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Effects of caloric restriction on the expression of lipocalin-2 and its receptor in the brown adipose tissue of high-fat diet-fed mice

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dc.contributor.authorPark, Kyung-Ah-
dc.contributor.authorJin, Zhen-
dc.contributor.authorAn, Hyeong Seok-
dc.contributor.authorLee, Jong Youl-
dc.contributor.authorJeong, Eun Ae-
dc.contributor.authorChoi, Eun Bee-
dc.contributor.authorKim, Kyung Eun-
dc.contributor.authorShin, Hyun Joo-
dc.contributor.authorLee, Jung Eun-
dc.contributor.authorRoh, Gu Seob-
dc.date.accessioned2022-12-26T14:34:00Z-
dc.date.available2022-12-26T14:34:00Z-
dc.date.issued2019-09-
dc.identifier.issn1226-4512-
dc.identifier.issn2093-3827-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/8810-
dc.description.abstractObesity causes inflammation and impairs thermogenic functions in brown adipose tissue (BAT). The adipokine lipocalin 2 (LCN2) has been implicated in inflammation and obesity. Herein, we investigated the protective effects of caloric restriction (CR) on LCN2-mediated inflammation and oxidative stress in the BAT of high-fat diet (HFD)-fed mice. Mice were fed a HFD for 20 weeks and then either continued on the HFD or subjected to CR for the next 12 weeks. CR led to the browning of the white fat-like phenotype in HFD-fed mice. Increased expressions of LCN2 and its receptor in the BAT of HFD-fed mice were significantly attenuated by CR. Additionally, HFD+CR-fed mice had fewer neutrophils and macrophages expressing LCN2 and iron-positive cells than HFD-fed mice. Further, oxidative stress and mitochondrial fission induced by a HFD were also significantly attenuated by CR. Our findings indicate that the protective effects of CR on inflammation and oxidative stress in the BAT of obese mice may be associated with regulation of LCN2.-
dc.format.extent10-
dc.language영어-
dc.language.isoENG-
dc.publisher대한약리학회-
dc.titleEffects of caloric restriction on the expression of lipocalin-2 and its receptor in the brown adipose tissue of high-fat diet-fed mice-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.4196/kjpp.2019.23.5.335-
dc.identifier.scopusid2-s2.0-85072643747-
dc.identifier.wosid000487259000007-
dc.identifier.bibliographicCitationThe Korean Journal of Physiology & Pharmacology, v.23, no.5, pp 335 - 344-
dc.citation.titleThe Korean Journal of Physiology & Pharmacology-
dc.citation.volume23-
dc.citation.number5-
dc.citation.startPage335-
dc.citation.endPage344-
dc.type.docTypeArticle-
dc.identifier.kciidART002498131-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalResearchAreaPhysiology-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPhysiology-
dc.subject.keywordPlusINSULIN-RESISTANCE-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusPERILIPIN-
dc.subject.keywordPlusOBESITY-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusDYSFUNCTION-
dc.subject.keywordPlusHOMEOSTASIS-
dc.subject.keywordPlusREGULATOR-
dc.subject.keywordAuthorBrown adipose tissue-
dc.subject.keywordAuthorCaloric restriction-
dc.subject.keywordAuthorLipocalin 2-
dc.subject.keywordAuthorObesity-
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