Overnutrition, increased macronutritient intake, physical inactivity, and ageing are associated with expansion of adipose tissue mass and cytokines, favoring in genetically and metabolically susceptible subjects, the development of insulin resistance, metabolic syndrome and diabetes. Adipose tissue distribution in human is dependent on genetic and environmental factors. The control of the rate of filling of adipocytes seems to be the main factor determining the local, regional mass of adipose tissue. Causes of visceral fat accumulation include glucocorticoid excess or decreased estrogen/androgen ratio either in plasma or within adipose tissue. Intra-adipose sex steroid metabolism is a determinant of gynoid versus androgen patterns of body fat. Abdominal obesity is associated with greater risk for hypertension, dyslipidemia, type 2 diabetes and coronary heart disease, due to increased release of free fatty acids from visceral fat to the liver. Visceral fat is highly active metabolic and endocrine organ that secretes many adipokines with action at local and systemic level. Dysregulation of adipokines contributes to the pathogenesis of the obesity-associated metabolic syndrome, resulting in insulin resistance, type 2 diabetes, hypertension, hyperlipidemia and vascular disease. Sex differences in visceral fat lipolysis are responsible for more cardiovascular complications in men than in women. Obesity, insulin resistance and type 2 diabetes are characterized by chronic low-grade inflammation. Adipose tissue of obese insulin resistant subjects is characterized by increased expression and/or secretion of inflammatory molecules, including TNF-a, IL-6, PAI-1 and leptin while the insulin-sensitizing factor adiponectin is downregulated. Macrophage infiltration in adipose tissue in obesity contribute to the reported inflammatory profile in abdominal obesity. Local inflammation in the expanded adipose tissue mass among obese subjects is proposed to be a partly responsible for obesity-related insulin resistance. Visceral obesity might also be a marker of defective fat portioning between the adipose tissue, the skeletal muscle, the liver and the heart.
03 - 07 May 2008
European Society of Endocrinology