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2023 Fiscal Year Final Research Report

Research for elucidating the molecular mechanisms linking phosphorus metabolism and aging.

Research Project

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Project/Area Number 21H03359
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Review Section Basic Section 59040:Nutrition science and health science-related
Research InstitutionThe University of Tokushima

Principal Investigator

MASUDA Masashi  徳島大学, 大学院医歯薬学研究部(医学域), 講師 (50754488)

Co-Investigator(Kenkyū-buntansha) 安倍 知紀  国立研究開発法人産業技術総合研究所, 生命工学領域, 研究員 (00736605)
谷村 綾子  島根県立大学, 看護栄養学部, 准教授 (10610199)
金子 一郎  兵庫県立大学, 環境人間学部, 准教授 (40389515)
Project Period (FY) 2021-04-01 – 2024-03-31
Keywords生体内リン / 小胞体ストレス
Outline of Final Research Achievements

This study aims to elucidate the regulatory mechanism of intestinal phosphorus absorption by endoplasmic reticulum (ER) stress caused by aging. A comparison of intestinal phosphorus absorption activity between young and aged mice showed that the aged group had higher phosphorus absorption activity. Among the intestinal phosphate transporters (Npt2b and PiT1/2), Npt2b gene expression was low, but PiT1/2 expression was high. Among the ER stress response factors in the intestine, the expression level of sXBP1 was low in the aged group, while the expression level of C/EBPb was high in the aged group. Moreover, PiT1/2 gene transcriptional activity is promoted by C/EBPb, suggesting that the cause of increased intestinal phosphorus absorption in aging is increased PiT1/2 expression via increased expression of C/EBPb.

Free Research Field

老化

Academic Significance and Societal Importance of the Research Achievements

小胞体ストレスは細胞内外の環境変化に起因する小胞体内の異常タンパク質の蓄積により生じ、加齢によってもタンパク質の折り畳み機能が低下することで小胞体ストレスは増大する。軽度の小胞体ストレスは生体内防御反応を誘発するが、それでは処理しきれない程に過剰になると細胞に対して悪影響を及ぼして、糖尿病、神経変性疾患、脂質異常症、循環器疾患、がん等、種々の加齢性疾患を誘発する。これまで生体内リンも加齢性疾患や寿命に影響を与えることが報告されてきたが、その詳細な機序に関しては不明な点が多い。本研究の成果は、老化状態における小胞体ストレスと生体内リンを介した加齢性疾患発症機序の解明に繋がる可能性がある。

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Published: 2025-01-30  

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