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2017 Fiscal Year Final Research Report

Pathophysiological mechanism for the high incidence of overeating-induced obesity, NASH and hepatic carcinogenesis in post-menoposal women

Research Project

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Project/Area Number 15H04935
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Digestive surgery
Research InstitutionTokyo Women's Medical University

Principal Investigator

Yamamoto Masakazu  東京女子医科大学, 医学部, 教授 (60220498)

Co-Investigator(Kenkyū-buntansha) 橋本 悦子  東京女子医科大学, 医学部, 教授 (40130273)
有泉 俊一  東京女子医科大学, 医学部, 准教授 (40277158)
徳重 克年  東京女子医科大学, 医学部, 教授 (60188729)
正田 純一  筑波大学, 医学医療系, 教授 (90241827)
柳川 徹  筑波大学, 医学医療系, 准教授 (10312852)
後藤 直宏  東京海洋大学, 食品生産科学科, 教授 (60323854)
磯辺 智範  筑波大学, 医学医療系, 准教授 (70383643)
蕨 栄治  筑波大学, 医学医療系, 講師 (70396612)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywords脂肪性肝炎 / 肝癌 / 女性ホルモン / 転写因子 / 臓器連環
Outline of Final Research Achievements

DKO mice represent a phenotype similar to human NASH. This study investigated sex differences in the phenotypes in the mice. Both male and female mice at 8 weeks showed normal liver histology. At 30 weeks, while the livers of male mice became fatty and fibrotic, those of female mice showed only minimal changes of steatosis and no fibrosis. Even for the female mice at 50 weeks, while the large lipid droplets were found, only minimal changes of fatty and fibrotic changes were observed in the livers. The magnitude of NASH histological changes was found to be weaker in female than in male mice. The results importantly suggest that female hormones may attenuate NASH pathophysiology by inhibiting overeating obesity and LPS-induced inflammatory responses.

Free Research Field

肝臓外科学

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Published: 2019-03-29  

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