Type 2 diabetes is very different from type 1 diabetes in its underlying etiology and its natural history. Insulin resistance, which is defined as a less than normal effect of insulin on in vivo glucose uptake and metabolism, occurs in a high proportion of the population of societies embracing western culture (10,26). Factors responsible for the development of insulin resistance are only partially understood. Fetal malnutrition predisposes to insulin resistance in postnatal life (27). Excess calorie intake and reduced physical activity lead to exaggerated lipid deposits and obesity. The proportion of excess calories deposited as lipids in subcutaneous adipose tissue relative to visceral adipose tissue is both genetically and hormonally determined (28). An increase in visceral adiposity but not subcutaneous adiposity is highly correlated with insulin resistance and the components of the metabolic syndrome (29,30). There is a significant correlation between visceral adiposity and both liver and muscle triglycerides so that it is difficult to dissect the contribution that each of these makes to the insulin resistance (31,32). The normal compensatory response to insulin resistance is an increase in insulin secretion sufficient to overcome the insulin resistance. As long as the compensatory increase in insulin secretion is sufficient to overcome the insulin resistance, glucose metabolism and plasma glucose levels will remain normal (8,26). However, such individuals will have a cluster of metabolic abnormalities (Table 3) that are associated with the insulin resistance (10,26). These metabolic abnormalities are cardiovascular risk factors and the cluster is referred to as the insulin resistance syndrome, the metabolic syndrome, or, more recently, the dysmetabolic syndrome. This syndrome leads to the development of type 2 diabetes in those individuals with genetically predisposed beta cells (9).
Cardiovascular disease is two to four times more prevalent in patients with type 2 diabetes than in age-matched nondiabetic persons. The time course of the -o increase in cardiovascular disease is exemplified in Figures 3 and 4 which plot |
cumulative mortality from coronary heart disease during 24 years of follow-up £
of a cohort of patients whose diabetes was diagnosed between 35 and 64 years of age (type 2 diabetics) (14). The striking difference between the cumulative <j mortality curves in the type 2 diabetic patients as contrasted to the type 1 diabetic patients shown in Figures 1 and 2 are the early mortality noted at diagnosis and
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