Endogenous opioid modulation of pancreatic hormone secretion: studies in dogs.
Endogenous opioid modulation of pancreatic hormone secretion: studies in dogs.
复制标题
胰腺激素分泌的内源性阿片类药物调节：对狗的研究。
DOI：
10.1016/0026-0495(86)90096-x
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Mills,S
中科院分区：
文献类型：
--
作者：
Levin,ER;Yamada,T;Levin,S;Mills,S
本文研究了内源性阿片肽在调节内分泌胰腺激素分泌中的作用。在胰岛素诱导的低血糖反应中，血浆胰高血糖素分泌显著增加，随后血浆生长抑素免疫反应性增加。用阿片拮抗剂纳洛酮预处理，阻止生长抑素反应，但对胰高血糖素分泌增加没有影响。纳洛酮既不影响低血糖的程度，也不影响从诱导的葡萄糖最低点的恢复。精氨酸盐酸盐给药导致免疫反应性胰高血糖素和胰岛素分泌迅速增加，以及血清葡萄糖升高。纳洛酮预处理未能影响任何这些反应。我们的研究结果表明，内源性阿片肽介导的生长抑素反应后，低血糖诱导胰高血糖素分泌。
The role of endogenous opioid peptides in the modulation of secretion of hormones from the endocrine pancreas was studied in dogs. In response to insulin-induced hypoglycemia, plasma glucagon secretion significantly increased, followed by an increase in plasma somatostatin immunoreactivity. Pretreatment with the opiate antagonist, naloxone, prevented the somatostatin response but had no effect on the augmented glucagon secretion. Neither the degree of hypoglycemia nor recovery from the induced glucose nadir were affected by naloxone. Arginine Hcl administration resulted in prompt increases in immunoreactive glucagon and insulin secretion, as well as a rise in serum glucose. Pretreatment with naloxone failed to affect any of these responses. Our results suggest that endogenous opioid peptides mediate the somatostatin response following hypoglycemia-induced glucagon secretion.