Surge in the Ewe

To determine if glucose availability modulates the timing of the positive feedback action of oestrogen on gonadotropin secretion, we monitored the estradiol-induced luteinizing hormone (LH) surge in sheep (n=5/group) made transiently hypoglycemic by insulin. Experiment 1 determined an effective insulin treatment, one which would depress tonic LH secretion. Two injections of insulin (5 IU/kg iv) 4 h apart were found to induce extended hypoglycemia (10–13 h) and to decrease the LH pulse frequency for 8 h (5.0±0.32 pulses/4 h before versus 2.5±0.34 pulses/4 h after insulin; P<0.05; mean±SEM). Using this same paradigm, experiment 2 determined the influence of the transient hypoglycemia on the LH surge mechanism. In control sheep, estradiol (subcutaneous implants at hour 0) evoked an LH surge with a latency period of 12.4±0.5 h. When insulin was administered either before (hours −4 and 0) or after the estradiol stimulus (hours 4 and 8, or 12 and 16), the onset of the LH surge was delayed to 29.0±2.4 h (average of all three time groups, P<0.05). Infusion of glucose from hours 12–30, along with insulin, prevented hypoglycemia and restored the normal timing of the oestrogen-induced LH surge to that of controls (15.4±0.93 h, P>0.05). These findings suggest that not only is the tonic mode of LH secretion sensitive t