The possible significance of citrate for insulin release was elucidated by measuring the levels of this metabolite in isolated pancreatic islets from obese-hyperglycemic mice and their lean litter mates. The amount of islet citrate depended on the extracellular glucose concentration but was not affected by the insulin secretagogues, glibenclamide or dibutyryl cyclic-3,5-AMP. Increased β-cell levels of citrate do not necessarily result in stimulation of insulin release, as shown by the increased amounts of citrate in islets exposed to epinephrine. Octanoate (5 mM) had no effect on the level of citrate in islets exposed to 0.6 mg./ml. glucose. In the presence of 3 mg./ml. glucose, octanoate significantly depressed the citrate level. It seems unlikely that the citrate molecule has the important role in controlling insulin release that has previously been suggested.

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