Abdominal obesity and the metabolic syndrome

Abstract

Abdominal obesity in man is an integrated part of the Metabolic Syndrome, and is associated with a complex neuroendocrine disturbance. Its consequences for the metabolism of the periphery seems to be insulin resistance caused by a combination of a relative hypercortisolaemia and a relative deficiency of sex steroid hormones. This hormonal aberration, in combination with a relative insufficiency of growth hormone secretion, might also direct depot triglycerides to visceral adipose tissues, a consequence at least partly due to varying densities of the specific receptors for these hormones. Visceral fat accumulation may thus be a consequence of the neuroendocrine aberrations, and may amplify the metabolic symptoms via effects on the liver of free fatty acids released in abundance from the lipolytically sensitive enlarged visceral fat depots. The origin of the neuroendocrine disturbance is not known, but epidemiological and cross-sectional information suggest that psychosocial factors are intimately involved. Animal and human studies indicate that the mediating factor(s) may be stress-sensitivity, leading to the neuroendocrine consequences observed.