Abstract

Sulfated CCK-8 but not non-sulfated CCK-8 induced a dose-dependent increase in plasma insulin levels in fed mice. In fasted mice, however, the CCK peptides caused a non-significant to minimal elevation of plasma insulin. Refeeding fasted mice for 1 h prior to CCK-8-S administration was sufficient to cause a significant elevation of plasma insulin levels. The peripheral CCK antagonist, L-364,718, prevented the CCK-8-S-induced elevation of plasma insulin observed in fed mice. In conclusion, CCK produces a nutrition-dependent increase in plasma insulin levels in vivo via an action upon peripheral CCK receptors.

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