A study of molecular mechanisms by which D-dopachrome tautomerase improves insulin resistance in obesity

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592799
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Functional basic dentistry
• Research Institution: The University of Tokushima
• Principal Investigator: IWATA Takeo 徳島大学, ヘルスバイオサイエンス研究部, 助教 (10350399)
• Co-Investigator(Kenkyū-buntansha): YOSHIMOTO Katsuhiko 徳島大学, 大学院ヘルスバイオサイエンス研究部, 教授 (90201863) ; MIZUSAWA Noriko 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助教 (80254746) ; ISHIMOTO Kyoko 徳島大学, 大学病院, 診療支援医師 (60579952)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: アディポカイン / インスリン抵抗性 / 脂肪細胞 / 肥満

Outline of Final Research Achievements

D-dopachrome tautomerase (DDT), an adipokine, improves insulin resistance in obesity. To clarify the mechanisms, we performed analysis using transgenic mice overexpressing DDT in the adipocytes (TG mice), identification of genes whose expressions change in DDT-knockdown preadipocytes, and investigation of molecular mechanisms by which DDT inhibits adipogenesis. TG mice fed high fat diet tended to inhibit the insulin resistance. DDT-knockdown in adipocytes decreased expression of VEGF-A that was reported to accelerate insulin resistance, and increased expression of SEPP-1 that inhibits insulin signals in the adipose tissue and skeletal muscle. Adipogenesis inhibited by DDT was specific in a human preadipocyte cell line, SGBS cells. Expressions of LMO3 and c-Fos were decreased in SGBS cells treated with DDT in the presence of glucocorticoid, suggesting that these genes may be involved in adipogenesis inhibited by DDT in human preadipocytes.

Free Research Field

薬理学、内分泌学