2023 Fiscal Year Final Research Report
Toward Reducing the Risk of Fatty Liver Syndrome in Post-Growth Infants Caused by Undernutrition in Utero
Project/Area Number |
20K09666
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 56040:Obstetrics and gynecology-related
|
Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
伊東 宏晃 浜松医科大学, 医学部, 教授 (70263085)
内田 季之 浜松医科大学, 医学部附属病院, 准教授 (90570234)
成味 恵 浜松医科大学, 医学部附属病院, 診療助教 (50594321)
|
Project Period (FY) |
2020-04-01 – 2024-03-31
|
Keywords | DOHaD / 慢性炎症 / metaflamation |
Outline of Final Research Achievements |
We focused on endoplasmic reticulum stress as a mechanism involved in the exacerbation of chronic inflammation in tissues due to catch-up growth following prenatal malnutrition, and administered Tauroursodeoxycholic acid (TU), an endoplasmic reticulum stress reliever, in adult animals, and fat weight was significantly reduced. Microarray analysis of adipose tissue identified four Gene Ontologies (GOs) related to inflammation, which were common to both hypofertilization and TU administration. Mφ counts were increased by prenatal malnutrition and decreased by TU administration.
|
Free Research Field |
DOHaD
|
Academic Significance and Societal Importance of the Research Achievements |
マウス動物モデルの解析から、胎生期低栄養と出生後のcatch upにより、脂肪組織に炎症に関わる一群の遺伝子発現の変化ならびにマクロファージの集簇が明らかとなった。 二次胆汁酸であるTauroursodeoxycholic acid が、プログラムされたMetaflamtionを改善する可能性が指摘された。Developmental Origins of Metaflamationという新規視点から研究の展開が期待される。
|