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Luseogliflozin preserves the pancreatic beta-cell mass and function in db/db mice by improving mitochondrial function

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Title: Luseogliflozin preserves the pancreatic beta-cell mass and function in db/db mice by improving mitochondrial function
Authors: Yamauchi, Yuki Browse this author
Nakamura, Akinobu Browse this author →KAKEN DB
Yokota, Takashi Browse this author →KAKEN DB
Takahashi, Kiyohiko Browse this author
Kawata, Shinichiro Browse this author
Tsuchida, Kazuhisa Browse this author
Omori, Kazuno Browse this author
Nomoto, Hiroshi Browse this author →KAKEN DB
Kameda, Hiraku Browse this author →KAKEN DB
Cho, Kyu Yong Browse this author
Anzai, Toshihisa Browse this author →KAKEN DB
Tanaka, Shinya Browse this author →KAKEN DB
Terauchi, Yasuo Browse this author
Miyoshi, Hideaki Browse this author →KAKEN DB
Atsumi, Tatsuya Browse this author →KAKEN DB
Issue Date: 13-Jun-2022
Publisher: Nature Portfolio
Journal Title: Scientific reports
Volume: 12
Issue: 1
Start Page: 9740
Publisher DOI: 10.1038/s41598-022-13888-6
Abstract: We aimed to determine the mechanism by which the sodium glucose co-transporter 2 inhibitor, luseogliflozin, preserves pancreatic beta-cell mass and function in db/db mice. Six-week-old db/db mice were fed to standard chow or standard chow containing 0.01% luseogliflozin. After 4 weeks, DNA microarray analysis, real-time PCR analysis, and measurement of mitochondrial respiratory capacity and reactive oxygen species (ROS) generation were performed using isolated islets. Immunohistochemistry and electron microscopic analysis were performed using pancreatic tissues. Metabolites extracted from the islets were measured by capillary electrophoresis mass spectrometry. The expression of genes involved in the tricarboxylic acid (TCA) cycle and electron transport chain was upregulated by luseogliflozin. Luseogliflozin improved the mitochondrial complex II-linked oxidative phosphorylation capacity and reduced ROS generation. Mitochondrial morphology was normally maintained by luseogliflozin. Luseogliflozin increased NK6 homeobox 1 (NKX6.1) expression and TCA cycle metabolites. Relief of glucotoxicity by luseogliflozin may involve lower mitochondrial ROS generation and an improvement in complex II-linked mitochondrial respiration. Reducing ROS generation through preventing complex II damage likely increases NKX6.1 expression and ameliorate glucose metabolism in the TCA cycle, contributing to the protection of pancreatic beta-cells. Protection of complex II in pancreatic beta-cells represents a novel therapeutic target for type 2 diabetes.
Type: article
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

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