- 期刊
Pentagastrin-Induced Gastric Acid Secretion in the Diabetic Rats: Role of Insulin
並列摘要
Streptozotocin-induced diabetic rats have excessively pentagastrin-simulated acid output in which insulin seems to attenuate rather than further stimulate acid output. The aim of this study was to determine the insulin impact on pentagastrin-stimulated acid output of diabetic and non-diabetic rats to resolve whether an attenuated effect does exist. Diabetic rats were induced by the streptozotocin i.v. injection four days before acid study. Some streptozotocin-treated rats additionally received daily insulin (2.4 IU/kg) injection. Using an autotitrator, acid output was measured every five minutes by the titration of gastric perfusate. Basal output was collected for 45 mm before the 90-min pentagastrin infusion (0.89μ/kg/min). Plasma gastric inhibitory polypeptide (GIP) levels were measured. Both doses (0.067and 0.133 IU/kg/min) of insulin infusion resulted in stimulated acid output in normal rats. The subsequent insulin infusion (0.133 IU/kg/min) for non-diabetic rats undergoing pentagastrintreatment suppressed their stimulated acid output almost down to the basal level. Pentagastrmnstimulation led to the excessively increased acid output of diabetic rats throughout the whole infusion period (P＜0.01). Correction of hyperglycemia with insulin for diabetic rats normalized the stimulated acid output. Measured basal and stimulated plasma GIP levels of those diabetic rats during acid stimulation remained higher, regardless of insulin treatment (P＜0.05). Our results suggest that insulin has the ability to attenuate pentagastrin-stimulated acid output in rats, whereas GIP is not involved in this attenuation. This effect appears to be responsible for the excessive acid output of diabetic rats undergoing pentagastrin stimulation.