Effect of adipokine on feeding behavior of obese adolescents through dopaminergic reward circuits in the brain
Project/Area Number |
25350166
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Eating habits
|
Research Institution | Daiichi University, College of Pharmaceutical Sciences (2015) Fukuoka University (2013-2014) |
Principal Investigator |
Koyama Susumu 第一薬科大学, 薬学部, 教授 (60461505)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 食報酬 / ドパミン / レプチン / 腹側被蓋野 / 電気生理学 / ドパミン受容体 |
Outline of Final Research Achievements |
Feeding behavior independent of hunger and satiety causes maintenance or exacerbation of obesity. It has been suggested that leptin, an adipokine, and dopamine, a neurotransmitter, interact in the ventral tegmental area (VTA), which is the origin of the dopaminergic mesolimbic system and critical for food reward. In the electrophysiological research using mice, we found the following results; (1) leptin directly inhibited spontaneous activity of VTA dopamine neurons and attenuated dopamine receptor-mediated effect on these neurons, (2) recovery time from the leptin-induced direct inhibition of VTA dopamine neurons was negatively correlated with body weight in high fat diet-induced obese mice.
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Report
(4 results)
Research Products
(13 results)