Reversal of Glucose-Induced Inhibition of Insulin Release by Dibutyryl Cyclic AMP

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Abstract
Insulin release in response to glucose was measured after culture of islets from ob/obmice in a medium deficient in Ca2+. When present at a concentration of 6 mmol/1, glucose inhibited, insulin release. After activation of the <α2-adrenergic receptors by 1 µmol/1 clonidine also 20 mmol/1 glucose became inhibitory. The inhibitory action of glucose oa insulin release disappeared in the presence of 1 mmol/1 dibutyryl cyclic AMP. Raising the glucose concentration from 3 to 20 mmol/1 resulted in increased cytoplasmic Ca2+ after an initial depression. Whereas clonidine removed the Ca2+ increase, this phase was partly restored after simultaneous addition of dibutyryl cyclic AMP. It is concluded that cyclic AMP plays a major role in controlling the balance between the stimulatory and inhibitory components in the glucose action on insulin release.

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