Possible role of the adrenergic mechanism in gastric inhibitory polypeptide-and glucagon-like peptide-1 (7–36) amide-induced insulin release in the rat

Abstract Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1(7–36) amide (GLP-1) are thought to be the most probable candidates for incretin. However, the precise mechanism of incretin effect is unclear. In the present study, to elucidate the possible role of the autonomic nervous system in incretin effect, the effects of atropine, propranolol, metoprolol, and phentolamine on GIP- or GLP-1-induced insulin release were investigated in the rat. The GIP-induced (2 or 20μg) insulin release was partly inhibited by propranolol pretreatment (0.5 mg/kg subcutaneously [SC]), and GLP-1-induced (2 or 20 μg) insulin release was partly inhibited by propranolol or metoprolol (35 mg/kg SC). These results suggest that a β-adrenergic mechanism may be involved in the incretin effect, probably through a modulating effect on GIP- or GLP-1-induced insulin secretion.