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Testis; |
Department of Cell Biology and Physiology,3 Center for Research in Reproductive Physiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261
Department of Physical Therapy,4 School of Health Sciences, Duquesne University, Pittsburgh, Pennsylvania 15282
ABSTRACT
Testosterone shows circadian rhythms in monkeys with low serum levels in the morning hours. The decline relies on a diminished frequency of LH pulses. Inhibin B shows no diurnal patterns. In elderly men, the diurnal rhythm of testosterone is blunted and inhibin levels fall. Here we explore whether aging exerts similar effects in the rhesus monkey. We collected blood samples from groups of young (6–9 yr) and old (12–16 yr) male rhesus monkeys at 20-min intervals for a period of 24 h under remote sampling via a venous catheter. We determined moment-to-moment changes in plasma levels of testosterone, FSH, and LH by RIA, and of inhibin B by ELISA. We found significant diurnal patterns of testosterone in both groups. The circadian rhythm in testosterone was enhanced in older monkeys. Testosterone levels and pulse frequencies dropped significantly below those of young monkeys during midday hours. Diminished pulse frequency of LH appeared to be responsible for the midday testosterone decrease in old monkeys, while LH and testosterone pulse frequency did not change in young monkeys at corresponding time points. Old monkeys showed extended periods of LH-pulse quiescence in the morning and midday hours. Inhibin B and FSH levels were generally lower in old monkeys compared with the young group, but neither inhibin B nor FSH showed circadian rhythms. We conclude from these data that old rhesus monkeys have a more prominent circadian rhythm of LH and testosterone resulting from an extended midday period of quiescence in the hypothalamus-pituitary-gonadal axis.
aging, androgen, circadian rhythm, gonadotropins, inhibin, luteinizing hormone, monkey, testis, testosterone
1Supported by grant 1R21 AG024914 and startup funds from the University of Pittsburgh School of Medicine and by NICHD/NIH through cooperative agreement U54 08160 as part of the Specialized Cooperative Centers Program in Reproduction and Infertility Research.
Correspondence: 2Stefan Schlatt, Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, B301 Magee Womans Research Institute, 204 Craft Avenue, Pittsburgh, PA 15213. FAX: 412 641 7676; e-mail: schlatt{at}pitt.edu
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