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Nature. 2014 Jun 5;510(7503):84-91. doi: 10.1038/nature13478.

The role of hepatic lipids in hepatic insulin resistance and type 2 diabetes.

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  • 1Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
  • 21] Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA. [2] VA Connecticut Healthcare System West Haven, Connecticut 06516, USA.
  • 31] Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA. [2] Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen DK-2200, Denmark.
  • 41] Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA. [2] Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen DK-2200, Denmark. [3] Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. [4] Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06535-8012, USA.

Abstract

Non-alcoholic fatty liver disease and its downstream sequelae, hepatic insulin resistance and type 2 diabetes, are rapidly growing epidemics, which lead to increased morbidity and mortality rates, and soaring health-care costs. Developing interventions requires a comprehensive understanding of the mechanisms by which excess hepatic lipid develops and causes hepatic insulin resistance and type 2 diabetes. Proposed mechanisms implicate various lipid species, inflammatory signalling and other cellular modifications. Studies in mice and humans have elucidated a key role for hepatic diacylglycerol activation of protein kinase Cε in triggering hepatic insulin resistance. Therapeutic approaches based on this mechanism could alleviate the related epidemics of non-alcoholic fatty liver disease and type 2 diabetes.

PMID:
24899308
[PubMed - indexed for MEDLINE]
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