Succinic acid monomethyl ester protects rat pancreatic islet secretory potential against interleukin-1 beta (IL-1 beta) without affecting glutamate decarboxylase expression or nitric oxide production.
Rat pancreatic islets exposed to interleukin-1 beta (IL-1 beta) 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-1 beta alone. These beneficial effects of SAM were not accompanied by any decrease in IL-1 beta-induced nitric oxide (NO) production nor inhibition of aconitase activity. Moreover, SAM did not increase biosynthesis of glutamate decarboxylase. SAM apparently improves beta-cell function mostly by increasing the capacity of these cells to endure NO exposure and partial blockage of the Krebs cycle.
Eizirik
D L
DL
Department of Medical Cell Biology, Uppsala University, Sweden.
Welsh
N
N
Niemann
A
A
Velloso
L A
LA
Malaisse
W J
WJ
D000154:Aconitate Hydratase / Q000378:metabolism; D000818:Animals; D005947:Glucose / Q000494:pharmacology; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007375:Interleukin-1 / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D009569:Nitric Oxide / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000494:pharmacology; D013386:Succinates / Q000494:pharmacology*
D007328:Insulin; D007375:Interleukin-1; D011994:Recombinant Proteins; D013386:Succinates; D009569:Nitric Oxide; D005968:Glutamate Decarboxylase; D000154:Aconitate Hydratase; D005947:Glucose; C041105:monomethyl succinate