Elucidation of the pathophysiological roles of thyroid hormone metabolism in diabetes mellitus

2016 Fiscal Year Final Research Report

• Project/Area Number: 26293125
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Laboratory medicine
• Research Institution: Gunma University
• Principal Investigator: Murakami Masami 群馬大学, 医学(系)研究科(研究院), 教授 (30241871)
• Co-Investigator(Kenkyū-buntansha): 角野 博之 群馬大学, 医学部附属病院, 講師 (10375579) ; 常川 勝彦 群馬大学, 医学(系)研究科(研究院), 助教 (30436307) ; 奈良 誠人 群馬大学, 医学部附属病院, 助教 (80420165) ; 荒木 修 群馬大学, 医学部附属病院, 助教 (80589482) ; 木村 孝穂 群馬大学, 医学(系)研究科(研究院), 講師 (90396656) ; 荻原 貴之 群馬大学, 医学部附属病院, 助教 (80361377)
• Co-Investigator(Renkei-kenkyūsha): OKU Hiroyuki 群馬大学, 理工学研究院, 准教授 (20301749)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 糖尿病 / 甲状腺ホルモン / 遺伝子 / 一塩基多型 / 自己抗体

Outline of Final Research Achievements

We have studied the expression and regulation of thyroid hormone metabolism, including type 2 iodothyronine deiodinase (D2) which activates thyroid hormones and type 3 iodothyronine deiodinase (D3) which inactivates thyroid hormones.
We found the expression of D3 in cultured pancreatic beta cells, which is stimulated by GLP-1 via a cAMP-PKA mediated pathway. D3 is suggested to increases insulin secretion from pancreatic beta cells by decreasing intracellular T3. Furthermore, we discovered the expression of D2 in cultured human umbilical vein endothelial cells (HUVECs). Conversion of T4 to T3 by D2 is required for rapid nongenomic action of T4, which results in migration of HUVECs.
These results may open a novel perspective on understanding of the mechanisms of thyroid hormone action.

Free Research Field

内分泌代謝疾患における臨床化学を中心とした臨床検査医学