Abstract
The impact of muscarinic type 3 receptor knockout (M 3KO) on the cholinergic regulation of insulin secretion and phospholipase C (PLC) activation was determined. Islets isolated from control, wild-type mice or heterozygotes responded with comparable insulin secretory responses to 15 mM glucose. This response was markedly amplified by the inclusion of 10 μM carbachol. While 15 mM glucose-induced release remained similar to wild-type and heterozygote responses in M 3KO mice, the stimulatory impact of carbachol was abolished. Stimulation with 15 mM glucose plus 50 μM carbachol increased fractional efflux rates of myo-[2- 3H]inositol from control wild-type and heterozygote islets but not from M 3KO islets. Fed plasma insulin levels of M 3KO mice were reduced 68% when compared to values obtained from combined wild-type and heterozygote animals. These studies support the conclusion that the M 3 receptor in islets is coupled to PLC activation and insulin secretion and that cholinergic stimulation of the islets may play an important role in the regulation of plasma insulin levels.
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