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.
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Eizirik et al. (1994) studied this question.
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