2004 Fiscal Year Final Research Report Summary
Identification of a novel secreted satiety protein that is activated by PPARγ activation
| Project/Area Number |
15390291
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Endocrinology
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| Research Institution | Gunma University |
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Principal Investigator |
MORI M Gunma University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (80174382)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU H Gunma University, Associate Professor, 医学部, 講師 (20251100)
YAMADA M Gunma University, Associate Professor, 医学部, 講師 (90261833)
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| Project Period (FY) |
2003 – 2004
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| Keywords | Satiety factor / PPARγ / Obesity / NAP |
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| Research Abstract |
We identified a protein of unknown function, termed NAP, that is expressed in the feeding-related hypothalamic nuclei and fat in rodents, using subtraction cloning analysis of PPARγ-activated cells. Icv injection of NAP caused a dose-dependent decrease in food intake, and icv injection of its antibody increased this. Expressions of NAP gene and protein in the lateral hypothalamic nuclei were significantly decreased in over-night starved rats. The hypothalamic NAP was co-localized with prohormone convertases, and the band corresponding to NAP-1 was observed in the rat brain extracts and cerebrospinal fluids. Icv injection of NAP-1, but not another regions of NAP, produced satiety, and an antibody recognizing NAP-1 oppositely elevated feeding behavior. Chronic icv injection of NAP-1 caused a significant decrease in both food intake and body weight. In contrast, an increased feeding and consequent obesity were found in rats receiving chronic icv administration of both antisense against NAP gene. Icv injection of NAP-1 significantly reduced food intake in fa/fa rats. Data presented here show that NAP functions satiety in the hypothalamus and that its administration is efficient in a condition of leptin resistance.
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Research Products
(8 results)
