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Overexpression of NRK1 ameliorates diet- and age-induced hepatic steatosis and insulin resistance.

Abstract：

:NAD+ is a co-enzyme in redox reactions and a substrate required for activity of various enzyme families, including sirtuins and poly(ADP-ribose) polymerases. Dietary supplementation of NAD+ precursors nicotinamide mononucleotide (NMN) or nicotinamide riboside (NR) protects against metabolic disease, neurodegenerative disorders and age-related physiological decline in mammals. Here we sought to identify the roles of nicotinamide riboside kinase 1 (NRK1) plays in regulating hepatic NAD+ biosynthesis and lipid metabolism. Using adenovirus mediated gene transduction to overexpress or knockdown NRK1 in mouse liver, we have demonstrated that NRK1 is critical for maintaining hepatic NAD+ levels and triglyceride content. We have further shown that the hepatic expression of Nmrk1 mRNA is significantly decreased either in mice treated with high-fat diet or in aged mice. However, adenoviral delivery of NRK1 in these diet- and age-induced mice elevates hepatic NAD+ levels, reduces hepatic steatosis, and improves glucose tolerance and insulin sensitivity. Our results provide important insights in targeting NRK1 for treating hepatic steatosis.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Fan R,Cui J,Ren F,Wang Q,Huang Y,Zhao B,Wei L,Qian X,Xiong X

doi

10.1016/j.bbrc.2018.04.107

subject

Has Abstract

pub_date

2018-06-02 00:00:00

pages

476-483

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)30886-6

journal_volume

500

pub_type

杂志文章

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