Galanin and Pancreastatin Inhibit Stimulated Insulin Secretion in the Mouse: Comparison of Effects

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Abstract
The effects of the two intrapancreatic peptides galanin and pancreastatin on basal and stimulated insulin and glucagon secretion in the mouse were compared. It was found that at 2 min after intravenous injection of galanin or pancreastatin (4.0 nmol/kg), basal plasma glucagon and glucose levels were slightly elevated. Galanin was more potent than pancreastatin to elevate basal plasma glucagon levels: they increased from 60 ± 15 to 145 ± 19 pg/ml (p < 0.01) after galanin compared to from 35 ± 5 to 55 ± 8 pg/ml (p < 0.05) after pancreastatin. Plasma insulin levels were lowered by galanin (p < 0.05), but not by pancreastatin. CCK-8 (6.3 nmol/kg) or terbutaline (3.6 µmol/kg) markedly increased the plasma insulin levels. Galanin (4.0 nmol/kg) completely abolished the insulin response to CCK-8 (p < 0.001), but pancreastatin (4.0 nmol/kg) was without effect. Galanin inhibited the insulin response to terbutaline by approximately 60% (p < 0.01), but pancreastatin inhibited the insulin response to terbutaline by approximately 35% only (p < 0.05). CCK-8 and terbutaline did both elevate plasma glucagon levels by moderate potencies: neither pancreastatin nor galanin could affect these responses. Thus, in the mouse, galanin and pancreastatin both inhibit basal and stimulated insulin secretion, and stimulate basal glucagon secretion. Galanin is thereby more potent than pancreastatin. The study also showed that galanin potently inhibits insulin secretion stimulated by the octapeptide of cholecystokin and by the β2-adrenoceptor agonist terbutaline, and that pancreastatin inhibits terbutaline-induced insulin secretion.

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