期刊
FRONTIERS IN ENDOCRINOLOGY
卷 5, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fendo.2014.00221
关键词
O-GIcNAc; insulin; glucagon; liver metabolism; insulin resistance; NAFLD; liver fibrosis
资金
- NIH [R01 DK089098, P01 DK057751, CT DPH2014-0139]
- Ellison Medical Foundation
- China Scholarship Council-Yale World Scholars Program scholarships
- NATIONAL CANCER INSTITUTE [P30CA016359] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK089098, P01DK057751] Funding Source: NIH RePORTER
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 beta-N-acetylglucosamine (O-GIcNAc) 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-GIcNAc modification and discusses its pathophysiological implications in insulin resistance, non-alcoholic fatty liver disease, and fibrosis.
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