Authors: Eric Winkel Arick Sabin Rafael MejíaAlvarez
Publish Date: 2012/07/17
Volume: 42, Issue: 3, Pages: 746-748
Abstract
The lipodystrophy frequently observed with prolonged hypercortisolism ie Cushing’s disease is characterized by increased visceral adipose tissue VAT and decreased peripheral subcutaneous adipose tissue SAT A very similar lipodystrophy is seen in HIV patients particularly when they are using protease inhibitors 1 Although not demonstrated it has been suggested that this cushingoid lipodystrophy results from differences in insulin resistance between VAT and SAT However cortisol also affects lipid metabolism through glyceroneogenesis GLN wherein nonglucose substrates such as lactate pyruvate and amino acids are converted to glycerol to form triacylglycerol Regulation of GLN mainly occurs via expression of the enzyme phosphoenolpyruvatecarboxykinase PEPCK Specifically cortisol increases PEPCK expression in the liver while in adipose tissue induces the opposite effect Thus it is possible that the cushingoid lipodystrophy results from
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