Effect of Nicotine and Nicotine Metabolites on Insulin Secretion from Rabbit Pancreas Pieces

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Abstract
The effects of nicotine and the nicotine metabolites cotinine and γ–(3-pyridyl)-γ-oxobutyric acid on insulin secretion from rabbit pancreas pieces were studied with a radioimmunological method. High concentrations of nicotine inhibited a glucose (3.0 mg/ml) induced insulin secretion, while lower concentrations stimulated the secretion. The stimulating effect of nicotine was also demonstrated in a lower glucose concentration (0.6 mg/ml). A high concentration of cotinine stimulated the glucose induced insulin secretion, while inhibitory effects of cotinine were not observed. In further experiments it was shown that nicotine was not metabolised in the pancreas in vitro, thus the effect of nicotine on insulin secretion is not due to cotinine formation. Both the stimulatory and the inhibitory effects of nicotine as well as the stimulatory effect of cotinine were blocked by both atropine and hexamethonium. γ-(3-pyridyl)-γ-oxobutyric acid had no effect on the glucose induced insulin secretion. Several possibilities for the mechanism of nicotine action are discussed. The site of action may be at parasympathetic ganglia within the pancreas. Another possibility is a direct effect on the β-cells in the pancreatic islets, where nicotine might exert an effect on biogenic amines present within the islets and of importance for insulin release. This is discussed in view of the importance that biogenic amines have been shown to have on insulin secretion and also in view of the finding that aminergic mechanisms are operative in the islets. Since cotinine has been shown to have weak nicotine—like effects, it is postulated that the stimulating effect of high concentrations of cotinine on the insulin secretion is mediated via similar mechanisms as is the stimulatory effect of nicotine. (Endocrinology92: 1343, 1973)

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