Nutritional modulation of reproductive hormone secretion in adult male rhesus monkeys

One day of fasting suppresses pulsatile luteinizing hormone (LH) secretion in adult male rhesus monkeys. Conversely, refeeding following fasting leads to a rapid stimulation of LH secretion. The present experiments examined a possible pathway mediating these nutritional effects on the reproductive axis. Studies were conducted using male rhesus monkeys with chronically indwelling venous catheters. It was hypothesized that blood glucose levels are detected by the hepatic vagus nerves which then generate afferent signals to the caudal medulla where they activate hypothalamically-projecting catecholaminergic neurons. However, in fasted monkeys, meals which did not lead to a rise in blood glucose levels stimulated LH secretion as well as meals that did. The role of the hepatic vagus nerves in the nutritional regulation of LH secretion was examined in monkeys with unilateral left cervical vagotomy, used to remove hepatic vagal afferents. Unilateral vagotomy had no effect on the fasting-induced suppression of LH secretion or the feeding-induced stimulation of LH secretion, suggesting that hepatic vagal afferents do not provide a nutritional signal which modulates LH secretion. Similarly, bilateral cervical vagotomy did not prevent the fasting-induced suppression of LH secretion. The role of both vagus nerves in the feeding-induced stimulation of LH secretion could not be assessed because bilateral vagotomy led to marked metabolic disruption in response to feeding. Feeding activated catecholaminergic neurons in the caudal medulla (determined by the immunocytochemical detection of Fos) in areas known to project to the hypothalamus. The involvement of these neurons in LH secretion was assessed by pharmacological blockade of adrenergic receptors. Systemic injection of phentolamine prevented the feeding-induced stimulation of LH secretion; however, phentolamine also inhibited LH secretion when administered at a time removed from feeding. Thus, the role of adrenergic projections in LH secretion may not be specific to feeding. Overall, the results of these studies do not support a role for blood glucose or hepatic vagal afferents in the nutritional modulation of LH secretion. However, the possibility remains that activation of a small population of catecholaminergic neurons in the caudal medulla might play a role in altering LH secretion in response to changes in food intake.