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PIAS1 regulates systemic insulin sensitivity by inhibiting inflammation response

刘洋  葛辛  汤其群  
【摘要】:Over the last decade, an abundance of evidence has emerged demonstrating a close linkbetween metabolism and immunity. It is now clear that obesity is associated with a state ofchronic low-level inflammation. Obesity-induced inflammation contributes to diabetes. It iswell recognized that PIAS1(Protein Inhibitor of Activated STAT 1), a SUMO(small ubiquitinlike modifier) E3 ligase, modulates such cellular processes as cell proliferation, DNAdamage responses, and inflammation responses. Recent studies have shown that PIAS1 also involves in adipocyte differentiation and energy metabolism. However, the role of PIAS1 in insulin sensitivity remains unknown. Here we showed that PIAS1 protected bodyfrom insulin resistance induced by gene deficit or high fat diet. PIAS1 was downregulatedin the adipose tissue of diabetic models, including ob/ob, db/db and DIO mice. Ectopic expressionof PIAS1 in diabetic adipose tissue improved systemic insulin sensitivity. Similareffect of PIAS1 was shown in 3T3-L1 adipocytes. Cellular inflammation response may bethe underlying mechanism. We found that PIAS1 inhibited expression of NF-κB targetgenes, mainly including inflammation genes. Furtherstudies clarified that PIAS1 inhibitedmacrophage infiltration in adipose tissue, thus suppressing inflammation response. In conclusion,PIAS1 improved systemic insulin sensitivity by inhibiting cellular inflammation.

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