The effects of adequate blood glucose control on neurological dysfunction induced by septic shock

Research Project

Project/Area Number	15K10532
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Anesthesiology
Research Institution	Gunma University
Principal Investigator	KADOI YUJI 群馬大学, 医学部附属病院, 准教授 (10292591)
Project Period (FY)	2015-04-01 – 2020-03-31
Project Status	Completed (Fiscal Year 2019)
Budget Amount *help	¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000) Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000) Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000) Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords	敗血症 / 高血糖 / 中枢神経障害 / サイトカイン / 脳障害 / HMGB-1 / 神経障害 / インスリン / 脳細胞
Outline of Final Research Achievements	in neural cells, high glucose level induced nerual cell death, in contrast, adequate glucose level induced the improvement of neural cell death. In vitro patch clamping showed that high glucose level induced the decrse on the degree of long-term potential (LTP), in contrast adequate glucose level had no effects ontthe degree of long-term potential (LTP), In septic shock model rats, adequate blood glucose cntrol could not improve the blood levels of RAGE and HMGB-1. In addition, no effects of neurological dysfuvtion induced by sepsis was found even when keeping adequate blood glucose. These data showed that higher bllod glucose was not associated with neurological dysfunction inded by septic shock in rats.
Academic Significance and Societal Importance of the Research Achievements	In vitroの実験においては敗血症由来の中枢神経障害は高血糖を改善させることにより神経細胞活性を改善させたが、一方、動物実験では敗血症由来の中枢神経障害は高血糖を改善させるだけでは各種サイトカインレベルを減少させることが出来ず、中枢神経障害も改善させることは出来なかった。これらの知見は敗血症由来の中枢神経障害は高血糖由来ではないことを証明したものであり、他の因子が中枢神経障害に関与していることを推測するものである。