Testicular function in uremic rats: In vivo assessment of testosterone biogenesis
The Journal of Steroid Biochemistry and Molecular Biology(1991)
Abstract
The mechanism of testosterone (T) production defect in uremic rats has not yet been clearly defined and hypothalamo-hypophyseal impairment as well as primary testicular dysfunction have been suggested. In 42 rats followed monthly after subtotal nephrectomy up to 7.1 ± 0.3 months, we observed a progressive significant decline of T and androstenedione (A) compared to control rats. Two months before the terminal phase of chronic renal failure (CRF), T/A ratio abruptly declined. T and its precursors on the 4-ene pathway, A, progesterone (P) and 17-hydroxyprogesterone were evaluated in pampiniform plexus testicular vein (PPTV) and in peripheral blood (PV) in end stage uremic rats (blood urea > 30 mmol/1, creatinine clearance < 0.5 ml/min). Under basal conditions, all steroids but peripheral P were significantly lower in uremic rats than in controls as well as T/P and A/P ratios. After human chorionic gonadotropin (hCG) stimulation, T concentration in PV and PPTV remained highly significantly lower than in controls whereas T precursor concentrations were partially corrected by hCG administration. T/P ratio remained lower than in controls whereas A/P ratio was not significantly lower than in controls. Those data show a decline in all the steps of T biogenesis in uremic rats in basal conditions. The defect in 17β-hydroxysteroid dehydrogenase evidenced by T/A decrease at the end stage of CRF seems of primary testicular origin as it is not corrected by hCG administration as shown by T/P and A/P ratios in PPTV and in PV.
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Key words
Androstenedione,progesterone,17-hydroxyprogesterone,testosterone
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