Lack of a direct effect of the autonomic nervous system on glucose-stimulated gastric inhibitory polypeptide (GIP) secretion in man

Abstract

To determine whether the autonomic nervous system has a direct effect on GIP secretion, six normal subjects received a 4-hr intraduodenal perfusion of glucose (225 mg/min) and polyethylene glycol on four successive days. During the latter 2 hr, either normal saline, propranolol, phentolamine, or atropine were infused intravenously. Glucose absorption was calculated by measuring glucose and polyethylene glycol following luminal aspiration distal to the perfusion site. Basal and peak or nadir values in the saline study of plasma glucose, insulin, glucagon, and GIP were similar to the other three studies prior to autonomic blockade. During the latter 2 hr of the glucose perfusion, the plasma glucose and glucagon responses to saline did not differ from responses to the three blocking agents. Phentolamine but not atropine or propranolol resulted in a greater insulin response compared to saline (3247±762 vs 1348±388 μU/ml/120 min,P<0.01). GIP was not significantly affected by phentolamine (18,146±4574), propranolol (7585±5854), or atropine (15,797±6297) compared to saline (11,717±5204 pg/ml/120 min). Glucose absorption was unaffected by infusions of saline, phentolamine, and propranolol, but was increased following atropine infusion (5841±1120 vs 1044±808 mg/120 min,P<0.02). There appears to be no direct effect of the autonomic nervous system on glucose-induced secretion of GIP.