scholarly journals The effects of testosterone and testosterone propionate on adult male rats (compared with those on female rats)

1937 ◽  
Vol 31 (8) ◽  
pp. 1434-1437 ◽  
Author(s):  
Vladimir Korenchevsky ◽  
Marjorie Dennison ◽  
Kathleen Hall
Keyword(s):  
Adult Male ◽  
Testosterone Propionate ◽  
Female Rats ◽  
Male Rats

scholarly journals Altered sexual differentiation of hepatic uridine diphosphate glucuronyltransferase by neonatal hormone treatment in rats

1979 ◽  
Vol 180 (2) ◽  
pp. 313-318 ◽  
Author(s):  
Coral A. Lamartiniere ◽  
Cindy S. Dieringer ◽  
Etsuko Kita ◽  
George W. Lucier
Keyword(s):  
Enzyme Activity ◽  
Adult Male ◽  
Sexual Differentiation ◽  
Reproductive Tract ◽  
Testosterone Propionate ◽  
Hormone Treatment ◽  
Male Rats ◽  
Ventral Prostate ◽  
Uridine Diphosphate ◽  
Neonatal Administration

The hepatic microsomal enzyme UDP-glucuronyltransferase undergoes a complex developmental pattern in which enzyme activity is first detectable on the 18th day of gestation in rats. Prepubertal activities are similar for males and females. However, postpubertal sexual differentiation of enzyme activity occurs in which male activities are twice those of females. Neonatal administration of testosterone propionate or diethylstilboestrol to intact animals resulted in lowered UDP-glucuronyltransferase activity in liver microsomal fractions of adult male rats, whereas no changes were observed in the adult females and prepubertal male and female animals. Neonatal administration of testosterone propionate and diethylstilboestrol adversely affected male reproductive-tract development as evidenced by decreased weights of testes, seminal vesicles and ventral prostate. Diethylstilboestrol also markedly decreased spermatogenesis. Hypophysectomy of adult male rats resulted in negative modulation of microsomal UDP-glucuronyltransferase and prevented the sexual differentiation of enzyme activity. In contrast hypophysectomy had no effect on female UDP-glucuronyltransferase activity. A pituitary transplant under the kidney capsule was not capable of reversing the enzyme effects of hypophysectomy, therefore suggesting that the male pituitary factor(s) responsible for positive modulation of UDP-glucuronyltransferase might be under hypothalamic control in the form of a releasing factor. Neonatal testosterone propionate and diethylstilboestrol administration apparently interfered with the normal sequence of postpubertal UDP-glucuronyltransferase sexual differentiation.

Insulin sensitivity, leptin, adiponectin, resistin, and testosterone in adult male and female rats after maternal-neonatal separation and environmental stress

2018 ◽  
Vol 314 (1) ◽  
pp. R12-R21 ◽  
Author(s):  
Hershel Raff ◽  
Brian Hoeynck ◽  
Mack Jablonski ◽  
Cole Leonovicz ◽  
Jonathan M. Phillips ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adult Male ◽  
Rat Model ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Neonatal Hypoxia ◽  
Male And Female Rats ◽  
Plasma Leptin ◽  
Neonatal Separation

Care of premature infants often requires parental and caregiver separation, particularly during hypoxic and hypothermic episodes. We have established a neonatal rat model of human prematurity involving maternal-neonatal separation and hypoxia with spontaneous hypothermia prevented by external heat. Adults previously exposed to these neonatal stressors show a sex difference in the insulin and glucose response to arginine stimulation suggesting a state of insulin resistance. The current study used this cohort of adult rats to evaluate insulin resistance [homeostatic model assessment of insulin resistance (HOMA-IR)], plasma adipokines (reflecting insulin resistance states), and testosterone. The major findings were that daily maternal-neonatal separation led to an increase in body weight and HOMA-IR in adult male and female rats and increased plasma leptin in adult male rats only; neither prior neonatal hypoxia (without or with body temperature control) nor neonatal hypothermia altered subsequent adult HOMA-IR or plasma adiponectin. Adult male-female differences in plasma leptin were lost with prior exposure to neonatal hypoxia or hypothermia; male-female differences in resistin were lost in the adults that were exposed to hypoxia and spontaneous hypothermia as neonates. Exposure of neonates to daily hypoxia without spontaneous hypothermia led to a decrease in plasma testosterone in adult male rats. We conclude that neonatal stressors result in subsequent adult sex-dependent increases in insulin resistance and adipokines and that our rat model of prematurity with hypoxia without hypothermia alters adult testosterone dynamics.

scholarly journals Different mechanisms of regulation of nuclear reduced nicotinamide–adenine dinucleotide phosphate-dependent 3-oxo steroid 5α-reductase activity in rat liver, kidney and prostate

1974 ◽  
Vol 142 (2) ◽  
pp. 273-277 ◽  
Author(s):  
Jan-Åke Gustafsson ◽  
Åke Pousette
Keyword(s):  
Testosterone Propionate ◽  
Reductase Activity ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Female Rats ◽  
Male Rats ◽  
Regulatory Mechanisms ◽  
Oestradiol Benzoate ◽  
Liver And Kidney ◽  
Reduced Nicotinamide Adenine Dinucleotide ◽  
Hydroxy Steroid

The regulatory mechanisms involved in the control of the nuclear NADPH-dependent 3-ketosteroid 5α-reductase (5α-reductase) activity were studied in liver, kidney and prostate. The substrate used was [1,2-3H]androst-4-ene-3,17-dione (androstenedione) (for liver and kidney) or [4-14C]androstenedione (for prostate). The hepatic nuclear 5α-reductase activity was greater in female than in male rats, was greater in adult than in prepubertal female rats, increased after castration of male rats, but was not affected by treatment with testosterone propionate or oestradiol benzoate. These regulatory characteristics are in part different from those previously described for the hepatic microsomal 5α-reductase. The renal nuclear metabolism of androstenedione, i.e. 5α reduction and 17β-hydroxy steroid reduction, was relatively unaffected by sex, age, castration and treatment with testosterone propionate. However, treatment of castrated male rats with oestradiol benzoate led to a significant increase in the 5α-reductase activity and a significant decrease in the 17β-hydroxy steroid reductase activity. Finally, the nuclear 5α-reductase activity in prostate was androgen-dependent, decreasing after castration and increasing after treatment with testosterone propionate. In conclusion, the nuclear 5α-reductase activities in liver, kidney and prostate seem to be under the control of distinctly different regulatory mechanisms. The hypothesis is presented that whereas the prostatic nuclear 5α-reductase participates in the formation of a physiologically active androgen, 5α-dihydrotestosterone, this may not be the true function of the nuclear 5α-reductase in liver and kidney. These enzymes might rather serve to protect the androgen target sites in the chromatin from active androgens (e.g. testosterone) by transforming them into less active androgens (e.g. 5α-androstane-3,17-dione and/or 5α-dihydrotestosterone).

EFFECTS OF TESTOSTERONE MEDIATED OR MODULATED BY PITUITARY FACTORS

1975 ◽  
Vol 67 (1) ◽  
pp. 71-79 ◽  
Author(s):  
P. DE MOOR ◽  
M. ADAM-HEYLEN ◽  
H. VAN BAELEN ◽  
G. VERHOEVEN
Keyword(s):  
Body Weight ◽  
Testosterone Propionate ◽  
Total Body Weight ◽  
Seminal Vesicles ◽  
Female Rats ◽  
Male Rats ◽  
Intact Male ◽  
Adult Rats ◽  
Organ Weights ◽  
Total Body

SUMMARY Adult rats of both sexes were either gonadectomized or hypophysectomized and gonadectomized. Three to eight weeks later they were treated for 14 consecutive days with oil or with 75 or 200 μg testosterone propionate (TP) per 100 g body weight. The animals were killed and for each sex the gonadectomized animals were compared with the hypophysectomized-gonadectomized animals as far as their NADPH- and NADH-dependent 3α-hydroxysteroid dehydrogenases (3α-HSD) in renal microsomes, transcortin levels in serum and five organ weights relative to total body weight were concerned. For two of the latter, i.e. the relative kidney and prostatic weights, no significant differences were found. Transcortin levels, relative adrenal weights and renal NADPH-dependent 3α-HSD activities were higher in oil-treated gonadectomized animals than in oil-treated hypophysectomized-gonadectomized animals. The opposite was found for the relative weights of uterus and seminal vesicles and renal NADH-dependent 3α-HSD activities. These differences between gonadectomized and hypophysectomized-gonadectomized animals disappeared after TP treatment as far as transcortin levels were concerned but remained for the five other parameters. After gonadectomy sexual differences subsisted for all parameters studied. But whereas intact male rats had higher NADH-dependent 3α-HSD activities than female rats the opposite was found after gonadectomy. After gonadectomy plus hypophysectomy the between sex differences disappeared as far as transcortin levels were concerned but remained in the other parameters studied.

INFLUENCE OF SEX HORMONES ON AMIDINOTRANSFERASE LEVELS. METABOLIC CONTROL OF CREATINE BIOSYNTHESIS

1966 ◽  
Vol 53 (4) ◽  
pp. 655-662 ◽  
Author(s):  
István Kriskó ◽  
James B. Walker
Keyword(s):  
Testosterone Propionate ◽  
De Novo ◽  
Specific Activity ◽  
Hormonal Control ◽  
Mature Male ◽  
Female Rats ◽  
Male Rats ◽  
Enzyme Protein ◽  
Wet Weight ◽  
Mammalian Enzyme

ABSTRACT Arginine: glycine amidinotransferase is the first of two enzymes involved in creatine biosynthesis. The amidinotransferase specific activity (micromoles of hydroxyguanidine formed per hour per g wet weight of tissue) of kidney homogenates of mature male rats was about twice that of females of the same age, whereas activities were equal before puberty. Castration decreased the activity of males and increased that of females. The administration of testosterone propionate to young adult female rats resulted in a significant increase in enzyme activity. The same enzyme had previously been shown to be repressible by its end-product, creatine. Although there are numerous enzymes whose synthesis is known to be under hormonal control, amidinotransferase is the only mammalian enzyme described up to now on which there appears to operate both an end-product repression mechanism and a hormonal control on the de novo synthesis of the enzyme protein.

PROLACTIN STIMULATION TEST WITH PERPHENAZINE: AN EVALUATION OF PLASMA PROLACTIN LEVELS AND PITUITARY SECRETORY ACTIVITY IN THE RAT

1976 ◽  
Vol 68 (3) ◽  
pp. 355-368 ◽  
Author(s):  
A. A. VAN DER GUGTEN ◽  
P. C. SAHULEKA ◽  
G. H. VAN GALEN ◽  
H. G. KWA
Keyword(s):  
Adult Male ◽  
Secretory Activity ◽  
Female Rats ◽  
Male Rats ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Oestrogen Treatment ◽  
Endocrine Status ◽  
Pituitary Prolactin ◽  
Single Plasma

SUMMARY Many investigations of the regulation of prolactin synthesis and release are based on single plasma prolactin determinations. The purpose of the present experiment was to ascertain whether groups of rats (i.e. young or adult, male or female animals, being either intact, gonadectomized or gonadectomized and treated with oestrone), differing in age and/or endocrine status, will react to a single dose of perphenazine by an acute release of pituitary prolactin in proportion to their initial plasma prolactin levels. No consistent relation existed between the classification of the twelve groups of rats into three categories of basal plasma prolactin levels (i.e. < 20, 25–50, > 125 ng/ml) and their response to perphenazine. Even though all groups showed a highly significant increase of plasma prolactin levels the magnitude of the maximum prolactin response at 30 min varied greatly within the groups of one category and thus was not related to the initial prolactin levels. The effect of 14 days of oestrone treatment in increasing plasma prolactin levels in gonadectomized animals was greatest in young and adult male rats, less in young females and not significant in adult females. The results obtained after perphenazine treatment in the latter group made it clear that the effect of oestrogen treatment on prolactin release can be completely blocked by increasing synthesis and/or release of the prolactin-release inhibiting factor (PIF). Since perphenazine induces decrease of pituitary prolactin and a concomitant increase of plasma prolactin levels through lowered PIF-action, the positive effect of oestrogens on prolactin release (as observed in gonadectomized male and young female rats) apparently is caused by a different mode of action. The implications of these findings for the regulation of prolactin release, as affected by the endocrine status of the rat, is discussed. Moreover, comparison of prolactin lost from the pituitary and gained in the circulation of the experimental animals, with amounts of prolactin that were observed to disappear from plasma during the experiment, provided suggestive evidence that the capacity to synthesize and/or eliminate prolactin, after a sudden provoked release of the hormone, differed among the groups. The rates of synthesis by the pituitary, of release from the pituitary into the circulation as well as of elimination of the hormone from the circulation (equally involved in determining actual plasma levels) are thought, therefore, to be far more important for the elucidation of prolactin regulation than single plasma prolactin determinations.

EFFECTS OF 17β-HYDROXY-4-ANDROSTEN-19-OL-3-ONE (19-HYDROXYTESTOSTERONE) AND 5α-ANDROSTAN-17β-OL-3-ONE (DIHYDROTESTOSTERONE) ON ASPECTS OF SEXUAL BEHAVIOUR IN CASTRATED MALE RATS

1974 ◽  
Vol 61 (1) ◽  
pp. 105-115 ◽  
Author(s):  
R. F. PARROTT
Keyword(s):  
Adult Male ◽  
Sexual Behaviour ◽  
Testosterone Propionate ◽  
Male Rats ◽  
Organ Weights ◽  
Refractory Periods ◽  
Peripheral Effect ◽  
Rate Of Decline ◽  
The Brain ◽  
Experienced Adult

SUMMARY The ability of 19-hydroxytestosterone propionate (150 μg/day) to maintain sexual behaviour, accessory organ weights and the number of penile spines in experienced adult male rats in the 5 weeks after castration was compared with intact males and castrated animals receiving testosterone propionate (75 μg/day) or oil treatment. In a second experiment a group of male rats receiving dihydrotestosterone propionate (150 μg/day) was also included. 19-Hydroxytestosterone did not maintain ejaculatory performance but animals that ejaculated had refractory periods similar to those in intact and testosterone-treated groups. Dihydrotestosterone, however, slowed the rate of decline of ejaculatory performance but the refractory periods were comparable to those in castrated controls. The former action of dihydrotestosterone was attributed to its stimulatory effect on peripheral structures, especially the penile spines. 19-Hydroxytestosterone was shown to have no peripheral effect at doses up to 1800 μg every other day. The results are discussed in terms of a theory of testosterone action involving aromatization in the brain and 5α-reduction peripherally.

PREVENTION OF CENTRAL DEFEMINIZATION BUT NOT MASCULINIZATION IN MALE RATS BY INHIBITION NEONATALLY OF OESTROGEN BIOSYNTHESIS

1977 ◽  
Vol 74 (3) ◽  
pp. 375-382 ◽  
Author(s):  
J. T. M. VREEBURG ◽  
PAULA D. M. VAN DER VAART ◽  
P. VAN DER SCHOOT
Keyword(s):  
Sexual Function ◽  
Ovarian Function ◽  
Testosterone Propionate ◽  
Neonatal Period ◽  
Female Rats ◽  
Male Rats ◽  
Normal Male ◽  
Male And Female ◽  
Male And Female Rats ◽  
Copulatory Behaviour

SUMMARY An inhibitor of aromatization, androsta-1,4,6-triene-3,17-dione (ATD), was administered to newborn male and female rats and various parameters of gonadal and sexual function were examined in adulthood. Males injected with 1 mg ATD on the day of birth (day 1) and on days 3, 5, 10 and 15 postnatally, subsequently (day 55) showed normal male and female copulatory behaviour, but were not able to maintain cyclicity in ovarian transplants. When the ATD was administered by Silastic implants, however, cyclicity in ovarian transplants did occur. Neither form of treatment brought about significant changes in neonatal plasma or testicular testosterone concentrations. Female rats implanted on day 3 of life with Silastic capsules containing ATD and then given an injection of 0·25 mg testosterone propionate on day 5 subsequently showed normal ovarian function, whereas the controls receiving only testosterone propionate showed persistent vaginal cornification, anovulation and polyfollicular ovaries. The results support the view that the central conversion of testicular androgens to oestrogens during the neonatal period is necessary to abolish cyclic gonadotrophin release and to suppress female copulatory behaviour.

scholarly journals Male-specific suppression of hepatic microsomal UDP-glucuronosyl transferase activities toward sex hormones in the adult male rat administered bisphenol A

2002 ◽  
Vol 368 (3) ◽  
pp. 783-788 ◽  
Author(s):  
Noriaki SHIBATA ◽  
Junya MATSUMOTO ◽  
Ken NAKADA ◽  
Akira YUASA ◽  
Hiroshi YOKOTA
Keyword(s):  
Bisphenol A ◽  
Mrna Expression ◽  
Sex Hormones ◽  
Adult Male ◽  
Endocrine Disruptor ◽  
Liver Microsomes ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Blotting Analysis

Various adverse effects of endocrine disruptors on the reproductive organs of male animals have been reported. We found that UDP-glucuronosyltransferase (UGT) activities towards bisphenol A, testosterone and oestradiol were significantly decreased in liver microsomes prepared from adult male Wistar rats administered with the endocrine disruptor bisphenol A (1mg/2 days for 2 or 4 weeks). However, suppression of the transferase activities was not observed in female rats, even after bisphenol A treatment for 4 weeks. Diethylstilbestrol, which is well known as an endocrine disruptor, had the same effects, but p-cumylphenol had no effect on UGT activities towards sex hormones. Co-administration of an anti-oestrogen, tamoxifen, inhibited the suppression of the transferase activities by bisphenol A. Western blotting analysis showed that the amount of UGT2B1, an isoform of UGT which glucuronidates bisphenol A, was decreased in the rat liver microsomes by the treatment. Northern blotting analysis also indicated that UGT2B1 mRNA in the liver was decreased by bisphenol A treatment. The suppression of UGT activities, UGT2B1 protein and UGT2B1 mRNA expression did not occur in female rats. The results indicate that bisphenol A treatment reduces the mRNA expression of UGT2B1 and other UGT isoforms that mediate the glucuronidation of sex hormones in adult male rats, and this suggests that the endocrine balance may be disrupted by suppression of glucuronidation.

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