Insulin Resistance And Impaired Insulin Secretion As Predictors Of Type Diabetes

Type 2 diabetes is caused by impaired insulin action (insulin resistance) and/or impaired insulin secretion. Insulin resistance is a characteristic metabolic defect in the great majority of patients, and it also precedes the development of frank hyperglycemia. Impaired insulin action is observed in several tissues, e.g., skeletal muscle, adipose tissue, and the liver. It leads to increased insulin secretion from the pancreas to overcome impaired insulin action. Compensatory hyperinsulinemia maintains glucose levels within the normal range but in individuals destined to develop diabetes, beta-cell function eventually declines and leads to hyperglycemic diabetic state. In a minority of subjects diabetes develops as a consequence of a primary defect in insulin secretion. Between 2% and 14% (on average about 5%) of people with IGT progress to type 2 diabetes each year (34). The progression rate is influenced by age, ethnicity, and the degree of glucose intolerance.

The degree of insulin resistance varies between different ethnic groups. For example, in the Insulin Resistance Atherosclerosis Study (35) including 1100 healthy subjects African-Americans and Mexican Americans had a lower insulin sensitivity than non-Hispanic whites. The first study to demonstrate that a combination of insulin resistance and impaired insulin secretion predicts type 2 diabetes was published on Pima Indians. Lillioja et al. (36) showed that low insulin secretory response and increased insulin resistance were both predictors of type 2 diabetes. Furthermore, both impaired insulin secretion and insulin resistance acted as an independent risk factor. Quite similar results were published on Mexican Americans. During the 7-year follow-up baseline high-fasting insulin level (indicator of insulin resistance) predicted the conversion to diabetes (37). Furthermore, low insulin secretion assessed by insulin response (30 min insulin minus fasting insulin divided by 30 min glucose minus fasting glucose) also predicted the development of diabetes. When these two parameters were combined they had an additive effect on the risk of developing diabetes. High degree of insulin resistance and normal insulin secretion increased the risk by 4.5-fold, and high insulin sensitivity but low insulin secretion increased the risk by 5.4-fold, whereas the combination of these two increased the risk by 13.9-fold (Fig. 2).

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