Few data exist on predictors of non-insulin-dependent (type II) diabetes mellitus. We examined body mass index (BMI), ratio of subscapular-to-triceps skin fold (centrality index), and fasting glucose and insulin concentrations as predictors of decompensation to type II diabetes in Mexican Americans, a population at high risk for this disorder. Twenty-eight of 474 initially nondiabetic Mexican Americans developed type II diabetes after 8 yr of follow-up. Converters to diabetes were older and had higher BMIs, centrality indices, and fasting glucose and insulin concentrations than nonconverters. Subjects in the highest quartile of the insulin distribution had 6.6 times the risk of developing type II diabetes as subjects in the remaining three quartiles combined (95% confidence interval [CI] = 3.14-13.7). In multivariate analysis, fasting glucose (odds ratio [OR] = 5.80, 95% CI = 2.57-13.1) and insulin (OR = 3.12, 95% CI = 1.36-7.14) remained significantly related to conversion to diabetes. However, BMI and centrality index, which were significantly related to conversion in the univariate analysis, were no longer significant in the multivariate analysis once glucose and insulin concentrations were taken into consideration, suggesting that the effect of these variables may be mediated by insulin resistance. Nearly half of the incident cases developed in a subset of the population who were simultaneously in the highest quartile of both fasting insulin and glucose concentrations (population-attributable risk 44.2%). Our results support the insulin resistance/pancreatic exhaustion theory of type II diabetes.

Insulin resistance is thought by many to be the primary defect that results in non-insulin-dependent diabetes mellitus (NIDDM). An implication of this theory is that prediabetic persons have higher serum insulin levels than normal subjects. We assessed serum insulin concentrations in a cohort of 1497 nondiabetic Mexican Americans, a population at high risk for NIDDM, according to whether their parents or siblings had diabetes. It was assumed that prediabetic persons would be more likely to have strong family histories of diabetes. We found a stepwise increase in fasting insulin levels in nondiabetics with neither, one, or both parents with diabetes (69.8, 77.8, and 94.6 pmol per liter, respectively; P = 0.002). Similar results were observed for insulin sum (the total of insulin concentrations in the fasting state and at 30, 60, and 120 minutes after a 75-g oral glucose load). The differences in insulin sums according to family history remained statistically significant in analyses of covariance, which controlled for variations in body-mass index, body-fat distribution, and level of blood glucose. Subjects without diabetes who had a diabetic sibling had higher fasting concentrations of insulin than subjects without a diabetic sibling (83.2 vs. 69.6 pmol per liter), but the difference was not statistically significant. We conclude that prediabetic persons, who would be expected to be more numerous in kindreds with progressively stronger family histories of diabetes, have hyperinsulinemia. This supports the insulin-resistance hypothesis.

Microalbuminuria is associated with progression to renal disease In Insulindependent diabetes and wtth Increased mortality in noninsulln-dependent diabetes. In contrast, few studies have addressed the effect of mlcroalbumlnurla on cardiovascular risk In nondlabetics. We, therefore, determined the level of microalbuminuria In 316 nondiabetic subjects from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular risk factors. Microalbuminuria (£30 mg/l) was found In 42 of these 316 subjects (13%). Subjects wtth mlcroalbumlnurla had significantly higher blood pressure, trlglyceride concentration, sum of Insulin concentrations during a glucose tolerance test, and prevalence of hypertension and of self-reported myocardlal Infarction than subjects without microalbuminuria. When subjects with hypertension were excluded (n=27), normotensive subjects with mlcroalbumlnurla (n=31) still had significantly higher trlglyceride concentrations and Insulin sum than normotensive subjects without microalbuminuria (n=258), suggesting that an increased atherogenlc risk factor pattern exists even In normotensive subjects with microalbuminuria. Microalbuminuria may be a marker for cardiovascular risk, although It Is not certain whether microalbuminuria causes these metabolic changes or results from some metabolic disturbance such as insulin resistance.

The incidence of type II diabetes in Mexican Americans is greater than in non-Hispanic whites, a difference that is not explained by ethnic differences in obesity, age, or level of educational attainment.

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