title: [Mediation by opioid peptides of anterior pituitary response to insulin-induced hypoglycemia (author's transl)].
abstract: A 1.6 mg dose of the specific opiate antagonist naloxone was administered to normal volunteers, either separately or in conjunction with insulin-induce hypoglycemia, in order to study the possible mediation by opioid peptides of the release of adrenocorticotrophin (ACTH), lipotropins (LPH), human growth hormone (GH) and prolactin (PRL). Administered separately, naloxone was associated with a significant fall in PRL levels (p less than 0.01), a significant and unexpected rise in GH levels (p less than 0.02), and a suppression of the circadian decrease of ACTH and LPH levels. The association of naloxone with insulin-induced hypoglycemia significantly reduced the PRL peak (p less than 0.05), did not affect the rise of GH and lowered the ACTH peak, without altering the LPH peak. These data suggest the existence of a positive opioid tone to PRL secretion, as well as an opioid peptide role in the PRL response to hypoglycemia. They argue against the likelihood of an opioid pathway in the GH response to hypoglycemia. Furthermore, the data favor a paradoxical effect of naloxone on ACTH release during insulin-induced hypoglycemia.
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001786:Blood Glucose / Q000502:physiology*; D004723:Endorphins / Q000502:physiology*; D005260:Female; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D010903:Pituitary Gland, Anterior / Q000378:metabolism*; D010908:Pituitary Hormones, Anterior / Q000378:metabolism*; D011388:Prolactin / Q000097:blood; D008083:beta-Lipotropin / Q000097:blood
chemical_list: D001786:Blood Glucose; D004723:Endorphins; D007328:Insulin; D010908:Pituitary Hormones, Anterior; D009270:Naloxone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D013006:Growth Hormone; D008083:beta-Lipotropin
vernacular_title: Médiation par les peptides opioïdes de la réponse antéhypophysaire à l'hypoglycémie insulinique.