Visceral obesity, androgens and the risks of cardiovascular disease and diabetes mellitus

Abstract

The sex difference in cardiovascular morbidity is traditionally ascribed to the effects of testosterone on the lipid profile. Epidemiological studies show, however, that men with cardiovascular disease have low rather than high circulating testosterone. The factor responsible for both the higher prevalence of cardiovascular disease and the low testosterone might be visceral obesity. Men and women differ in their pattern of fat distribution. Women have predominantly gluteofemoral fat depots and men preferential abdominal/visceral depots. In puberty testosterone favors abdominal/visceral fat deposition. Visceral fat has a high metabolic turnover and the free fatty acids drain on the portal vein. With a large visceral fat depot the liver is flooded with free fatty acids inducing high levels of triglycerides and low high-density lipoprotein cholesterol, impairment of insulin metabolism and reducing insulin sensitivity. These factors contribute to the development of cardiovascular disease and diabetes type II. High insulin levels suppress sex hormone-binding globulin thus lowering circulating testosterone. The fat cell produces leptin signalling to the brain to reduce food intake and increase energy expenditure. High leptin levels suppress testosterone. Some studies suggest that testosterone supplementation reduces visceral obesity and improves cardiovascular risks but more evidence is needed.

• VISCERAL OBESITY
• ANDROGENS
• LEPTIN
• CARDIOVASCULAR DISEASE
• DIABETES MELLITUS