Effect of ethanol on amylase secretion and cellular calcium homeostasis in pancreatic acini from normal and ethanol-fed rats.
Effect of ethanol on amylase secretion and cellular calcium homeostasis in pancreatic acini from normal and ethanol-fed rats.
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乙醇对正常和乙醇喂养大鼠胰腺腺泡淀粉酶分泌和细胞钙稳态的影响。
DOI：
10.1016/0006-2952(87)90383-2
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发表时间：
1987
影响因子：
5.8
通讯作者：
Rubin,E
中科院分区：
文献类型：
--
作者：
Ponnappa,BC;Hoek,JB;Waring,AJ;Rubin,E
通过研究离体大鼠胰腺腺泡中淀粉酶的释放、Ca2+稳态和膜物理性质的变化，评估乙醇对刺激-分泌耦合的影响。在正常大鼠的腺泡中，体外乙醇（50 mM 及以上）会引起剂量依赖性的淀粉酶释放刺激和胞质游离 Ca2+ 浓度增加。乙醇不影响胆囊收缩素八肽 (CCK8) 刺激的淀粉酶分泌，CCK8 是一种通过增加胞质游离 Ca2+ 水平发挥作用的促分泌剂，但确实增强了血管活性肠肽 (VIP) 诱导的淀粉酶分泌，血管活性肠肽 (VIP) 提高了细胞内 cAMP。乙醇还增加了45Ca2+交换速率。在用自旋探针 12-doxyl 硬脂酸标记的腺泡中，乙醇扰乱了胰腺质膜。相比之下，在长期（6-7周）摄入乙醇的动物的腺泡中，膜对乙醇的这种紊乱作用具有抵抗力。长期喂食乙醇会降低细胞总钙含量和腺泡钙离子载体 (A23187) 释放池（分别为 11% 和 24%），并导致 45Ca2+ 交换率降低 15-30%。长期摄入乙醇也降低了淀粉酶分泌的基础率，但体外乙醇比对照制剂更能刺激淀粉酶分泌。然而，基础淀粉酶分泌和乙醇诱导的淀粉酶分泌的这些差异并不伴随细胞内游离Ca2+的相应变化。数据表明，乙醇会扰乱细胞膜，还会扰乱细胞 Ca2+ 稳态。这些作用可以解释其作为弱 Ca2+ 介导的促分泌剂的作用。然而，长期乙醇喂养引起的细胞膜改变并不能阻止乙醇引起的对细胞钙稳态的干扰。
The effects of ethanol on stimulus-secretion coupling were assessed by studying amylase release, Ca2+-homeostasis, and changes in physical properties of membranes in isolated rat pancreatic acini. In acini from normal rats, ethanol (50 mM and above)in vitrocaused a dose-dependent stimulation of amylase release and an increase in cytosolic free Ca2+concentration. Ethanol did not affect amylase secretion stimulated by cholecystokinin-octapeptide (CCK8), a secretagogue that acts by increasing cytosolic free Ca2+levels, but did potentiate the secretion of amylase induced by vasoactive intestinal peptide (VIP) which raises intracellular cAMP. Ethanol also increased the rate of45Ca2+exchange. In acini labeled with the spin-probe 12-doxyl stearic acid, ethanol disordered the pancreatic plasma membranes. By contrast, in acini from animals that had chronically (6–7 weeks) ingested ethanol, the membranes were resistant to this disordering effect of ethanol. Chronic ethanol feeding lowered the total cellular calcium content and ionophore (A23187)-releasable pools of acinar calcium (11 and 24% respectively), and led to a 15–30% decrease in the rate of45Ca2+exchange. Chronic ethanol ingestion also lowered the basal rate of amylase secretion, but ethanolin vitrostimulated amylase secretion more than in control preparations. However, these differences in basal and ethanol-induced amylase secretion were not accompanied by corresponding changes in intracellular free Ca2+. The data suggest that ethanol perturbs cell membranes and also disturbs cellular Ca2+homeostasis. These effects may explain its actions as a weak Ca2+-mediated secretagogue. However, the membrane alterations induced by chronic ethanol feeding do not prevent the ethanol-induced interference with cellular calcium homeostasis.
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DOI：
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期刊：
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