Insulin biosynthesis: the monoaminergic mechanisms and the specificity of "glucoreceptor".

Islets of Langerhans, isolated from the rat, did not synthesize insulin in the presence of L-glucose, fructose, galactose, 3-0-methyl glucose or sorbitol. A small amount of insulin was synthesized in the presence of glucosamine. Addition of caffeine to these compounds did not enhance the biosynthesis of insulin. It is suggested that the specificity of the membrane surface "glucoreceptor", if it exists, may be rather narrow, at least with respect to insulin biosynthesis. Serotonin, dopamine and isoproterenol did not inhibit or enhance insulin biosynthesis induced by glucose. Propranolol also failed to modify insulin synthesis in the absence or presence of isoproterenol. It is concluded that the monoaminergic mechanisms do not affect insulin biosynthesis in spite of their significant regulatory influence on insulin release. Methysergide, at the concentration reported to potentiate insulin release induced by glucose and tolbutamide in rabbit, strongly inhibited insulin biosynthesis.