A. Glucose Metabolism f„

Within the population satisfying the criteria for normal glucose tolerance, the <j greater their degree of insulin resistance, the higher their plasma glucose concentration. In a smaller subset of insulin-resistant individuals, the degree of compensatory hyperinsulinemia is not sufficient to maintain normal glucose tolerance, and they are classified as having either impaired fasting glucose or impaired glu-

Table 1 Manifestations of Insulin Resistance/ Compensatory Hyperinsulinemia (Syndrome X)

A. Glucose Metabolism

1. Impaired fasting glucose

2. Impaired glucose tolerance

B. Uric Acid Metabolism

1. T Plasma uric acid concentration

2. - Plasma renal uric acid clearance

C. Dyslipidemia

1. T Triglyceride concentration

2. T Postprandial lipemia

3. - HDL cholesterol concentration

4. - LDL particle diameter

D. Blood Pressure

1. T Blood pressure

2. T Sympathetic nervous system activity

3. T Renal sodium retention

E. Procoagulant Activity

1. T Plasminogen activator inhibitor-1

2. T Fibrinogen

F. Reproductive System

1. Polycystic ovary syndrome cose tolerance. In an even smaller number of insulin-resistant individuals, insulin secretory function fails to the degree that permits manifest hyperglycemia to develop. Such individuals have type 2 diabetes. Syndrome X and type 2 diabetes share insulin resistance as a basic metabolic defect, but the designation of syndrome X should be limited to individuals who have maintained sufficient insulin secretory function to remain nondiabetic.

B. Uric Acid Metabolism

An association between increases in plasma uric acid concentration and increased CHD risk has been known for many years. Hyperuricemia is commonly seen in -o individuals with glucose intolerance, dyslipidemia, and hypertension. Significant correlations exist between plasma uric acid concentration and both insulin resistance and the plasma insulin response to an oral glucose challenge in healthy volunteers, and individuals with asymptomatic hyperuricemia have higher plasma insulin responses to oral glucose; higher TG and lower high-density lipoprotein (HDL) cholesterol concentrations; and higher blood pressure when compared to volunteers with normal serum uric acid concentrations.

The increase in plasma uric concentrations in insulin-resistant, nondiabetic individuals appears to result from a decrease in renal uric acid clearance secondary to the effect of compensatory hyperinsulinemia on the handling of uric acid by the kidney. This is one of several instances in which a manifestation of syndrome X occurs because one organ system remains sensitive to insulin action, in this case the kidney, whereas the muscle in the same individual is insulin resistant.

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