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Enhanced hypothalamic leptin signaling in mice lacking dopamine D2 receptors

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dc.contributor.authorKim, Kyu Seok-
dc.contributor.authorYoon, Ye Ran-
dc.contributor.authorLee, Hyo Jin-
dc.contributor.authorYoon, Sehyoun-
dc.contributor.authorKim, Sa-Yong-
dc.contributor.authorShin, Seung Woo-
dc.contributor.authorAn, Juan Ji-
dc.contributor.authorKim, Min-Seon-
dc.contributor.authorChoi, Se-Young-
dc.contributor.authorSun, Woong-
dc.contributor.authorBaik, Ja-Hyun-
dc.date.accessioned2011-10-14T01:12:26Z-
dc.date.available2011-10-14T01:12:26Z-
dc.date.issued2010-03-
dc.identifier.citationJournal of Biological Chemistry 285,8905-8917en
dc.identifier.issn0021-9258-
dc.identifier.urihttps://hdl.handle.net/10371/74130-
dc.description.abstractThe dopamine D2 receptor (D2R) plays a critical role in diverse neurophysiological functions. D2R knock-out mice (D2R-/-) show reduced food intake and body weight while displaying an increased basal energy expenditure level, compared with their wild type littermates. Thus, these mice show a lean phenotype. D2R-/- mice displayed increased leptin sensitivity, and leptin injection induced increased phosphorylation of the hypothalamic signal transducer and activator of transcription 3 (STAT3) in D2R-/- mice relative to wild type littermates. Using double immunofluorescence histochemistry, we have demonstrated that D2Rs are present in leptin-sensitive STAT3-positive cells in the arcuate nucleus of the hypothalamus and that leptin injection induces STAT3 phosphorylation in hypothalamic neurons expressing D2Rs. Stimulation of D2R by the D2R agonist quinpirole suppressed the leptin-induced STAT3 phosphorylation and nuclear trans-localization of phospho-STAT3 in the hypothalamus of wild type mice. However, this regulation was not detected in the D2R-/- mice. Treatment of D2R agonist and antagonist could modulate the leptin-induced food intake and body weight changes in wild type mice but not in D2R-/- mice. Together, our findings suggest that the interaction between the dopaminergic system and leptin signaling in hypothalamus is important in control of energy homeostasis.en
dc.description.sponsorshipThis work was supported by Korea Research Grant KRF-2006-311-C00478, funded by the Korean Government(MOEHRD), Grants M103KV010015-07K2201-01510 and M103KV010014-08K2201-01410 from the Brian Research Center of the 21st Century Frontier Research Program, Grant M1-0311-00-0069 from the Korea Science and Engineering Foundation, funded by the Korean Ministry of Science and Technology, and a grant award from the AstraZeneca VRI Program.en
dc.language.isoenen
dc.publisherAmerican Society for Biochemistry and Molecular Biologyen
dc.titleEnhanced hypothalamic leptin signaling in mice lacking dopamine D2 receptorsen
dc.typeArticleen
dc.contributor.AlternativeAuthor김규석-
dc.contributor.AlternativeAuthor윤예란-
dc.contributor.AlternativeAuthor이효진-
dc.contributor.AlternativeAuthor윤세현-
dc.contributor.AlternativeAuthor김사용-
dc.contributor.AlternativeAuthor신승우-
dc.contributor.AlternativeAuthor김민선-
dc.contributor.AlternativeAuthor최세영-
dc.contributor.AlternativeAuthor선웅-
dc.contributor.AlternativeAuthor백자현-
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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