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论文题目: Ethanol-induced hepatic steatosis is modulated by glycogen level in the liver
英文论文题目: Ethanol-induced hepatic steatosis is modulated by glycogen level in the liver
第一作者: Gu, J; Zhang, YX; Xu, DQ; Zhao, ZL; Zhang, YX; Pan, Y; Cao, PJ; Wang, ZZ; Chen, Y
英文第一作者: Gu, J; Zhang, YX; Xu, DQ; Zhao, ZL; Zhang, YX; Pan, Y; Cao, PJ; Wang, ZZ; Chen, Y
联系作者: Chen, Y (reprint author), Chinese Acad Sci, Grad Sch, Key Lab Nutr & Metab, Inst Nutr Sci,Shanghai Inst Biol Sci, Shanghai 200031, Peoples R China.
英文联系作者: Chen, Y (reprint author), Chinese Acad Sci, Grad Sch, Key Lab Nutr & Metab, Inst Nutr Sci,Shanghai Inst Biol Sci, Shanghai 200031, Peoples R China.
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发表年度: 2015
卷: 56
期: 7
页码: 1329-1339
摘要: Alcoholic liver disease (ALD) is a major health problem worldwide and hepatic steatosis is an early response to alcohol consumption. Fat and glycogen are two major forms of energy storage in the liver; however, whether glycogen metabolism in the liver impacts alcohol-induced steatosis has been elusive. In this study, we used a mouse model with overexpression of PPP1R3G in the liver to dissect the potential role of glycogen on alcohol-induced fatty liver formation. PPP1R3G is a regulatory subunit of protein phosphatase 1 and stimulates glycogenesis in the liver. Chronic and binge ethanol (EtOH) feeding reduced glycogen level in the mouse liver and such inhibitory effect of EtOH was reversed by PPP1R3G overexpression. In addition, PPP1R3G overexpression abrogated EtOH-induced elevation of serum levels of alanine aminotransferase and aspartate aminotransferase, increase in liver triglyceride concentration, and lipid deposition in the liver. EtOH-stimulated sterol regulatory element-binding protein (SREBP)1c, a master regulator of lipogenesis, was also reduced by PPP1R3G overexpression in vivo. In AML-12 mouse hepatocytes, PPP1R3G overexpression could relieve EtOH-induced lipid accumulation and SREBP-1c stimulation. In conclusion, our data indicate that glycogen metabolism is closely linked to EtOH-induced liver injury and fatty liver formation.
英文摘要: Alcoholic liver disease (ALD) is a major health problem worldwide and hepatic steatosis is an early response to alcohol consumption. Fat and glycogen are two major forms of energy storage in the liver; however, whether glycogen metabolism in the liver impacts alcohol-induced steatosis has been elusive. In this study, we used a mouse model with overexpression of PPP1R3G in the liver to dissect the potential role of glycogen on alcohol-induced fatty liver formation. PPP1R3G is a regulatory subunit of protein phosphatase 1 and stimulates glycogenesis in the liver. Chronic and binge ethanol (EtOH) feeding reduced glycogen level in the mouse liver and such inhibitory effect of EtOH was reversed by PPP1R3G overexpression. In addition, PPP1R3G overexpression abrogated EtOH-induced elevation of serum levels of alanine aminotransferase and aspartate aminotransferase, increase in liver triglyceride concentration, and lipid deposition in the liver. EtOH-stimulated sterol regulatory element-binding protein (SREBP)1c, a master regulator of lipogenesis, was also reduced by PPP1R3G overexpression in vivo. In AML-12 mouse hepatocytes, PPP1R3G overexpression could relieve EtOH-induced lipid accumulation and SREBP-1c stimulation. In conclusion, our data indicate that glycogen metabolism is closely linked to EtOH-induced liver injury and fatty liver formation.
刊物名称: JOURNAL OF LIPID RESEARCH
英文刊物名称: JOURNAL OF LIPID RESEARCH
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学科: Biochemistry & Molecular Biology
英文学科: Biochemistry & Molecular Biology
影响因子: 4.421
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论文类别: Article
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