Vascular thrombosis in type II diabetes mellitus.

One prevailing point of view is that many individuals with established type II diabetes have gone through years of impairment of glucose tolerance and hyperinsulinism before the appearance of fasting hyperglycemia (1,2). Peripheral insulin resistance plus a pancreatic p-cell insulin secretory defect presumably wage a battle over the years that results ultimately in clinically apparent type II diabetes (3). If this sequence of events is correct, many individuals with type II diabetes have had years of hyperinsulinism, in contrast to their ageand sex-matched control subjects. Further, there may be a disproportionate elevation of plasma proinsulin levels in individuals with IGT and frank diabetes (4,5). These individuals are at a high risk for cardiovascular events, and this increased risk does not appear to be completely explained by the association of IGT or type II diabetes with such classical risk factors as hypertension, hypercholesterolemia, or cigarette smoking (6). These observations have led to numerous studies directed at determining the pathogenesis of accelerated cardiovascular disease in diabetes; a daunting challenge, for atherosclerosis in nondiabetic individuals is an extraordinarily complex process (7). The early events appear to involve macrophage adherence to endothelium, followed by macrophage migration to the subendothelial space. Here, macrophages may be transformed into foam cells.