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Glucose-induced production of hydrogen sulfide may protect the pancreatic beta-cells from apoptotic cell death by high glucose |
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| Authors: | Yukiko Kaneko Toshihide Kimura Midori Souma Yuka Kimura Ichiro Niki |
| Affiliation: | a Department of Pharmacology, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama, Oita 879-5593, Japan b Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka 52-1 Yada, Suruga-ku, Shizuoka 422-8526, Japan c Department of Molecular Genetics, National Institute of Neuroscience, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8551, Japan |
| Abstract: | We examined the expression of the major H2S-producing enzymes, cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE). CBS was ubiquitously distributed in the mouse pancreas, but CSE was found only in the exocrine. Freshly isolated islets expressed CBS, while CSE was faint. However, high glucose increased the CSE expression in the beta-cells. l-Cysteine or NaHS suppressed islet cell apoptosis with high glucose, and increased glutathione content in MIN6 beta-cells. Pretreatment with l-cysteine improved the secretory responsiveness following stimulation with glucose. The CSE inhibitor dl-propargylglycine antagonized these l-cysteine effects. We suggest H2 S may function as an ‘intrinsic brake’ which protects beta-cells from glucotoxicity. |
| Keywords: | Hydrogen sulfide Pancreatic beta-cell Cystathionine-γ-lyase (CSE) Cystathionine-β-synthase (CBS) Apoptosis l-Cysteine |
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