2000 Fiscal Year Final Research Report Summary
A comprehensive study on the role of the obese gene product, leptin in reproduction and fetal development
| Project/Area Number |
11470348
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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 |
SAGAWA Norimasa Kyoto University, Graduate School of Medicine, Associate Professor, 医学研究科, 助教授 (00162321)
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| Co-Investigator(Kenkyū-buntansha) |
OGAWA Yoshihiro Kyoto University, Graduate School of Medicine, Instructor, 医学研究科, 助手 (70291424)
KARIYA Masatoshi Kyoto University, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (90243013)
KONISHI Ikuo Shinshu University, School of Medicine, Professor, 医学部, 教授 (90192062)
ITOH Hiroaki Kyoto University, Graduate School of Medicine, Instructor, 医学研究科, 助手 (70263085)
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| Project Period (FY) |
1999 – 2000
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| Keywords | leptin / transgenic mice / reproduction / ovarian function / pregnancy / ingestion / fetal development / placenta |
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| Research Abstract |
Leptin is an adipocyte-derived hormone that is involved in the regulation of food intake and energy expenditure. Short-term administration of leptin accelerates the onset of puberty in normal mice and corrects the sterility of leptin-deficient ob/ob mice. These findings suggest a putative role of leptin as an endocrine signal between fat depots and the reproductive axis. However, the effect of hyperleptinemia on the initiation and maintenance of reproductive function has not been elucidated. To address this issue, we examined the reproductive phenotypes of female transgenic skinny mice(Tg-mice) with elevated plasma leptin concentrations comparable to those in obese subjects. With no apparent adipose tissue, female Tg-mice exhibit accelerated puberty and intact fertility at younger ages followed by successful delivery of healthy pups. However, at older ages, they develop hypothalamic hypogonadism characterized by prolonged menstrual cycles, atrophic ovary, reduced hypothalamic gonadotro
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pin releasing hormone (GnRH) contents and poor pituitary luteinizing hormone secretion. This study has demonstrated for the first time that accelerated puberty and late onset hypothalamic hypogonadism are associated with chronic hyperleptinemia.
We previously demonstrated that leptin is a novel placenta-derived hormone in humans (Nat Med.3 : 1029, 1997). Intrauterine growth retardation (IUGR) of the fetus due to placental hypoperfusion is one of the most common complications in preeclampsia. In this study, we compared the maternal plasma leptin levels with maternal mean blood pressure and degree of fetal growth restriction. Plasma leptin levels were correlated well with mean blood pressure, but not with body mass index (BMI). Plasma leptin levels in preeclamptic women with IUGR were significantly elevated, compared to those without IUGR (P<0.05). Moreover, plasma leptin levels were negatively correlated with relative birth weight (ΔSD). These dada ggest the possibility that maternal plasma leptin may be useful as a clinical marker of maternal hypertension as well as fetal growth restriction. Less
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