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■c impaired fasting glucose. IFG is defined as a fasting plasma glucose >110 mg/ dL (6.2 mmol/dL) and <126 mg/dL (7.0 mmol/dL). The introduction of this category has created much controversy. Many analyses of data bases, including those in the DECODE study, have shown that IFG consists of some who would be diagnosed as type 2 diabetics by the 2-h post-glucose-challenge plasma glucose >200 mg/dL (11.1 mmol/L), some who have IGT, and a small subset who have only IFG (39,40). Some series show that IFG predicts CV disease while others show little or no predictive value (41). In studies where IFG predicts future CVD (as in the CARE secondary prevention study employing pravastatin in patients post myocardial infarction), the IFG cohort has the insulin resistance syndrome with increased BMI and waist circumference, increased systolic blood pressure, and the characteristic dyslipidemia (42).

Insulin resistance can occur very early in life. Data from an ongoing prospective study of low-birth-weight infants in India indicate that these children can develop the insulin resistance syndrome as early as 8 years of age. Many studies have found insulin resistance in young adults who are first degree relatives of individuals who have type 2 diabetes. Insulin resistance is a characteristic of individuals who have visceral obesity. Individuals who are obese as assessed by BMI are not necessarily insulin resistant nor do they have the insulin resistance syndrome. Brochu et al. examined the metabolic characteristics of 43 obese, sedentary, postmenopausal women (44). Despite comparable BMI (31.5 vs. 34.7 kg/ m2) and fat mass (37.3 vs. 39.0 kg), 17 individuals had normal insulin sensitivity and 26 were insulin resistant as assessed by the euglycemic hyperinsulinemic clamp. The obese individuals with normal insulin sensitivity had 49% less visceral adipose tissue than the resistant individuals, and had normal fasting and post-glucose-challenge plasma glucose and insulin and mean plasma triglycerides of 1.50 mmol/L (133 mg/dL) and plasma HDL cholesterol of 1.16 mmol/L (45 mg/dL). The insulin-resistant individuals had hyperinsulinemia and the classic dyslipidemia of insulin resistance as well as borderline increases in fasting and post-glucose-challenge plasma glucose levels.

The evidence suggesting that the insulin resistance syndrome plays a central role in the development of macrovascular disease in type 2 diabetic patients comes from many sources. In 1989, Banerji and Lebovitz described two variants of type 2 diabetes: one with impaired insulin action (insulin-resistance variant) and one with normal insulin action (insulin-sensitive variant) (6). Their insulinsensitive patients had none of the components of the insulin resistance syndrome, while the insulin-resistant patients had the classic insulin resistance syndrome (17). These observations were extended by Haffner et al., who showed that insu- g lin-sensitive type 2 diabetic patients had lower BMI and waist circumference, lower plasma triglyceride and higher plasma HDL cholesterol levels and larger, more buoyant, LDL particles, and lower plasma fibrinogen and plasminogen u

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