The role of intracerebral insulin in the effect of nutrition on gonadotrophin secretion in mature male sheep

Abstract

Abstract The effect of nutrition on gonadotrophin secretion may be exerted through a central metabolic signal that reflects nutritional status. We have previously found that glucose and insulin concentrations are elevated in the cerebrospinal fluid (CSF) of rams in which the secretion of gonadotrophins has been stimulated by a nutritional supplement of lupin grain (Lupinus angustifolius). In the present study, we tested the hypothesis that insulin and/or glucose is a metabolic modulator of GnRH secretion and mediates the effects of nutrition on gonadotrophin secretion. Six mature rams were fed a diet that maintained live weight and then given a series of infusions, each for 12 h/day for 4 days, in a cross-over design. The treatments were: artificial CSF (aCSF), glucose (50 μmol/h) in aCSF, insulin (0·6 ng/h) in aCSF, and glucose (50 μmol/h) plus insulin (0·6 ng/h) in aCSF; all infused at a rate of 5 μl/min. At the same time as the infusion treatments, two other groups of four rams without cerebral cannulae were fed either the maintenance diet or the same diet supplemented with 750 g lupin grain per head per day for 4 days, again in a cross-over design. Rams fed the lupin supplement showed an increase in both LH pulse frequency and mean FSH on day 4 (P<0·05). Infusion of aCSF or glucose did not affect gonadotrophin secretion. Rams infused with insulin or insulin plus glucose showed an increase (P<0·05) in LH pulse frequency but no increase in FSH concentrations on day 4 of infusion. The magnitude of the LH response to insulin was similar to the nutritional response of feeding lupin supplements. There was no effect of any of the infusion treatments on plasma prolactin or insulin secretion. These data show that changes in insulin concentrations in the CSF lead to changes in LH secretion and support the hypothesis that insulin is a metabolic modulator of GnRH secretion and mediates the effects of nutrition on gonadotrophin secretion. Journal of Endocrinology (1995) 147, 321–329