Vierhapper H, Bratusch-Marrain P, Waldhäusl W, Nowotny P, Panzer S
Clin Endocrinol (Oxf). 1983 Jun;18(6):613-9. doi: 10.1111/j.1365-2265.1983.tb00599.x.
The effect of acetyl-salicylic acid (ASA, 3 g/d for three days) on basal and arginine-stimulated concentrations of insulin and growth hormone was studied in seven type II diabetics. From 120 min before until 120 min after the infusion of arginine-hydrochloride (30 g/30 min) blood glucose concentrations were clamped at hyperglycaemic levels both during treatment with ASA (blood glucose: 12.7 +/- 1.2 mmol/l) and during a control experiment without ASA (blood glucose: 12.9 +/- 1.3 mmol/l). Concentrations of serum insulin in the hyperglycaemic state prior to arginine infusion were increased during treatment with ASA, whereas increments of serum insulin induced by i.v. arginine were unaffected. No difference was seen in either basal or stimulated concentrations of growth hormone. Thus, ASA enhances glucose-induced secretion of insulin in type II diabetics but fails to potentiate the glucose-dependent suppression of arginine-stimulated growth hormone release. In contrast to the pancreatic beta-cell the glucose-sensitive regulatory mechanism of growth hormone release appears to be unaffected by the inhibition of endogenous prostaglandin synthesis.
研究了乙酰水杨酸（ASA，3克/天，共三天）对7名II型糖尿病患者基础状态以及精氨酸刺激后的胰岛素和生长激素浓度的影响。在用盐酸精氨酸（30克/30分钟）输注前120分钟至输注后120分钟期间，在使用ASA治疗时（血糖：12.7±1.2毫摩尔/升）以及在不使用ASA的对照实验期间（血糖：12.9±1.3毫摩尔/升），血糖浓度均维持在高血糖水平。在精氨酸输注前的高血糖状态下，使用ASA治疗期间血清胰岛素浓度升高，而静脉注射精氨酸诱导的血清胰岛素增量未受影响。基础状态或刺激状态下的生长激素浓度均未观察到差异。因此，ASA可增强II型糖尿病患者葡萄糖诱导的胰岛素分泌，但未能增强精氨酸刺激的生长激素释放的葡萄糖依赖性抑制作用。与胰腺β细胞不同，生长激素释放的葡萄糖敏感调节机制似乎不受内源性前列腺素合成抑制的影响。
