Inhibitory effect of an intravenous glucose load on basal and insulin-stimulated gastric acid secretion in man.
The effect of intravenous glucose on basal and insulin-stimulated gastric acid secretion was investigated in a crossover study on four healthy subjects. Acid output was measured by means of intragastric titration and a telemetering capsule; serum-gastrin and blood glucose levels were measured in 15-minute-intervals. Two different experiments were carried out on each subject. After one basal hour in series (a), 2 ml saline, and in series (b), 0.2 U/kg b. w. glucagon-free insulin were injected intravenously. Two hours later, in both series 0.66 g/kg b. w. glucose were given by rapid i.v. infusion, and the experiment continued for another hour. Hyperglycemia was found to depress significantly basal as well as insulin-stimulated acid secretion, while serum-gastrin levels showed no systematic variation. On the basis of these findings and of earlier studies in animals, it is concluded that the inhibitory effect of hyperglycemia is due to a central action, i.e., an increased activity of the satiety center.
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005750:Gastric Juice / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D007031:Hypothalamus / Q000502:physiology; D007263:Infusions, Parenteral; D007328:Insulin / Q000494:pharmacology; D008297:Male; D012527:Satiation
D001786:Blood Glucose; D007328:Insulin; D005947:Glucose