Androgens and abdominal obesity

Central or visceral obesity is recognized as a main risk factor for cardiov ascular disease and type 2 diabetes mellitus. The co-existence of visceral obesity, increased blood lipid levels, hypertension and impaired glucose to lerance defines the metabolic syndrome that today is widely recognized as o ne of the prime factors behind cardiovascular morbidity and mortality. Endocrine disorders such as insulinoma, hypothyroidism and hypercortisolism are known to cause obesity. However, it is only hypercortisolism that is a ssociated with increased abdominal fat accumulation. Recently, new findings have shed light on subtle endocrinopathies that are prevalent in individuals presenting with the metabolic syndrome. Such deran gements are of borderline character and often fall within the normal refere nce range. Intervention studies demonstrate that correction of relative hyp ogonadism in men with visceral obesity and other manifestations of the meta bolic syndrome seem to decrease the abdominal fat mass and reverse the gluc ose intolerance, as well as lipoprotein abnormalities in the serum. Further analysis of the underlying mechanism has also disclosed a regulatory role for testosterone in counteracting visceral far accumulation. Longitudinal e pidemiological data demonstrates that relatively low testosterone levels ar e a risk factor for development of visceral obesity. The primary event that triggers the initial development of visceral obesity is not known, but it seems plausible that increased activity in the hypoth alamus-pituitary-adrenal axis can be of major importance.