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Circadian clock control of hepatic lipid metabolism: role of small heterodimer partner (Shp)
  1. Li Wang1,2,3,4,
  2. Suthat Liangpunsakul5,6,7
  1. 1Department of Physiology & Neurobiology, University of Connecticut, Storrs, Connecticut, USA
  2. 2Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut, USA
  3. 3Department of Internal Medicine, Section of Digestive Diseases, Yale University, New Haven, Connecticut, USA
  4. 4School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China
  5. 5Division of Gastroenterology and Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA
  6. 6Roudebush Veterans Administration Medical Center, Indianapolis, Indiana, USA
  7. 7Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA
  1. Correspondence to Dr Suthat Liangpunsakul, Division of Gastroenterology and Hepatology, 550 N. University Blvd, UH 4100, Indianapolis, IN 46202, USA; sliangpu{at}iupui.edu

Abstract

Hepatic steatosis, the accumulation of triglyceride droplets in the hepatocytes, is a common hepatic pathology seen in subjects with obesity/metabolic syndrome and those with excessive alcohol use. The pathogenesis underlying hepatic steatosis is complex. Recent studies have shown the specific role played by the molecular clock mechanism in the control of lipid metabolism and that the disruption of these tissue clocks may lead to the disturbances in lipid homeostasis. This review reports a novel role of small heterodimer partner in maintaining triglyceride and lipoprotein homeostasis through neuronal PAS domain protein 2.

  • Lipid Metabolism

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