Tissu adipeux viscéral : rôle majeur dans le syndrome métabolique

The relationship between excess visceral fat and insulin resistance seems to play a central role in the development of the metabolic syndrome. The portal fat hypothesis is based on a unique venous drainage of visceral fat depot and its increased lipolytic activity, that could explain hepatic insulin resistance. On the other hand the offensives (visfatine, TNFα, PAI-1 and IL6) or defensives cytokines (adiponectine) secreted by visceral fat contribute to the pathogenesis of hepatic and systemic insulin resistance. Obesity can be considered as a low grade systemic inflammatory disease with a particular role for macrophage infiltration in omental adipose tissue. Numerous cross-sectional and a few longitudinal studies are in favour of this third paradigm. Nevertheless, intra abdominal obesity is not the only culprit. Increased subcutaneous abdominal fat and decreased leg fat mass have independent and opposite associations with metabolic abnormalities of the metabolic syndrome. The ectopic fat storage syndrome and the lipodystrophic adiposity hypothesis give a major role to the dysregulation of free fatty acid fluxes between white adipose tissue and other tissues, i.e. the muscle, the liver and probably the beta cell. As far as insulin resistance is concerned, increased visceral fat could have a dramatic effect at the beginning of abdominal obesity development or for patients with severe metabolic syndrome associated with partial lipodystrophy.