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PLoS One. 2015 Aug 28;10(8):e0136597. doi: 10.1371/journal.pone.0136597. eCollection 2015.

Suppressive Role of PPARγ-Regulated Endothelial Nitric Oxide Synthase in Adipocyte Lipolysis.

Author information

1
Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
2
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Shriners Hospitals for Children, Harvard Medical School, Boston, Massachusetts, United States of America.
3
Department of Geriatric Medicine, Kyorin University School of Medicine, Tokyo, Japan.

Abstract

INTRODUCTION:

Metabolic syndrome causes insulin resistance and is associated with risk factor clustering, thereby increasing the risk of atherosclerosis. Recently, endothelial nitric oxide synthase deficient (eNOS-/-) mice have been reported to show metabolic disorders. Interestingly, eNOS has also been reported to be expressed in non-endothelial cells including adipocytes, but the functions of eNOS in adipocytes remain unclear.

METHODS AND RESULTS:

The eNOS expression was induced with adipocyte differentiation and inhibition of eNOS/NO enhanced lipolysis in vitro and in vivo. Furthermore, the administration of a high fat diet (HFD) was able to induce non-alcoholic steatohepatitis (NASH) in eNOS-/- mice but not in wild type mice. A PPARγ antagonist increased eNOS expression in adipocytes and suppressed HFD-induced fatty liver changes.

CONCLUSIONS:

eNOS-/- mice induce NASH development, and these findings provide new insights into the therapeutic approach for fatty liver disease and related disorders.

PMID:
26317347
PMCID:
PMC4552558
DOI:
10.1371/journal.pone.0136597
[Indexed for MEDLINE]
Free PMC Article

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