Hdl Handle:
http://hdl.handle.net/10675.2/802
Title:
Palmitoleate Induces Hepatic Steatosis but Suppresses Liver Inflammatory Response in Mice
Authors:
Guo, Xin; Li, Honggui; Xu, Hang; Halim, Vera; Zhang, Weiyu; Wang, Huan; Ong, Kuok Teong; Woo, Shih-Lung; Walzem, Rosemary L.; Mashek, Douglas G.; Dong, Hui; Lu, Fuer; Wei, Lai; Huo, Yuqing ( 0000-0001-9847-0120 ) ; Wu, Chaodong
Abstract:
The interaction between fat deposition and inflammation during obesity contributes to the development of non-alcoholic fatty liver disease (NAFLD). The present study examined the effects of palmitoleate, a monounsaturated fatty acid (16⠶1n7), on liver metabolic and inflammatory responses, and investigated the mechanisms by which palmitoleate increases hepatocyte fatty acid synthase (FAS) expression. Male wild-type C57BL/6J mice were supplemented with palmitoleate and subjected to the assays to analyze hepatic steatosis and liver inflammatory response. Additionally, mouse primary hepatocytes were treated with palmitoleate and used to analyze fat deposition, the inflammatory response, and sterol regulatory element-binding protein 1c (SREBP1c) activation. Compared with controls, palmitoleate supplementation increased the circulating levels of palmitoleate and improved systemic insulin sensitivity. Locally, hepatic fat deposition and SREBP1c and FAS expression were significantly increased in palmitoleate-supplemented mice. These pro-lipogenic events were accompanied by improvement of liver insulin signaling. In addition, palmitoleate supplementation reduced the numbers of macrophages/Kupffer cells in livers of the treated mice. Consistently, supplementation of palmitoleate decreased the phosphorylation of nuclear factor kappa B (NF-κB, p65) and the expression of proinflammatory cytokines. These results were recapitulated in primary mouse hepatocytes. In terms of regulating FAS expression, treatment of palmitoleate increased the transcription activity of SREBP1c and enhanced the binding of SREBP1c to FAS promoter. Palmitoleate also decreased the phosphorylation of NF-κB p65 and the expression of proinflammatory cytokines in cultured macrophages. Together, these results suggest that palmitoleate acts through dissociating liver inflammatory response from hepatic steatosis to play a unique role in NAFLD.
Citation:
PLoS One. 2012 Jun 29; 7(6):e39286
Issue Date:
29-Jun-2012
URI:
http://hdl.handle.net/10675.2/802
DOI:
10.1371/journal.pone.0039286
PubMed ID:
22768070
PubMed Central ID:
PMC3387145
Type:
Article
ISSN:
1932-6203
Appears in Collections:
Department of Cellular Biology and Anatomy: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorGuo, Xinen_US
dc.contributor.authorLi, Hongguien_US
dc.contributor.authorXu, Hangen_US
dc.contributor.authorHalim, Veraen_US
dc.contributor.authorZhang, Weiyuen_US
dc.contributor.authorWang, Huanen_US
dc.contributor.authorOng, Kuok Teongen_US
dc.contributor.authorWoo, Shih-Lungen_US
dc.contributor.authorWalzem, Rosemary L.en_US
dc.contributor.authorMashek, Douglas G.en_US
dc.contributor.authorDong, Huien_US
dc.contributor.authorLu, Fueren_US
dc.contributor.authorWei, Laien_US
dc.contributor.authorHuo, Yuqingen_US
dc.contributor.authorWu, Chaodongen_US
dc.date.accessioned2012-10-26T20:30:46Z-
dc.date.available2012-10-26T20:30:46Z-
dc.date.issued2012-06-29en_US
dc.identifier.citationPLoS One. 2012 Jun 29; 7(6):e39286en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid22768070en_US
dc.identifier.doi10.1371/journal.pone.0039286en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/802-
dc.description.abstractThe interaction between fat deposition and inflammation during obesity contributes to the development of non-alcoholic fatty liver disease (NAFLD). The present study examined the effects of palmitoleate, a monounsaturated fatty acid (16⠶1n7), on liver metabolic and inflammatory responses, and investigated the mechanisms by which palmitoleate increases hepatocyte fatty acid synthase (FAS) expression. Male wild-type C57BL/6J mice were supplemented with palmitoleate and subjected to the assays to analyze hepatic steatosis and liver inflammatory response. Additionally, mouse primary hepatocytes were treated with palmitoleate and used to analyze fat deposition, the inflammatory response, and sterol regulatory element-binding protein 1c (SREBP1c) activation. Compared with controls, palmitoleate supplementation increased the circulating levels of palmitoleate and improved systemic insulin sensitivity. Locally, hepatic fat deposition and SREBP1c and FAS expression were significantly increased in palmitoleate-supplemented mice. These pro-lipogenic events were accompanied by improvement of liver insulin signaling. In addition, palmitoleate supplementation reduced the numbers of macrophages/Kupffer cells in livers of the treated mice. Consistently, supplementation of palmitoleate decreased the phosphorylation of nuclear factor kappa B (NF-κB, p65) and the expression of proinflammatory cytokines. These results were recapitulated in primary mouse hepatocytes. In terms of regulating FAS expression, treatment of palmitoleate increased the transcription activity of SREBP1c and enhanced the binding of SREBP1c to FAS promoter. Palmitoleate also decreased the phosphorylation of NF-κB p65 and the expression of proinflammatory cytokines in cultured macrophages. Together, these results suggest that palmitoleate acts through dissociating liver inflammatory response from hepatic steatosis to play a unique role in NAFLD.en_US
dc.rightsGuo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectBiochemistryen_US
dc.subjectLipidsen_US
dc.subjectFatty Acidsen_US
dc.subjectImmunologyen_US
dc.subjectImmune Systemen_US
dc.subjectCytokinesen_US
dc.subjectImmunityen_US
dc.subjectInflammationen_US
dc.subjectModel Organismsen_US
dc.subjectAnimal Modelsen_US
dc.subjectMouseen_US
dc.subjectMedicineen_US
dc.subjectEndocrinologyen_US
dc.subjectDiabetic Endocrinologyen_US
dc.subjectInsulinen_US
dc.subjectGastroenterology and Hepatologyen_US
dc.subjectLiver Diseasesen_US
dc.subjectNonalcoholic Steatohepatitisen_US
dc.subjectNutritionen_US
dc.subjectObesityen_US
dc.titlePalmitoleate Induces Hepatic Steatosis but Suppresses Liver Inflammatory Response in Miceen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3387145en_US
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomy-

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