Effects of leptin on lipid metabolism and gene expression of differentiation-associated growth factors and transcription factors during differentiation and maturation of 3T3-L1 preadipocytes = 지방대사와 지방전세포주의 분화관련 유전자에의 렙틴의 영향

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dc.contributor.authorWon Kon-Kim-
dc.contributor.authorC Y Lee-
dc.contributor.authorM S Kang-
dc.contributor.authorM H Kim-
dc.contributor.authorY H Ryu-
dc.contributor.authorKwang-Hee Bae-
dc.contributor.authorS J Shin-
dc.contributor.authorSang Chul Lee-
dc.contributor.authorY Ko-
dc.date.accessioned2017-04-19T09:11:59Z-
dc.date.available2017-04-19T09:11:59Z-
dc.date.issued2008-
dc.identifier.issn0918-8959-
dc.identifier.uri10.1507/endocrj.K08E-115ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/8650-
dc.description.abstractThe present study was designed to determine the effects of leptin on lipid metabolism and gene expression during differentiation and maturation of the 3T3-L1 murine preadipocyte. The preadipocytes were induced to differentiate in a growth medium containing 10% calf serum and a hormonal cocktail for 2 days. The cells were next allowed to maturate for 14 days in the growth medium supplemented with 10 μg/ml insulin or 500 ng/ml insulin-like growth factor (IGF)-I in the absence or presence of supplemented leptin. Leptin, at a dose of 5 to 500 ng/ml, had no effect on proliferation of undifferentiated 3T3-L1 cells. However, leptin suppressed the insulin- or IGF-I-stimulated lipid accumulation and enhanced the release of glycerol, a measure of lipolysis, in a dose-dependent manner during and after the maturation of the cell. Moreover, leptin at a dose of 50 ng/ml inhibited IGF-I gene expression during the entire differentiation and maturation and also peroxisome proliferator activated receptor (PPAR)-γ expression during late maturation as monitored by semi-quantitative reverse transcription-polymerase chain reaction. However, leptin exerted no effect on the expression of transforming growth factor-β, CCAT/enhancer binding protein-α and PPAR-δ. Taken together, results suggest the anti-lipogenic and lipolytic effects of leptin in differentiating and mature adipocytes may have been partly mediated by suppressing the expression of PPAR-γ and IGF-I genes.-
dc.publisherJapan Endocrine Soc-
dc.titleEffects of leptin on lipid metabolism and gene expression of differentiation-associated growth factors and transcription factors during differentiation and maturation of 3T3-L1 preadipocytes = 지방대사와 지방전세포주의 분화관련 유전자에의 렙틴의 영향-
dc.title.alternativeEffects of leptin on lipid metabolism and gene expression of differentiation-associated growth factors and transcription factors during differentiation and maturation of 3T3-L1 preadipocytes-
dc.typeArticle-
dc.citation.titleEndocrine Journal-
dc.citation.number5-
dc.citation.endPage837-
dc.citation.startPage827-
dc.citation.volume55-
dc.contributor.affiliatedAuthorWon Kon-Kim-
dc.contributor.affiliatedAuthorKwang-Hee Bae-
dc.contributor.affiliatedAuthorSang Chul Lee-
dc.contributor.alternativeName김원곤-
dc.contributor.alternativeName이철영-
dc.contributor.alternativeName강문성-
dc.contributor.alternativeName김민호-
dc.contributor.alternativeName유양환-
dc.contributor.alternativeName배광희-
dc.contributor.alternativeName신성재-
dc.contributor.alternativeName이상철-
dc.contributor.alternativeName고용-
dc.identifier.bibliographicCitationEndocrine Journal, vol. 55, no. 5, pp. 827-837-
dc.identifier.doi10.1507/endocrj.K08E-115-
dc.subject.keywordAdipocyte-
dc.subject.keywordDifferentiation-
dc.subject.keywordIGF-I-
dc.subject.keywordLeptin-
dc.subject.keywordLipid-
dc.subject.keywordPPAR-
dc.subject.localAdipocyte-
dc.subject.localadipocyte-
dc.subject.localAdipocytes-
dc.subject.localadipocytes-
dc.subject.localdifferentiation-
dc.subject.localDifferentiation-
dc.subject.localIGF-I-
dc.subject.localLeptin-
dc.subject.localleptin-
dc.subject.locallipids-
dc.subject.localLipids-
dc.subject.locallipid-
dc.subject.localLipid-
dc.subject.localPPAR-
dc.description.journalClassY-
Appears in Collections:
Division of A.I. & Biomedical Research > Metabolic Regulation Research Center > 1. Journal Articles
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