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Succinic acid monomethyl ester protects rat pancreatic islet secretory potential against interleukin‐1β (IL‐1β) without affecting glutamate decarboxylase expression or nitric oxide production
Author(s) -
Eizirik Décio L.,
Welsh Nils,
Niemann Audrey,
Velloso Licio A.,
Malaisse Willy J.
Publication year - 1994
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 - 10.1016/0014-5793(94)80213-0
Subject(s) - nitric oxide , pancreatic islets , chemistry , beta cell , medicine , endocrinology , islet , nitric oxide synthase , insulin , biochemistry , biology
Rat pancreatic islets exposed to interleukin‐1β (IL‐1β) in the presence of succinic acid monomethyl ester (SAM) have a higher insulin release in response to glucose and higher glucose oxidation rates, as compared to islets exposed to IL‐1β alone. These beneficial effects of SAM were not accompanied by any decrease in IL‐1β‐induced nitric oxide (NO) production nor inhibition of aconitase activity. Moreover, SAM did not increase biosynthesis of glutamate decarboxylase. SAM apparently improves β‐cell function mostly by increasing the capacity of these cells to endure NO exposure and partial blockage of the Krebs cycle.