Feed Restriction in Prepubertal Lambs: Effect on Puberty Onset and on in vivo Release of Luteinizing-Hormone-Releasing Hormone, Neuropeptide Y and Beta-Endorphin from the Posterior-Lateral Median Eminence

Abstract

The exact nature of the interaction between energy balance and reproduction is still elusive. Theoretically, nutrition-related variables must reach the hypothalamic luteinizing-hormone-releasing hormone (LHRH) network and/or its neuronal inputs, to alter plasma luteinizing hormone (LH) and therefore reproductive activity. In an attempt to assess the potential mechanism of such interaction at the median eminence (ME) level, the area of hypophysiotropic LHRH neuronal terminals and release, we used a decreased caloric intake lamb model which delays the onset of puberty. Thus, we determined the in vivo release of neuro-peptides, by push-pull cannula (PPC) sampling from the posterior-lateral ME, in feed-restricted (FR) ewe lambs and in full-fed (FF), age-matched, contemporary control animals. Specifically, we assessed: (1) serum LH and ME in vivo release of LHRH, β-endorphin (β-END) and neuropeptide Y (NPY); β-END and NPY are two putative neuronal inputs to LHRH neuronal terminals at the ME, reported to be involved in the control of both reproduction and feed intake; (2) the effect that exogenous infusion of β-END through the PPC might have on the release of ME LHRH and NPY, and on plasma LH. In contrast to other works, the present results were obtained in lambs with intact ovaries. Furthermore, FR lambs were always compared statistically with FF contemporary paired controls that had attained puberty. Feed restriction decreased ME LHRH release, lowered plasma LH and prevented the onset of puberty. The changes induced by feed restriction in both LHRH and LH release were associated predominantly with decreases in pulse amplitude, rather than alterations in pulse frequency. The decreased LHRH and LH release occurred in the presence of a decreased β-END but unchanged NPY release from the ME. Exogenous infusion of β-END into the posterior-lateral ME decreased both LHRH and NPY release from this site and decreased plasma LH. In conclusion, decreased caloric intake lowers LH release and prevents puberty onset by decreasing the amplitude of the LHRH output from the hypothalamic hypophysiotropic network. A compensatory but unsuccessful mechanism for the FR status might be a lower β-END-inhibitory tone on ME LHRH neuronal terminals. The unchanged release of NPY at this site supports the specificity of the changes induced by feed restriction on LHRH and β-END in vivo release.

Diurnal Variation in Luteinizing Hormone-Releasing Hormone and β-Endorphin Release in Pituitary Portal Plasma during the Rat Estrous Cycle1

“…The increase in 13-EP release was observed each day in the late morning and early afternoon and was followed by an increase in LHRH release. The pulsatile nature of the portal blood LHRH and P-EP levels is consistent with the data obtained from ewe portal blood samples [26-281, from rat and ewe median eminence push-pull perfusates [11,12,24,29], and from in vitro perfusion of rat hypothalamic tissues [30]. The early morning increase in P-EP release prior to the preovulatory LHRH release on the day of proestrus has been previously documented in rats [18].…”

“…Studies using intra-cranial administration of P-EP or the opiate antagonist naloxone into the discrete areas of the hypothalamus and using measurement of the levels of immunoreactive 3-EP and of the 3-EP precursor proopiomelanocortin (POMC) mRNA in the hypothalamus revealed that the opioid peptide regulates LHRH secretion by acting both at the preopticanterior hypothalamus and the median eminence during the rat estrous cycle [8][9][10][11][12]. In accordance with this is the anatomical evidence that the P-EP immunoreactive neurons have direct contact with the LHRH neurons in the hypothalamus and that the opiate receptors are in proximity to LHRH-containing neurons in the hypothalamus [13][14][15][16].…”

Increased Galanin and Neuropeptide-Y Immunoreactivity within the Hypothalamus of Ovariectomised Ewes following a Prolonged Period of Reduced Body Weight Is Associated with Changes in Plasma Growth Hormone but Not Gonadotropin Levels

“…76]. There is also a reduction of GnRH release into the hypophysial portal vessels of the feed-restricted ewe [77], although some studies have not noted significant changes in GnRH release, or only a decrease in GnRH pulse amplitude in underfed ewes [72,73,78]. GnRH biosynthesis at the lev el of the POA also remains unchanged in such animals [53].…”

The effect of intracerebroventricular infusions of ghrelin or short fasting on the gene expression and immunoreactivity of neuropeptide Y in the hypothalamic neurons in prepubertal female lambs: A morphofunctional study

“…Global feed restrictions increase the expression of NPY mRNA in the ARC nucleus of ovariectomised ewe lambs (Mc Shane et al, 1993), but the release of NPY within the median eminence did not change (Prasad et al, 1993). In ovariectomised The role of exogenous ghrelin in the regulation of neuropeptide Y (NPY) neuronal system in the hypothalamus of intact lambs has not been yet determined.…”