HYPERGLYCEMIA REDUCES GASTRIN-STIMULATED GASTRIC-ACID SECRETION IN HUMANS

Background Recent studies have pointed to the role of plasma glucose i n the regulation of gastrointestinal function. Methods We have investi gated the effect of acute hyperglycaemia on gastric acid secretion and pancreatic polypeptide (PP) release. Gastric acid output was measured under basal conditions and in response to intravenous infusion of gas trin-17 in two doses: 5 pmol kg(-1) h for 60 min and 15 pmol kg(-1) h for another 60 min. Seven healthy subjects were studied during normogl ycaemia and during acute hyperglycaemia at 15 mmol L-1. Acid output wa s measured by continuous aspiration using phenol red as recovery marke r. Plasma PP levels were determined at regular intervals. Results Gast rin infusion at 5 pmol kg(-1) h significantly (P < 0.05) increased aci d output both. during normoglycaemia and during hyperglycaemia. Gastri n infusion at 15 pmol kg(-1) h further and significantly (P<0.05) incr eased the acid output during both experiments. Hyperglycaemia signific antly (P<0.05) reduced basal acid output (2.5 +/- 0.9 vs. 6.3 +/- 1.9 mmol h(-1)), low-dose gastrin stimulated acid output (6.5 +/- 1.7 vs. 13.0 +/- 1.8 mmol h(-1)) and high-dose gastrin stimulated acid output (11.7 +/- 3.0 vs. 19.4 +/- 3.0 mmol h(-1)) compared with normoglycaemi a. Plasma FP levels were not stimulated by gastrin-17 infusion and wer e significantly (P < 0.05) reduced during hyperglycaemia. Conclusions (a) Basal and gastrin-17-stimulated gastric acid secretion are reduced during hyperglycaemia; (b) infusion of gastrin-17 to physiological po st-prandial levels does not affect plasma PP levels; (c) plasma PP lev els are reduced during hyperglycaemia, suggesting vagal-cholinergic in hibition of gastric acid secretion during hyperglycaemia.