Endogenous opioid modulation of pancreatic hormone secretion: studies in dogs.
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.
Levin
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Yamada
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Levin
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Mills
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D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001786:Blood Glucose / Q000378:metabolism; D004285:Dogs; D004723:Endorphins / Q000502:physiology*; D005260:Female; D005934:Glucagon / Q000378:metabolism; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D010187:Pancreatic Hormones / Q000378:metabolism*; D013004:Somatostatin / Q000378:metabolism
D001786:Blood Glucose; D004723:Endorphins; D007328:Insulin; D010187:Pancreatic Hormones; D009270:Naloxone; D013004:Somatostatin; D005934:Glucagon; D001120:Arginine