol, a hypercoagulable state characterized by alterations in both thrombosis and fibrinolysis and increased

How Our Lifestyle Has Made Us Vulnerable to Diabetes

In 1985, an estimated 30 million cases of diabetes existed worldwide. This number increased to 177 million in 2000 and is estimated to rise to at least 370 million by 2030, almost all from type 2 diabetes associated with aging, obesity, and inactivity. In the United States, the numbers of cases of diabetes and obesity have risen in parallel. Diabetes and prediabetes affect 18 million and almost 40 million persons, respectively, and the metabolic syndrome affects almost 25 percent of the U.S. population.

Risk Factors For Stroke In Diabetic Subjects

Metabolic Syndrome (MS) as Stroke Risk Factor The term metabolic syndrome (MS) refers to a cluster of risk factors, including hypertension, dyslipidemia, obesity, and abnormalities in glucose metabolism that are closely associated with DM (in particular type 2 DM) and with cardiovascular disease, including stroke. Although the fact that these risk factors often co-occur is not debated, it is yet uncertain if the whole concept of the MS entails more than its individual components. The clustering of risk factors complicates the assessment of the contribution of individual components to the risk of vascular events, as well as assessment of synergistic or interacting effects. In addition, there is no general agreement on the actual definition of the syndrome (NCEP, 2001, 2005 WHO, 1999 IDF, 2005), and it is yet unclear if the presence of the MS has a higher predictive value for cardiovascular disease than widely used prediction scores such as Framingham, PROCAM, and SCORE (73-75). In the...

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