Obesity, Atherosclerosis and Diabetes Mellitus
Obesity, non-insulin dependent diabetes mellitus (NIDDM) and atherosclerosis are three prevalent conditions which might be causally related. Recent studies have reemphasized the importance of abdominally localized obesity as a risk factor for the development of both NIDDM and atherosclerosis in prospective studies. Abdominally localized obesity is also associated with other male features in women such as an elevated muscle mass which is relatively insulin resistant, and containing less of insulin sensitive red (slow twitch) muscle fibers. Furthermore, such women have endocrine abnormalities including elevated plasma free testosterone and low sex hormone binding globuline. Obesity in terms of elevated total body fat mass is not always present in the android syndrome. Speculatively, an increased peripheral insulin resistance, a cardinal prerequisite for the development of NIDDM, might be caused by a number of factors in this android syndrome. First, the lipolytically sensitive enlarged abdominal adipose tissues might produce excess free fatty acids to create peripheral insulin sensitivity. Second, the primary fault might be in the insulin resistant muscle, due to its low contents of red muscle fibers. Third, this in turn might be a consequence of the excess of circulating free testosterone. Fourth, an unknown factor might cause the various symptoms of the android syndrome in parallel. Whatever the mechanism, there are several possibilities to understand why the android syndrome is associated with an early insulin resistance and a hyperinsulinemia. It is of considerable interest that hyperinsulinemia has been shown to be an independent risk factor for myocardial infarction, and to be able to induce other established risk factors for this disease such as hyperlipidemia and, perhaps, hypertension. In this way one might visualize a speculative chain of events starting out from the android syndrome, in which insulin resistance is developing early, followed by on the one hand NIDDM and on the other atherosclerotic manifestations directly or via the promotion of development of other established risk factors for myocardial infarction.
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