The investigation of pathophysiological role of ghtelin and CRF on anorexia nervosa and discovery of a new therapeutic medication.
| Project/Area Number |
22791144
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Psychiatric science
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| Research Institution | Nippon Medical School |
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Principal Investigator |
MANO Asuka 日本医科大学, 医学部, 講師 (50343588)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ストレス / 生理学 / 脳・神経 / グレリン / CRF / 摂食障害 |
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| Research Abstract |
Corticotropin-releasing factor (CRF), the most important regulator of the response of the hypothalamic-pituitary-adrenal axis to stress, mediates stress-induced inhibition of food intake, and ghrelin, an endogenous ligand for growth hormone secretagogue receptor, stimulates food intake. Anorexia nervosa (AN) is an eating disorder characterized by immoderate food restriction and irrational fear of gaining weight. Therefore CRF and ghrelin may be involved in pathophysiology of AN. The goal of this study is to clarify important roles of CRF and ghrelin on pathophysiology of AN. Stress-induced inhibition of food intake was decreased by administration of ghrelin after stress. Suppression of the expression of endogenous ghrelin receptor in the hypothalamic arcuate nucleus decreased food intake and increased spontaneous activity in rats. These results show that ghrelin is effective on stress-induced inhibition of food intake, and impairment of the function of ghrelin receptor in the hypothalamic arcuate nucleus induces anorectic effect in rats. Further experiment is needed to clarify an important role of CRF and ghrelin in stress-induced anorexia, and a participation of CRF and ghrelin with pathophysiology of AN.
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Report
(4 results)
Research Products
(8 results)
