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Enhanced Hypothalamic Leptin Signaling in Mice Lacking Dopamine D-2 Receptors

Authors
Kim, Kyu SeokYoon, Ye RanLee, Hyo JinYoon, SehyounKim, Sa-YongShin, Seung WooAn, Juan JiKim, Min-SeonChoi, Se-YoungSun, WoongBaik, Ja-Hyun
Issue Date
19-3월-2010
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Citation
JOURNAL OF BIOLOGICAL CHEMISTRY, v.285, no.12, pp.8905 - 8917
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume
285
Number
12
Start Page
8905
End Page
8917
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/116792
DOI
10.1074/jbc.M109.079590
ISSN
0021-9258
Abstract
The dopamine D-2 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.
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