Novel phosphorylation of PPARγ ameliorates obesity-induced adipose tissue inflammation and improves insulin sensitivity.

摘要: Chronic inflammation in adipose tissue is highly associated with insulin resistance. Herein, we demonstrate that a novel modification of PPARγ strongly inflammatory responses tissue. c-Src kinase directly phosphorylated at Tyr78, and this process was reversed by protein tyrosine phosphatase-1B (PTP-1B). In adipocytes, phosphorylation suppressed the expression pro-inflammatory genes as well secretion chemokines cytokines, thus reducing macrophage migration. Importantly, pharmacological inhibition aggravated resistance obese mice concomitant increase These data suggest key regulatory mechanism response tissue, which glucose tolerance sensitivity. Furthermore, these our understanding mechanical aspects developing anti-diabetic drugs targeting phosphorylation.