Hepatocyte TRAF3 promotes insulin resistance and type 2 diabetes in mice with obesity

Molecular Metabolism
Zheng ChenLiangyou Rui

Abstract

Metabolic inflammation is believed to promote insulin resistance and type 2 diabetes progression in obesity. TRAF3, a cytoplasmic signaling protein, has been known to mediate/modulate cytokine signaling in immune cells. The goal is to define the metabolic function of hepatic TRAF3 in the setting of obesity. Hepatocyte-specific TRAF3 knockout mice were generated using the loxp/albumin-cre system. Liver TRAF3 was deleted in adult obese mice via Cre adenoviral infection. Both high fat diet-induced and genetic obesity were examined. TRAF3 levels and insulin signaling were measured by immunoblotting. Insulin sensitivity, hepatic glucose production, and glucose metabolism were examined by glucose, insulin, and pyruvate tolerance tests. Hepatic steatosis was examined by Oil red O staining of liver sections and measuring liver triacylglycerol levels. Liver TRAF3 levels were lower in the fasted states in normal mice, and were aberrantly higher in obese mice and in mice with streptozotocin-induced hyperglycemia. Glucose directly increased TRAF3 levels in primary hepatocytes. Hepatocyte-specific deletion of TRAF3 decreased hyperinsulinemia, insulin resistance, glucose intolerance, and hepatic steatosis in mice with either high fat diet-in...Continue Reading

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Citations

May 1, 2016·Nucleic Acids Research·Wangshu QinZheng Chen
Sep 15, 2016·Heart Failure Reviews·Li TaoZheng Chen
Oct 19, 2016·Scientific Reports·Nurbek MambetsarievGail A Bishop
May 31, 2018·Medicinal Research Reviews·Jingjing CaiHongliang Li
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Jun 6, 2020·Nature·Cassandra N SpracklenXueling Sim

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