Neuroendocrine mechanism of precocious puberty caused by fetal stress in utero

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K16123
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 48020:Physiology-related
• Research Institution: Iwate Medical University (2021-2022); Nippon Medical School (2020)
• Principal Investigator: Minabe Shiori 岩手医科大学, いわて東北メディカル・メガバンク機構, 特命助教 (40781571)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 思春期早発症 / 神経内分泌学 / 性成熟 / 胎児プログラミング / 視床下部 / Kisspeptin / ゴナドトロピン

Outline of Final Research Achievements

This study aims to examine the neuroendocrine mechanisms of precocious puberty induced by fetal stress to experimentally prove the DOHaD hypothesis, which states that the growth environment during development influences health and disease onset in later life. In this study, female rats born to mothers whose food intake was restricted to 50% of that of the control group were used as a model of fetal nutritional stress (UN group) to analyze their reproductive function. The results showed that nutritional deficiency during the fetal period induces fetal programming in the hypothalamus of female rats and changes in KNDy gene expression at different life stages, resulting in altered reproductive function.

Free Research Field

生殖神経内分泌学

Academic Significance and Societal Importance of the Research Achievements

思春期早発症は第二次性徴が早期に現れる疾患である。本症の問題点として、本人の心理的・社会的な問題を引き起こすことや、骨年齢の促進による最終的な低身長などがあげられるが、発症機序の詳細は不明である。本研究により、思春期早発症が視床下部の生殖中枢の胎児プログラミングが関与することが示されたことで、これまで発症機序が謎であった思春期早発症の神経内分泌メカニズムの一端を解明でき、学術的な意義は極めて高い。