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Hyperglycaemia reduces gastrin-stimulated gastric acid secretion in humans
W F Lam1, A A Masclee, S Y De Boer
1Leiden University Medical Center, The Netherlands.
Background:
Recent studies have pointed to the role of plasma glucose in the regulation of gastrointestinal function.
Methods:
We have investigated 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 gastrin-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 normoglycaemia and during acute hyperglycaemia at 15 mmol L-1. Acid output was measured by continuous aspiration using phenol red as recovery marker. Plasma PP levels were determined at regular intervals.
Results:
Gastrin infusion at 5 pmol kg-1 h significantly (P < 0.05) increased acid output both during normoglycaemia and during hyperglycaemia. Gastrin infusion at 15 pmol kg-1 h further and significantly (P < 0.05) increased the acid output during both experiments. Hyperglycaemia significantly (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 normoglycaemia. Plasma PP levels were not stimulated by gastrin-17 infusion and were 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 post-prandial levels does not affect plasma PP levels; (c) plasma PP levels are reduced during hyperglycaemia, suggesting vagal-cholinergic inhibition of gastric acid secretion during hyperglycaemia.