期刊
IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
卷 32, 期 2, 页码 251-257出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/08923970903252220
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资金
- KRF(Korea Research Foundation) [2007-314-E00111, 2007-531-E00015]
- KOSEF
- Ministry of Science & Technology, Republic of Korea
- National Research Foundation of Korea [2007-531-E00015, 2007-314-E00111] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The excessive supply of fatty acids to the liver contributes to hepatic insulin resistance and endoplasmic reticulum (ER) stress associated with obesity or type 2 diabetes mellitus. Furthermore, excess and/or prolonged ER stress contributes to hepatic cell death deteriorating nonalcoholic fatty liver disease to steatohepatitis. The aim of this study was to investigate the effects of metformin on palmitate-induced ER stress and hepatic insulin resistance in HepG2 cells. Metformin significantly inhibited palmitate-induced cell death and apoptosis via caspase-3 activation. Metformin also blocked the induction of ER stress proteins (GRP78, Chop, Cleaved ATF-6, p-eIF2 alpha and XBP-1) and regulated serine phosphorylation of IRS-1. Metformin may therefore protect hepatocytes from death induced by saturated fatty acids. These data may also provide a further rationale for exploring the use of metformin in the treatment of non-alcoholic fatty liver disease, revealing its blocking effect for hepatic insulin resistance evoked by saturated fatty acids.
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