NAMPT overexpression alleviates alcohol-induced hepatic steatosis in mice

• DOI: 10.1371/journal.pone.0212523
• Publication Date: 2019-02-22T19:14:41Z
• Authors: Xiwen Xiong; Jiahui Yu; Rui Fan; Cuicui Zhang; Lin Xu; Xupeng Sun; Yanmei Huang; Qingzhi Wang; Hai-Bin Ruan; Xinlai Qian
• Keywords: Nicotinamide phosphoribosyltransferase; Steatosis; Alcoholic fatty liver

Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)+ biosynthesis. Through its NAD+-biosynthetic activity, NAMPT influences the activity of NAD+-dependent enzymes, such as sirtuins. able to modulate processes involved pathogenesis non-alcohol induced fatty liver disease (NAFLD), but roles plays development alcoholic (ALD) still remain unknown. Here, we show that ethanol treatment suppresses expression Nampt hepatocytes. Consistently, chronic administration also reduces mouse liver. We next demonstrate hepatocytes infected with Ad-NAMPT adenovirus exhibit significantly elevated intracellular NAD+ levels and decreased ethanol-induced triglyceride (TG) accumulation. Similarly, adenovirus-mediated overexpression mice ameliorates hepatic steatosis. Moreover, SIRT1 required mediate effects on reduction TG accumulation serum ALT, AST ethanol-fed mice. Our results provide important insights targeting for treating disease.