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Tumor necrosis factor alpha receptor 1 deficiency in hepatocytes does not protect from non-alcoholic steatohepatitis, but attenuates insulin resistance in mice

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World Journal of Gastroenterology 2020年第33期26卷 4933-4944页

作者： sena bluemel Yanhan Wang Suhan Lee Bernd Schnabl Department of Medicine University of California San DiegoLa JollaCA 92093United States Division of Gastroenterology and Hepatology University Hospital ZurichZurich 8091Switzerland Department of Medicine VA San Diego Healthcare SystemSan DiegoCA 92161United States

BACKGROUND End-stage liver disease caused by non-alcoholic steatohepatitis(NASH)is the second leading indication for liver *** date,only moderately effective pharmacotherapies exist to treat *** the pathogenesis of NASH is therefore crucial for the development of new *** inflammatory cytokine tumor necrosis factor alpha(TNF-α)is important for the progression of liver *** signaling via TNF receptor 1(TNFR1)has been hypothesized to be important for the development of NASH and hepatocellular carcinoma in whole-body knockout animal *** To investigate the role of TNFR1 signaling in hepatocytes for steatohepatitis development in a mouse model of diet-induced *** NASH was induced by a western-style fast-food diet in mice deficient for TNFR1 in hepatocytes(TNFR1ΔHEP)and their wild-type littermates(TNFR1fl/fl).Glucose tolerance was assessed after 18 wk and insulin resistance after 19 wk of *** 20 wk mice were assessed for features of NASH and the metabolic syndrome such as liver weight,liver steatosis,liver fibrosis and markers of liver *** Obesity,liver injury,inflammation,steatosis and fibrosis was not different between TNFR1ΔHEP and TNFR1fl/fl ***,Tnfr1 deficiency in hepatocytes protected against glucose intolerance and insulin *** Our results indicate that deficiency of TNFR1 signaling in hepatocytes does not protect from diet-induced ***,improved insulin resistance in this model strengthens the role of the liver in glucose homeostasis.

关键词： Tumor necrosis factor alpha receptor 1 Non-alcoholic steatohepatitis Nonalcoholic fatty liver disease Type 2 diabetes Insulin resistance Glucose intolerance

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