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Silent information regulator 1 ( SIRT 1) is a nicotinamide adenine dinucleotide ( NAD  + )‐dependent protein deacetylase. In mice,  mS irt1 deficiency causes the onset of fatty liver via regulation of the hepatic nutrient metabolism pathway. In this study, we demonstrate  SIRT 1 expression, activity and  NAD  +  regulation using noncancerous liver tissue specimens from hepatocellular carcinoma patients with non‐B non‐C ( NBNC ) hepatitis.  SIRT 1 expression levels were higher in  NBNC  patients than in healthy donors, while  SIRT 1 histone H3K9 deacetylation activity was suppressed in  NBNC  patients. In the liver of hepatitis patients, decreased  NAD  +  amounts and its regulatory enzyme nicotinamide phosphoribosyltransferase expression levels were observed, and this led to inhibition of SIRT1 activity.  SIRT 1 expression was associated with  HIF 1 protein accumulation in both the  NBNC  liver and liver cancer cell lines. These results may indicate that the  NBNC  hepatitis liver is exposed to hypoxic conditions. In HepG2 cells, hypoxia induced inflammatory chemokines, such as  CXCL 10 and  MCP ‐1. These inductions were suppressed in rich  NAD  +  condition, and by  SIRT 1 activator treatment. In conclusion, hepatic  SIRT 1 activity was repressed in  NBNC  patients, and normalization of  NAD  +  amounts and activation of  SIRT 1 could improve the inflammatory condition in the liver of  NBNC  hepatitis patients.

cancer science

Suppression of silent information regulator 1 activity in noncancerous tissues of hepatocellular carcinoma: Possible association with non‐B non‐C hepatitis pathogenesis