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PubMed1983

[The central nervous system-endocrine pancreas axis].

Some results suggesting the existence of gluco- and/or insulin-sensitive sites within the central nervous system (CNS) are recalled. In summary, it seems that when these sites are activated by the presence of glucose or insulin, there is an activation of the parasympathetic nervous system which is responsible for an increased peripheral insulin secretion and/or an hypoglycemia. This could possibly favour glucose disposal. Inversely, when the CNS lacks energy substrates, a cascade of events occurs which tend to increase peripheral glycemia. Bilateral lesions of the ventromedial hypothalamus (VMH) bring about a very early occurring hypersecretion of insulin which can be rapidly and completely abolished by vagotomy. It has also been shown that genetically pre-obese rats (fa/fa) do hypersecrete insulin in response to an i.v. glucose load. This suggests that hypersecretion of insulin of these animals could play a causative role in the development of their obesity. Moreover, this hypersecretion of insulin observed in genetic pre-obesity is abolished by acute atropine administration indicating the involvement of the parasympathetic nervous system in the development of their hyperinsulinemia and subsequent obesity. Cephalic phase insulin secretion seems to "optimalize" insulin secretion that occurs following a meal, as it appears to permit adequate glucose utilization and therefore glucose tolerance. Indeed, animals which are lacking cephalic phase insulin secretion do hypersecrete insulin while remaining hyperglycemic for a longer period of time when compared to animals which have a cephalic phase insulin secretion. Hypothalamic factors present in the ventromedial or the ventrolateral hypothalamus have been shown to have insulin secretion promoting activity when administered in vivo or in vitro to donor rats. It remains to be shown whether such factors are indeed released into the blood (humoral factors) or whether they are neuromodulators and/or neurotransmitters.

Afferent Pathways↗
PubMed1985

The effects of dermorphin on the endocrine system in man.

This paper summarizes the results of our recent studies in a group of healthy subjects on the endocrine effects of the new potent opioid peptide, dermorphin (H-Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2), originally isolated from amphibian skin. Intravenous infusion (5.5 microgram/kg/min for 30 min) of dermorphin (D) significantly increased plasma levels of prolactin (PRL), growth hormone (GH), thyrotropin (TSH) and renin activity (PRA), but decreased plasma levels of cortisol. D produced a small decrease in ACTH, and a small increase in plasma aldosterone. Pretreatment with the opioid receptor antagonist naloxone (N) suppressed the PRL and TSH response to D, blunted the D-induced GH and PRA increase, and completely prevented the D-induced plasma cortisol decrease, but enhanced plasma cortisol and ACTH levels. These data indicate that the action of D is mediated through opioid receptors, and are consistent with the conclusion that: (1) D, a new opioid peptide, can stimulate PRL, GH and TSH release in humans; (2) D increases PRA levels, perhaps via activation of the sympathetic nervous system, providing evidence that opioid peptides may exert an influence on renin secretion; (3) D suppresses plasma cortisol levels, by affecting ACTH secretion, corroborating previous observations that opioid peptides might affect the function of the pituitary-adrenocortical axis.

Adrenocorticotropic Hormone↗