Format

Send to

Choose Destination
Front Endocrinol (Lausanne). 2014 Dec 17;5:221. doi: 10.3389/fendo.2014.00221. eCollection 2014.

O-GlcNAc: A Bittersweet Switch in Liver.

Author information

1
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine , New Haven, CT , USA ; Section of Comparative Medicine, Yale University School of Medicine , New Haven, CT , USA ; Department of Cellular and Molecular Physiology, Yale University School of Medicine , New Haven, CT , USA.
2
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine , New Haven, CT , USA ; Section of Comparative Medicine, Yale University School of Medicine , New Haven, CT , USA ; Department of Cell Biology, Yale University School of Medicine , New Haven, CT , USA.

Abstract

The liver is a vital organ responsible for maintaining nutrient homeostasis. After a meal, insulin stimulates glycogen and lipid synthesis in the liver; in the fasted state, glucagon induces gluconeogenesis and ketogenesis, which produce glucose and ketone bodies for other tissues to use as energy sources. These metabolic changes involve spatiotemporally co-ordinated signaling cascades. O-linked β-N-acetylglucosamine (O-GlcNAc) modification has been recognized as a nutrient sensor and regulatory molecular switch. This review highlights mechanistic insights into spatiotemporal regulation of liver metabolism by O-GlcNAc modification and discusses its pathophysiological implications in insulin resistance, non-alcoholic fatty liver disease, and fibrosis.

KEYWORDS:

NAFLD; O-GlcNAc; glucagon; insulin; insulin resistance; liver fibrosis; liver metabolism

Supplemental Content

Full text links

Icon for Frontiers Media SA Icon for PubMed Central
Loading ...
Support Center