Any steroid that is used in a dose to promote anabolism is going to shut down the HPTA in days.
Acta Endocrinol (Copenh). 1992 Feb;126(2):173-8. Related Articles, Links
The effects of an anabolic steroid (oxandrolone) on reproductive development in the male rat.
Grokett BH, Ahmad N, Warren DW.
Department of Exercise Science, University of Southern California, Los Angeles 90033.
Oxandrolone is a 5 alpha-reduced anabolic steroid that is administered for the treatment of short stature disease in children. It is a commonly used substance beginning as early as prepuberty by some individuals who are seeking to enhance athletic performance or personal appearance. Because of the lack of data on the effects of anabolic steroids on the reproductive system, we have examined the effects of oxandrolone treatment on reproductive development in male rats with treatment beginning two days after weaning. Male, Sprague-Dawley rats (N = 12) received a daily subcutaneous injection of oxandrolone (32.7 mumol.kg-1.day-1) and the control group (N = 12) received vehicle only (dimethyl sulfoxide). Treatment began at age 23 days and continued to 60 days of age. The weights of the testes, prostate glands, and seminal vesicles in the treatment group were 69%, 50% and 29% below control levels, respectively and were all significantly decreased (p less than 0.01). Testicular testosterone production in a 3-h incubation was inhibited in the treated animals to 1.3% of control values (p less than 0.001). Serum FSH (11.7% of control) and LH (undetectable) in the treated animals were both significantly less than controls. Histological findings indicated an arrest of advanced spermatids and a severe depletion of Leydig cells in the interstitial compartment. It was concluded that treatment of immature male rats with oxandrolone results in effects on the adult male reproductive system which are profound and occur at several levels. The most likely affected sites are the hypothalamus, pituitary gland, and the Leydig cells.
Clin Endocrinol (Oxf). 1997 Feb;46(2):209-16. Related Articles, Links
Effect of low dose oxandrolone and testosterone treatment on the pituitary-testicular and GH axes in boys with constitutional delay of growth and puberty.
Crowne EC, Wallace WH, Moore C, Mitchell R, Robertson WH, Holly JM, Shalet SM.
Department of Endocrinology, Christie Hospital Trust, Manchester, UK.
OBJECTIVE: To investigate the effect of low dose oxandrolone and testosterone on the pituitary-testicular and GH-IGF-I axes. DESIGN: Prospective double-blind placebo-controlled trial. PATIENTS: Sixteen boys with constitutional delay of growth and puberty (CDGP) with testicular volumes 4-6 ml were randomized to 3 months treatment: Group 1 (n = 5), daily placebo: Group 2 (n = 5), 2.5 mg oxandrolone daily or Group 3 (n = 6), 50 mg testosterone monthly intramuscular injections with assessment (growth, pubertal development and overnight hormone profiles) at 0, 3, 6 and 12 months. MAIN OUTCOME MEASURES: LH and GH profiles (15-minute samples) were analysed by peak detection (Pulsar), Fourier transformation and autocorrelation. Testosterone levels were measured hourly and insulin, SHBG, IGF-I, and IGFBP-3 levels at 0800 h. Statistical analysis was by multivariate analysis of variance for repeated measures. RESULTS: LH and testosterone parameters increased significantly with time in all 16 (LH AUC, P < 0.001; peak amplitude, P = 0.02; number of peaks, P = 0.02; testosterone AUC, P = 0.02; morning testosterone, P = 0.002). In Group 2, however, LH and testosterone parameters decreased at 3 months followed by a rebound increase at 6 and 12 months. SHBG levels were markedly reduced at 3 months (P = 0.006) and a wider range of dominant GH frequencies was present although GH AUC was not increased until 6 months, with an increase in GH pulse frequency but not amplitude. IGF-I levels were increased at both 3 and 12 months. In Group 3, pituitary-testicular suppression was not apparent, but GH levels increased with an increase in GH amplitude at 3 and 12 months. CONCLUSION: Oxandrolone transiently suppressed the pituitary-testicular axis and altered GH pulsatility. Testosterone increased GH via amplitude modulation.
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