Arrest of pulsatile luteinizing hormone (LH) secretion during insulin-induced hypoglycemia (IIH): Improvement by intrahypothalamic perfusion with glucose

Summary

Insulin-induced hypoglycemia (IIH), as with many other acute stressors, restrains the activity of the reproductive axis, reducing luteinizing hormone (LH) release. In adult ovariectomized, steroid-primed rats, we investigated the effect of IIH and of mediobasal intrahypothalamic perfusion with glucose (200 mg/dl) on pulsatile LH secretion. IIH led to a significant decrease in all pulsa-tility parameters studied using PC-Pulsar analysis, e.g. pulse amplitude and frequency, maximum and baseline LH levels (p < 0.05 versus control), and LH overall mean release (p < 0.01 versus control). Intrahypothalamic perfusion with glucose normalized LH pulse frequency, improved maximum and baseline levels, and partially ameliorated LH pulse amplitude and overall mean release. Thus, our results show that the glucoprivic cessation of LH release is restored, at least partially, by an adequate glucose supply to the hypothalamus; it is proposed, in view of these and previous results, that different mechanisms in the CNS may be involved in LH suppression observed during IIH.

Luteinizing hormone - insulin hypoglycemia - push pull perfusion - mediobasal hypothalamus