2004 Fiscal Year Final Research Report Summary
Mechanism for leptin resistance and obesity in ventromedial hypothalamus lesioned rats
| Project/Area Number |
15590204
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | University of Fukui (2004)
福井医科大学 (2003) |
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Principal Investigator |
HIGUCHI Takashi University of Fukui, Faculty of Medical Sciences, Professor, 医学部, 教授 (70106326)
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| Co-Investigator(Kenkyū-buntansha) |
MURATA Takuya University of Fukui, Faculty of Medical Science, Associate Professor, 医学部, 助教授 (70281186)
NARITA Kazumi University of Fukui, Faculty of Medical Science, Assistant Professor, 医学部, 助手 (80270958)
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| Project Period (FY) |
2003 – 2004
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| Keywords | ventromedial hypothalamus / hyperphagia / odesity / orexin / melanin-concentrating hormone / immunohisto chemistry |
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| Research Abstract |
The ventromedial hypothalamus (VMH) has long been known as a satiety center because the lesion of the VMH results in hyperphagia and obesity. Recently leptin that inhibits food intake, can not exert its effect in VMH-lesioned rats (leptin resistance). We hypothesize that orexigenic neurons which produce orexigenic peptides such as orexin or melamocyte-concentrating hormone (MCH) may increase their activity after VMH lesion. Otherwise, since there is melanocortin receptor in the VMH, VMH lesion may deplete the receptor, resulting in leptin resistance and unresponsiveness to anorexic peptide such as α-melanocyte stimulating hormone (MSH). Our results show that orexin and MCH contents in the lateral hypothalamus are decreased in the VMH-lesioned rats suggesting that these orexigenic neurons may be inhibited their activity after VMH lesion. These results are published in the Journal of Neruoendocrinology 15, 51-60, 2002 and 16, 79-83, 2003. In addition, MSH as well as other anorexia peptides such as corticotropin releasing hormone (CRH) and cholecystokinin (CCK) is effective in the VMH-lesioned rats (unpublished). Thus the hyperphagia and leptin resistance is neither due to the hyperactivity of orexigenic neurons that produce orexin or MCH nor unresponsiveness to anorexia peptides such as MSH, CRH or CCK. We are conducting experiments to testify a new hypothesis in stead of that the VMH is a satiety center.
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[Journal Article] Orexin a Elicits Arousal Electroencephalography Without Sympathetic Cardiovascular Activation in Isoflurane-Anesthetized Rats2003
Author(s)
Yasuda, Y., A.Takeda, S.Fukuda, H.Suzuki, M.Ishimoto, Y.Mori, H.Eguchi, R.Saitoh, H.Fujihara, K.Honda, T.Higuchi.
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Journal Title
Anesth Analg 97
Pages: 1663-1666
Description
「研究成果報告書概要(欧文)」より
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