Journal
NATURE
Volume 510, Issue 7503, Pages 84-91Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature13478
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Funding
- National Institutes of Health [R01 DK-40936, R01 DK-49230, R24 DK-085836, R01 AG-23686, U24 DK-059635, UL1 RR-024139, P30 DK-45735, T32-DK101019, I01-BX000901]
- Novo Nordisk Foundation for Basic Metabolic Research, University of Copenhagen
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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 C epsilon 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.
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