2013 Fiscal Year Final Research Report
Regulation by Na-K pump of glucose-sensitive NPY neurons and feeding behavior, and its dysfunction in hyperphagia and obesity
| Project/Area Number |
24659101
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKATA Masanori 自治医科大学, 医学部, 准教授 (10305120)
MAEJIMA Yuko 自治医科大学, 医学部, 助教 (40438669)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | 弓状核 / グルコース / Na,K-ATPase / Neuropeptide Y / 摂食 / ATP |
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| Research Abstract |
In the glucose-sensitive neurons (GSNs) in the hypothalamic arcuate nucleus (ARC), lowering glucose concentration increases cytosolic Na+ concentration ([Na+]) that is inhibited by activator of Na,K-ATPase (NKA), SSA412. The results indicate that suppression of NKA is implicated in the response to lowering glucose. The NKA suppression is mediated by decrease in intracellular ATP. The NKA suppression, possibly by inducing depolarization, activates voltage-dependent Ca channels and increases [Ca2+]. Pharmacologic inhibition of NKA increases neuropeptide Y (NPY) mRNA expression and food intake.In ARC GSNs, lowering glucose, via intracellular ATP reduction, causes NKA suppression, which activates NPY neurons to promote feeding.
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