Singh J, Yago M D, Adeghate E
Department of Biological Sciences, University of Central Lancashire, Preston, UK.
Arch Physiol Biochem. 2001 Jul;109(3):252-9. doi: 10.1076/apab.109.3.252.11585.
This study investigates the effects of the islet hormones insulin (Ins), glucagon (Glu), and somatostatin (Som) with nerve stimulation (EFS) acetylcholine (ACh) and cholecytokinin-octapeptide (CCK-8) on amylase secretion and intracellular free calcium concentration Ca(2+) in the pancreas of age-matched control and diabetic rats. Either Ins, Glu or Som elicited small increases in amylase secretion from the pancreas of age-matched control animals compared to a much larger increase in amylase secretion with either EFS, ACh or CCK-8. Combining the islet hormones with either EFS, ACh or CCK-8 resulted in marked potentiation of amylase output. In the diabetic pancreas, the islet hormones had no effect on amylase secretion compared to diabetic control. Moreover, either EFS, ACh or CCK-8 evoked a much smaller increase in amylase output compared to age-matched control. In addition, the islet hormones failed to potentiate the secretory effects of either EFS, ACh or CCK-8. In fura-2 loaded acinar cells from age-matched control pancreas either Ins or Glu elicited a small increase in Ca(2+) whereas Som had no effect. Both ACh and CCK-8 evoked large increases in Ca(2+) compared to control. Combining either Ins, Glu or Som with either ACh or CCK-8 resulted in a marked elevation in Ca(2+) compared to the responses obtained with either the islet hormones, ACh or CCK-8 alone. In diabetic fura-2 loaded pancreatic acinar cells, the islet hormones had no effect on Ca(2+) compared to control and moreover, the responses were much smaller than those obtained in acinar cells from age-matched control. Both ACh and CCK-8 induced large increases in Ca(2+) in diabetic acinar cells. However, combining the islet hormones with either ACh or CCK-8 failed to enhance Ca(2+) compared to the reponses obtained in acinar cells from age-matched control. The results suggests that Ca(2+) homeostasis is deranged during diabetes mellitus and this in turn is probably associated with reduced pancreatic amylase secretion.
本研究调查了胰岛激素胰岛素（Ins）、胰高血糖素（Glu）和生长抑素（Som）与神经刺激（EFS）、乙酰胆碱（ACh）和八肽胆囊收缩素（CCK-8）对年龄匹配的对照大鼠和糖尿病大鼠胰腺淀粉酶分泌及细胞内游离钙浓度Ca(2+)的影响。与EFS、ACh或CCK-8引起的淀粉酶分泌大幅增加相比，Ins、Glu或Som引起年龄匹配的对照动物胰腺淀粉酶分泌小幅增加。将胰岛激素与EFS、ACh或CCK-8联合使用导致淀粉酶分泌显著增强。在糖尿病胰腺中，与糖尿病对照组相比，胰岛激素对淀粉酶分泌无影响。此外，与年龄匹配的对照相比，EFS、ACh或CCK-8引起的淀粉酶分泌增加要小得多。此外，胰岛激素未能增强EFS、ACh或CCK-8的分泌作用。在来自年龄匹配的对照胰腺的fura-2负载腺泡细胞中，Ins或Glu引起Ca(2+)小幅增加，而Som无作用。与对照相比，ACh和CCK-8均引起Ca(2+)大幅增加。将Ins、Glu或Som与ACh或CCK-8联合使用导致Ca(2+)显著升高，与单独使用胰岛激素、ACh或CCK-8所获得的反应相比。在糖尿病fura-2负载的胰腺腺泡细胞中，与对照相比，胰岛激素对Ca(2+)无影响，而且，反应比年龄匹配的对照腺泡细胞中获得的反应小得多。ACh和CCK-8均在糖尿病腺泡细胞中诱导Ca(2+)大幅增加。然而，与年龄匹配的对照腺泡细胞中获得的反应相比，将胰岛激素与ACh或CCK-8联合使用未能增强Ca(2+)。结果表明，糖尿病期间Ca(2+)稳态紊乱，这反过来可能与胰腺淀粉酶分泌减少有关。
