| Project/Area Number |
16390475
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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 |
Obstetrics and gynecology
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| Research Institution | Kyoto University |
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Principal Investigator |
ITOH Hiroaki Kyoto University, Graduate School of Medicine, Associate Professor, 医学研究科, 講師 (70263085)
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| Co-Investigator(Kenkyū-buntansha) |
SAGAWA Norimasa Mie University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (00162321)
YURA Shigeo Kyoto University, Graduate School of Medicine, Assistant Professor, 医学研究科, 助手 (60335289)
OGAWA Yoshihiro Tokyo Medical and Dental University, Department of molecular Medicine and Metabolism, Professor, 難治疾患研究所, 教授 (70291424)
菅 真一 国立循環器病センター, 研究所・病因部, 室長 (70273456)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥14,300,000 (Direct Cost: ¥14,300,000)
Fiscal Year 2005: ¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 2004: ¥7,400,000 (Direct Cost: ¥7,400,000)
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| Keywords | pregnancy / fetus / metabolic syndrome / nutrition / medical welfare / IUGR / 栄養 / fetal programming / 肥満 / 高血圧 / 糖尿病 |
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| Research Abstract |
The purpose of the present study was to investigate a possible mechanism of developmental origins of metabolic syndrome.
We developed a mouse animal model of fetal undernutrition (UN offspring) by maternal food restriction. The UN offspring developed an acceleration of obesity on high fat diet, dyslipidemia, impaired glucose tolerance and blood pressure increase in adulthood. In the UN offspring, we reveled a premature onset of leptin surge during neonatal period, which programmed permanent low leptin sensitivity in the hypothalamic energy regulation, concomitant with structural changes of hypothalamic neuronal circuit, such as neuropeptide Y (NPY) and cocaine and amphetamine regulated transcript (CART), contributing to an acceleration of obesity on high fat diet as well as impaired glucose metabolism (Yura S, Itoh H et al., Cell Metab, 2005,1,371).
Thus, we here demonstrated that premature leptin surge during neonatal period plays a pivotal role in the developmental origins of obesity and associated detrimental metabolic disorders.
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