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Elevating Circulating Leptin in Prepubertal Male Rhesus Monkeys (Macaca mulatta) Does Not Elicit Precocious Gonadotropin-Releasing Hormone Release, Assessed Indirectly

Department of Cell Biology & Physiology (M.L.B.-G., A.S., T.M.P.), University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261; and Department of Physical Therapy (C.R.P.), School of Health Sciences, Duquesne University, Pittsburgh, Pennsylvania 15282

Address all correspondence and requests for reprints to: Dr. Tony M. Plant, Department of Cell Biology & Physiology, University of Pittsburgh School of Medicine, S-828A Scaife Hall, Pittsburgh, Pennsylvania 15261. E-mail: plant1{at}pitt.edu.

Abstract

The purpose of this study was to examine the hypothesis that the pubertal reaugmentation of pulsatile GnRH release in male primates is triggered by a rise in circulating leptin concentrations. Agonadal juvenile male rhesus monkeys (n = 7) were implanted with indwelling venous catheters and housed in specialized cages that allow continuous access to the venous circulation. GnRH release was monitored indirectly using LH secretion from the in situ pituitary sensitized to the LH releasing action of GnRH as a bioassay for the hypothalamic peptide. Infusion of recombinant human leptin (5 µg/kg body weight ·h for 16 d resulted in a marked square wave increment in circulating leptin concentration from approximately 2–20 ng/ml but did not elicit precocious GnRH release. GH secretion, however, was stimulated confirming that the heterologous leptin preparation was bioactive in the monkey. Parenthetically, recombinant human leptin was found to be immunogenic in the monkey and circulating antileptin IgG was demonstrable 22–35 d after the initial exposure to the human protein. These findings further support the view that circulating leptin is unlikely to provide the signal that triggers the onset of puberty in male primates.

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