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Journal of Clinical Endocrinology & Metabolism, Vol 76, 1280-1285, Copyright © 1993 by Endocrine Society


ARTICLES

Hypoglycemia-induced inhibition of luteinizing hormone secretion in the rhesus monkey is not mediated by endogenous opioid peptides

LE Heisler, CM Pallotta, RL Reid and DA Van Vugt
Department of Physiology, Queen's University, Kingston, Ontario, Canada.

A role for endogenous opioid peptides in stress-induced inhibition of LH secretion has been suggested based on the observation in rats, humans, and nonhuman primates that LH inhibition in response to a variety of different stresses could be blocked by the administration of opiate antagonists. In the present study, we have examined in rhesus monkeys whether suppression of LH secretion by insulin-induced hypoglycemia is prevented by administration of the opiate antagonist naloxone. The administration of 1.0 U insulin/kg to chair-restrained ovariectomized monkeys (n = 6) decreased blood glucose levels from 4.98 +/- 0.17 to 2.08 +/- 0.05 mmol/L and increased cortisol levels from 1279 +/- 205 to 2191 +/- 475 nmol/L. LH levels declined to 62% of the levels observed in the pretreatment control period (P < 0.05). Infusion of naloxone (2-mg bolus plus 2 mg/h or 10-mg bolus plus 10 mg/h) did not reverse the effects of insulin-induced hypoglycemia on LH concentrations. The administration of 1.0 U insulin/kg to nonrestrained monkeys produced a similar hypoglycemic state. Blood glucose levels declined from 4.08 +/- 0.11 to 2.45 +/- 0.05 mmol/L, while cortisol concentrations increased from 577 +/- 53 to 1324 +/- 294 mmol/L. However, LH concentrations did not decline in response to hypoglycemia. These data indicate that hypoglycemia-induced inhibition of LH secretion in chair-restrained ovariectomized monkeys is not mediated by endogenous opiates, since naloxone failed to reverse this effect. The observation that hypoglycemia inhibited LH levels only during a period of restraint suggests either an additive or synergistic effect of these two stresses on LH secretion.


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