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Glucose‐induced production of hydrogen sulfide may protect the pancreatic beta‐cells from apoptotic cell death by high glucose
Author(s) -
Kaneko Yukiko,
Kimura Toshihide,
Taniguchi Shigeki,
Souma Midori,
Kojima Yumiko,
Kimura Yuka,
Kimura Hideo,
Niki Ichiro
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.12.026
Subject(s) - cystathionine beta synthase , cystathionine gamma lyase , cysteine , apoptosis , hydrogen sulfide , islet , pancreas , chemistry , programmed cell death , medicine , endocrinology , beta cell , enzyme , pancreatic islets , stimulation , glutathione , biochemistry , biology , diabetes mellitus , sulfur , organic chemistry
We examined the expression of the major H 2 S‐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 H 2 S may function as an ‘intrinsic brake’ which protects beta‐cells from glucotoxicity.