Biomedical subjects
Publications and source records attributed to A Belanger.
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The metabolism in vitro of 4 androgens, namely testosterone, androstenedione, 5 alpha-dihydrotestosterone and 3 alpha-androstanediol has been studied in male and female rat anterior pituitary cells in primary culture. When testosterone was used as precursor, androstenedione, 5 alpha-dihydrotestosterone and 3 alpha-androstanediol were the main metabolites whereas androstendione was mainly converted into testosterone, 5 alpha-androstanedione, 5 alpha-dihydrotestosterone and androsterone. Studies on the metabolism of 5 alpha-dihydrotestosterone and 3 alpha-androstanediol showed that these compounds were easily interconverted and were also significantly metabolized to 5 alpha-androstanedione and androsterone. No aromatized compounds could be detected suggesting that androgen action in the pituitary cell occurs directly via the androgen receptor rather than through prior conversion into estrogens.
Inhibition of plasma prolactin levels by 2-bromo-alpha-ergocryptine (CB-154) caused a 60% decrease and potentiated the inhibitory effects of [D-Ala6,des-Gly-NH2(10)]LHRH ethylamide on testicular LH receptor levels. Animals treated with the LHRH agonist showed reduced plasma and testicular testosterone levels and elevated progesterone concentration. This progesterone rise was further increased in animals having high circulating prolactin levels but was prevented by CB-154. These data demonstrate that: (1) treatment with the LHRH agonist induces a blockage in the steroidogenic pathway at a step between progesterone and testosterone and (2) prolactin levels to an apparent accentuation of this blockage reflected by higher progesterone levels.
Intranasal administration of two doses of potent agonist of luteinizing hormone (LH)-releasing hormone (LHRH), [D-Ser(TBU)6,des-Gly-NH2(10)]LHRH ethylamide (500 micrograms), a 8 A.M. and 5 P.M. on 1 day between day 4 and 9 following the LH peak in six normal women during two consecutive menstrual cycles shortened the luteal phase from 13.6 +/- 0.3 days to 10.9 +/- 0.3 days (mean shortening, 2.7 days; range, 0.5 to 4.5 days) and reduced plasma progesterone levels to 61.3% +/- 9.2% of control. Hormone changes were followed by daily measurements of plasma LH, follicle-stimulating hormone, 17 beta-estradiol, and progesterone during two pretreatment cycles, two treatment cycles, and two post-treatment cycles. No side effect was observed, and apparently normal cycles occurred immediately after treatment. The present data indicate that the intranasal administration of a potent LHRH agonistic analog can induce luteolysis and control time of occurrence of menses in normal women. This finding opens the possibility of a new and physiologic approach to fertility control.
Following previous observations of the potent antifertility effects of acute treatment with LHRH or its agonistic analogs in male and female rats, this study describes the effect of long term (up to 12 weeks) treatment with an LHRH agonist, [D-Ala6, des-Gly-NH210]LHRH ethylamide (LHRH-A), on testicular and ovarian gonadotropin receptor levels and function in the rat. Treatment of adult male rats with 100 ng LHRH-A every third day led to a progressive decrease of testis, seminal vesicle, and prostate weight up to 12 weeks of treatment, while the inhibitory effect (70%) on LH receptor levels was already maximal at 1 week. When adult female rats were injected daily with 5 microgram LHRH-A for 12 weeks, ovarian LH, FSH, and PRL receptor levels were reduced 50--90%, while plasma estradiol and progesterone levels were inhibited 60% (compared with diestrus day 1). The effect of chronic administration of a low dose (5 IU) of hCG in the male rat was transient. By contrast, no sign of resistance developed up to 12 weeks of treatment with the LHRH agonist in either male or female animals.
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