Lam W F, Masclee A A, Muller E S, Lamers C B
Department of Gastroenterology-Hepatology, University Hospital Leiden, The Netherlands.
Am J Physiol. 1997 May;272(5 Pt 1):G1116-21. doi: 10.1152/ajpgi.1997.272.5.G1116.
We have examined the effect of an acute stable hyperglycemia on gastric acid secretion during the gastric phase of digestion. Gastric acid output was measured with a recovery marker (phenol red) under basal conditions and after repeated intragastric instillation of a liquid meal in seven healthy subjects on two separate occasions: during normoglycemia (serum glucose, 15 mM). Premeal gastric acid output was significantly (P < 0.05) reduced during hyperglycemia compared with during normoglycemia (2.6 +/- 1.0 vs. 5.8 +/- 1.8 mmol/h). Intragastric meal-stimulated incremental acid output during hyperglycemia was significantly (P < 0.05) reduced compared with during normoglycemia (19 +/- 4 vs. 38 +/- 9 mmol/120 min). Meal-stimulated gastrin release during hyperglycemia was significantly (P < 0.05) reduced compared with that during normoglycemia (4.9 +/- 1.3 vs. 6.6 +/- 1.6 micrograms.1(-1).120 min-1). The intragastric meal induced significant (P < 0.05) increases in pancreatic polypeptide concentrations only during normoglycemia. During hyperglycemia, recovery rates of gastric contents were significantly (P < 0.05) increased compared with during normoglycemia, both before (81 +/- 4 vs. 71 +/- 6%) and after (72 +/- 4 vs. 57 +/- 4%) meal ingestion, pointing to delayed gastric emptying of liquids during hyperglycemia. In conclusion, 1) gastric acid secretion under unstimulated conditions and during the gastric phase of digestion is reduced during hyperglycemia; 2) meal-stimulated gastrin release is significantly reduced during hyperglycemia; 3) the reduction in meal-stimulated acid output is correlated with the reduction in gastrin releases; and 4) pancreatic polypeptide secretion is significantly reduced during hyperglycemia, pointing to impaired vagal cholinergic tone.
我们研究了急性稳定高血糖对消化期胃相胃酸分泌的影响。在基础条件下以及在7名健康受试者两次分别重复胃内滴注流食后，用恢复标志物（酚红）测量胃酸分泌量：一次处于血糖正常状态（血清葡萄糖，15 mM），另一次处于高血糖状态（血清葡萄糖，30 mM）。与血糖正常期间相比，高血糖期间餐前胃酸分泌量显著降低（P < 0.05）（2.6±1.0 vs. 5.8±1.8 mmol/h）。与血糖正常期间相比，高血糖期间胃内餐食刺激后的胃酸分泌增量显著降低（P < 0.05）（19±4 vs. 38±9 mmol/120分钟）。与血糖正常期间相比，高血糖期间餐食刺激的胃泌素释放显著降低（P < 0.05）（4.9±1.3 vs. 6.6±1.6 μg·1⁻¹·120分钟⁻¹）。仅在血糖正常期间，胃内餐食导致胰多肽浓度显著升高（P < 0.05）。与血糖正常期间相比，高血糖期间胃内容物的恢复率在餐前（81±4 vs. 71±6%）和餐后（72±4 vs. 57±4%）均显著升高（P < 0.05），表明高血糖期间液体胃排空延迟。总之，1）高血糖期间未刺激条件下及消化期胃相的胃酸分泌减少；2）高血糖期间餐食刺激的胃泌素释放显著减少；3）餐食刺激的胃酸分泌减少与胃泌素释放减少相关；4）高血糖期间胰多肽分泌显著减少，表明迷走胆碱能张力受损。
