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      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

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          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.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1993
          1993
          08 April 2008
          : 57
          : 6
          : 1171-1181
          Affiliations
          Departments of Animal Sciences and Physiology, Rutgers University, New Brunswick, N.J.; Department of VCAAP, Washington State University, Pullman, Wash., USA
          Article
          126484 Neuroendocrinology 1993;57:1171–1181
          10.1159/000126484
          8232771
          © 1992 S. Karger AG, Basel

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          Page count
          Pages: 11
          Categories
          Original Paper

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