2023 Fiscal Year Final Research Report

Mechanism of high fat-induced myeloid hematopoiesis regulated by SOCS3

Research Project

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Project/Area Number	19K11716
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Review Section	Basic Section 59040:Nutrition science and health science-related
Research Institution	Niigata University
Principal Investigator	USHIKI TAKASHI 新潟大学, 医歯学系, 准教授 (80579152)
Co-Investigator(Kenkyū-buntansha)	平位秀世東京薬科大学, 生命科学部, 教授 (50315933) 増子正義新潟大学, 医歯学総合病院, 准教授 (70397115) 中川嘉富山大学, 学術研究部薬学・和漢系, 教授 (80361351)
Project Period (FY)	2019-04-01 – 2024-03-31
Keywords	SOCS3 / 顆粒球増多 / 高脂肪食 / 慢性炎症
Outline of Final Research Achievements	Systemic inflammation due to granulocytosis is induced without the formation of fatty liver, when SOCS3 knockout mice are fed a high-fat diet. As a mechanism, the saturated fatty acid/unsaturated fatty acid balance in liver fatty acid metabolism was only slightly changed, and changes in the intestinal microbiota were observed by 16S rRNA sequencing. Granulocytosis was canceled by administration of four types of antibiotics (ABPC+FRM+VCM+MNZ). Furthermore, increases in LSK, CD34 negative LSK, CMP, and GMP were observed in the bone marrow by fat diet, but these findings disappeared after intestinal sterilization. Based on the above, it was considered that abnormalities in the intestinal flora due to SOCS3 knockout and high-fat diet loading, which had the most influence on granulocytosis.
Free Research Field	血液学
Academic Significance and Societal Importance of the Research Achievements	慢性炎症は肥満、糖尿病、高血圧、高脂血症などのメタボリックシンドロームに関与しており、それらの疾患に伴う合併症の発症に関与している。このため、メタボリックシンドロームに伴う慢性炎症の発症メカニズムを明らかとすることは合併症予防において大きな社会的意義を有する。また慢性炎症は自己免疫疾患、がん、神経疾患の進展にも大きく関与している現象であり、これらの制圧するためのストラテジー構築においても本研究成果は大いに参考になるものであり、学術的意義を有するものである。