Levin E R, Yamada T, Levin S, Mills S
Metabolism. 1986 Jan;35(1):59-63. doi: 10.1016/0026-0495(86)90096-x.
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.
在犬类动物中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。对胰岛素诱导的低血糖反应时，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可阻止生长抑素反应，但对胰高血糖素分泌增加无影响。纳洛酮既不影响低血糖程度，也不影响诱导的血糖最低点后的恢复。给予盐酸精氨酸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。用纳洛酮预处理未能影响这些反应中的任何一个。我们的结果表明，内源性阿片肽介导低血糖诱导的胰高血糖素分泌后的生长抑素反应。
