Publication Date:
2014-06-06
Description:
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 Cepsilon 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.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4489847/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4489847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perry, Rachel J -- Samuel, Varman T -- Petersen, Kitt F -- Shulman, Gerald I -- I01 BX000901/BX/BLRD VA/ -- P30 DK-45735/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- R01 AG-23686/AG/NIA NIH HHS/ -- R01 DK-40936/DK/NIDDK NIH HHS/ -- R01 DK-49230/DK/NIDDK NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- R24 DK-085836/DK/NIDDK NIH HHS/ -- T32-DK101019/DK/NIDDK NIH HHS/ -- U24 DK-059635/DK/NIDDK NIH HHS/ -- UL1 RR-024139/RR/NCRR NIH HHS/ -- England -- Nature. 2014 Jun 5;510(7503):84-91. doi: 10.1038/nature13478.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA. ; 1] Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA. [2] VA Connecticut Healthcare System West Haven, Connecticut 06516, USA. ; 1] 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. ; 1] 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.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24899308" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Diabetes Mellitus, Type 2/drug therapy/*metabolism
;
Diglycerides/metabolism
;
Fatty Liver/drug therapy/metabolism
;
Humans
;
Hyperglycemia/metabolism
;
*Insulin Resistance
;
*Lipid Metabolism
;
*Lipids/biosynthesis
;
Lipodystrophy/metabolism
;
Lipogenesis
;
Liver/*metabolism
;
Muscle, Skeletal/metabolism
;
Non-alcoholic Fatty Liver Disease
;
Triglycerides/biosynthesis
Print ISSN:
0028-0836
Electronic ISSN:
1476-4687
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
,
Natural Sciences in General
,
Physics
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