Body Fat Distribution and Insulin Resistance

The effect of generalized obesity and particularly central body fat distribution on insulin resistance and incidence of type 2 diabetes was convincingly demonstrated in epidemiological and experimental studies. However, the impact of visceral and subcutaneous abdominal fat depots remains unclear. Various epidemiological data suggested an increased risk of insulin resistance and type 2 diabetes in individuals with visceral obesity. High free fatty acids, elevated activity of 11b-hydroxysteroid dehydrogenase type 1 in visceral adipose tissue, low levels of testosterone, growth hormone and IGF-1 or the increased secretion of plasminogen activator inhibitor-1 and of several cytokines, like TNF-alpha and IL-6 are candidates potentially mediating these effects. The impact of other abdominal fat compartments like subcutaneous abdominal adipose tissue is still under debate, even if some studies indicate a separate effect of this fat compartment on insulin resistance and glucose tolerance. Furthermore a growing body of evidence suggests insulin resistance inducing effects of increased intramyocellular lipid levels. However, the precise impact of the muscular lipid content and the mechanisms linking intramyocellular fat and insulin resistance are still not fully understood.