Study of the influence that the anesthetic which assumed metabolism mode analysis a key gives to the insulin secretion of pancreas beta cell

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K20063
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Anesthesiology
• Research Institution: Kyoto University (2016); Kansai Medical University (2015)
• Principal Investigator: Suzuki Kengo 京都大学, 医学研究科, 助教 (90734658)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: HIF-1 / インスリン / セボフルラン / イソフルラン

Outline of Final Research Achievements

Several animal and human studies have indicated that volatile anesthetics impair glucose-stimulated insulin secretion (GSIS).
Isoflurane and sevoflurane inhibited GSIS significantly in a concentration-dependent manner. Oxygen consumption rate in MIN6 cells but to a lesser extent than the mitochondrial uncoupler, CCCP (5 μM). Isoflurane and sevoflurane significantly suppressed glucose-induced HIF-1alpha protein expression in MIN6 cells. HIF-1alpha protein expression, which was not affected by isoflurane. Inhibition of HIF-1 activity by YC-1 treatment and RNA interference-mediated knockdown of HIF-1alpha expression significantly suppressed GSIS in MIN6 cells.
Both the anesthetics inhibited the glucose-induced increase of ATP, which is dependent on intracellular hypoxia-induced HIF-1 activity, and suppressed GSIS at a clinically relevant dose in MIN6 cells.

Free Research Field

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