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

Abstract

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.