In Obesity/Metabolic Syndrome, high plasma fatty acids regulate genes responsible for increase insulin resistance, visceral fat deposits, fatty acid oxidation, and thermogenesis. Many of these responses have a role in metabolic syndrome, obesity and diabetes. Glucocorticoid receptor (GR) regulates several genes that have been implicated in insulin sensitivity. The glucocorticoid receptor is activated by binding to cortisol which is supplied by the conversion of cortisone by corticosteroid 11-beta-dehydrogenase. The mechanism for increased visceral fat levels is the over expression of lipoprotein lipase from glucocorticoid receptor activity. Lipoprotein lipase increases free fatty acids in tissues by cleaving fatty acids from triacylglycerols. PPAR-gamma is a fatty acid activated transcription factor involved in a complicated regulatory network of transcription factors that modulated fatty acid oxidation, thermogenesis and mitochondria biogenesis.

Obesity / Metabolic Syndrome References