Serum concentrations of testosterone throughout pregnancy in rats

1982 ◽  
Vol 94 (1) ◽  
pp. 21-27 ◽  
Author(s):  
R. S. Bridges ◽  
R. B. Todd ◽  
C. M. Logue

Testosterone concentrations in serum of rats bled throughout pregnancy and post partum were measured using Celite microcolumn chromatography and a radioimmunoassay for testosterone. Mean serum levels of testosterone ranged from about 170 to 340 pmol/l during the first 10 days of pregnancy. Significant increases in concentrations of testosterone in serum of pregnant rats were found on days 12, 15 and 18 of gestation. The highest testosterone concentrations occurred on days 18 and 20 of pregnancy when mean levels were 3228 and 3685 pmol/l respectively. Testosterone levels declined before parturition on day 22 (mean = 1449 pmol/l and declined further after parturition (mean = 315 pmol/l). In order to determine whether serum testosterone concentrations varied during the day in the pregnant rat, samples were collected at 6-h intervals on days 6–7 and 14–15 of gestation. Diurnal variations in serum testosterone concentrations were not evident during early or late pregnancy, unlike the rhythmic changes in serum prolactin levels found at these times during early pregnancy. The possible sources of the increased titres of serum testosterone during the second part of gestation in rats are discussed.

1964 ◽  
Vol 206 (4) ◽  
pp. 796-804 ◽  
Author(s):  
Robert O. Scow ◽  
Sidney S. Chernick ◽  
Marlene S. Brinley

Pregnant rats fasted on the 18th or 19th day of gestation developed hypoglycemia, severe ketosis, and hyperlipemia. The latter, which consisted primarily of triglycerides, was accompanied by increased plasma free fatty acids and accumulation of fat in the liver and kidneys. The effects of fasting were diminished by starting the fast earlier in pregnancy or by hysterectomy. Both ketosis and hyperlipemia were corrected by administration of insulin, tolbutamide, or glucose. The findings indicate that increased fat mobilization and ketosis in fasting pregnant rats are the result of insulin lack. It is suggested that the high priority of the fetuses for glucose reduced the maternal blood glucose concentration to a level too low to stimulate insulin secretion during fasting. Fasting did not alter the rapid growth of the fetuses. Pregnant rats fed ad libitum also developed hypertriglyceridemia if the diet contained fat. This hyperlipemia, unlike that in the fasted rats, was not due to increased fat mobilization and was unaffected by insulin administration. It is concluded that the fractional clearance of blood triglycerides is greatly reduced during late pregnancy.


1975 ◽  
Vol 152 (3) ◽  
pp. 433-443 ◽  
Author(s):  
R G Rodway ◽  
N J Kuhn

Treatment of pregnant rats with human chorionic gonadotrophin, luteotrophin (luteinizing hormone), luteotrophin-releasing hormone, prostaglandin F2α, aminoglutethimide, or by foetoplacental removal or hysterectomy achieved a common multiple-response pattern, namely increased activity of luteal 20α-hydroxy steroid dehydrogenase with decreased activity of delta5-3β-hydroxy steriod dehydrogenase and release of delta4-3-oxo steroids in vitro. 2. Similar effects of foetoplacental removal are noted in pregnant mice. 3. Gonadotrophin induced lower activities of 20α-hydroxy steroid dehydrogenase, except at the very end of pregnancy, and partly inhibited the induction caused by foetoplacental removal. 4. The results suggest that existence of a placental factor that restrains these changes until the end of normal pregnancy, which is produced in amounts proportional to the number of placentae and is conveyed to the ovary via the blood. 5. This factor was not replaced by prolactin. 6. It is argued that neither placental lactogen nor pituitary luteotrophin participate in the induction of 20α-hydroxy steroid dehydrogenase at late pregnancy in the rat. 7. Aminoglutethimide induced 20α-hydroxy steroid dehydrogenase only in late pregnancy. This was partly reversed by progesterone, wholly reversed by progesterone plus oestrogen, and did not involve the pituitary.


1979 ◽  
Vol 83 (2) ◽  
pp. 131-139 ◽  
Author(s):  
W. BECK ◽  
W. WUTTKE

Six male rhesus monkeys were kept under rigidly controlled conditions for 1–2 years. During August of the first year a thyrotrophin releasing hormone (TRH) test was performed on each of the monkeys by giving 10 μg TRH as a bolus injection. Significantly increased serum prolactin levels occurred 15 min after the injection. After a training period of 2 months, during which blood samples were collected every other day by puncture of the saphenous vein, blood was collected three times a week for 14 months. Serum levels of prolactin, LH, FSH and testosterone were measured by radioimmunoassay. Mean serum prolactin levels increased significantly during June, July and August in all six animals. Peak levels were observed in August and September and then levels declined gradually to reach a minimum in April and May. Mean serum testosterone levels closely paralleled the annual pattern of prolactin. Mean serum LH levels significantly decreased during the time when mean serum prolactin and testosterone levels were increasing and they increased again at the time of decreasing mean prolactin levels, i.e. mean serum LH and prolactin were negatively correlated. In individual monkeys, however, a rigid negative correlation between serum prolactin and LH could not be demonstrated. Mean serum FSH levels did not change significantly.


1975 ◽  
Vol 67 (3) ◽  
pp. 371-383 ◽  
Author(s):  
J. P. MALTIER ◽  
F. CAVAILLE

SUMMARY Injection of a monoamine oxidase (MAO) inhibitor (nialamide) into the uterus of an anaesthetized and laparotomized rat on day 20 of pregnancy severely disturbed parturition. Injection of the solvent (0·9% isotonic NaCl solution) at the same stage of gestation produced the same but less frequent disturbances. When the rats were injected on days 19 or 21, impairment was less marked than on day 20. Therefore, day 20 seems to be a critical period for the onset of parturition. Injection of Ringer solution into the uterus on day 20 had effects analogous to those of saline injection at the same stage. Anaesthesia induced with ether, laparotomy of the pregnant rat on day 20, and handling of the uterine horns without injection of either Ringer or NaCl also disturbed parturition in 70% of the rats treated. Nevertheless, disorders were not as severe as those after injection. Laparotomy alone on day 20 did not disturb parturition. The effects on parturition of a saline injection into the uterus on day 20 were greatly decreased when the injection was performed on pregnant rats adrenalectomized on day 14, or on pregnant rats pretreated on days 18 and 19 with an agent blocking the adrenergic β receptors (propranolol); 70–80% of the treated rats had normal deliveries. In control rats, uterine catecholamine levels were markedly modified between days 21 and 22 of gestation. These changes did not occur in rats injected with MAO inhibitor or saline.


1987 ◽  
Vol 113 (1) ◽  
pp. 111-116 ◽  
Author(s):  
R. F. A. Weber ◽  
M. P. Ooms ◽  
J. T. M. Vreeburg

ABSTRACT The effects of hyperprolactinaemia on serum levels of LH were investigated in adult male rats of the R × U strain. Hyperprolactinaemia was induced by three pituitary grafts under the kidney capsule, transplanted on day 0 of each experiment. Special attention was paid to the contribution of prolactin-stimulated testes, adrenals and corticosterone. In experiment 1, hyperprolactinaemia significantly reduced the serum concentrations of LH in intact rats. In spite of a significant increase in the serum levels of corticosterone, serum testosterone was not significantly affected by hyperprolactinaemia. The weights of both the adrenals and accessory sex glands were significantly increased at autopsy. In experiment 2, treatment with 10 mg corticosterone s.c. daily from day 14 to day 28 after pituitary grafting significantly reduced serum levels of both LH and testosterone. The suppression of testosterone in the hyperprolactinaemic corticosterone-treated animals was significantly less than in the corticosterone-treated control animals. The weights of the accessory sex glands were significantly increased in the hyperprolactinaemic animals. In experiment 3, rats were adrenalectomized and half of them were substituted with corticosterone. Serum testosterone levels significantly increased in both hyperprolactinaemic adrenalectomized rats and in adrenalectomized corticosterone-treated animals without any significant effect on serum LH. Again the weights of the accessory sex glands were significantly increased in the hyperprolactinaemic animals. In experiment 4, rats were adrenalectomized, gonadectomized and corticosterone treated on day 0 and then implanted with a 2, 1·5 or 1 cm silicone elastomer capsule containing testosterone. On day 28 after pituitary grafting, LH levels were significantly suppressed in animals with a 2 or 1·5 cm testosterone implant. The weights of the accessory sex glands were not increased in the hyperprolactinaemic animals. These results show that in the male rat the inhibitory effects of hyperprolactinaemia on serum LH levels may be due to (1) increased sensitivity of the hypothalamic-pituitary axis to the negative feedback action of testosterone by prolactin and by the prolactin-stimulated corticosterone secretion and (2) stimulation of testicular testosterone secretion by prolactin, which can also explain the increased weights of the accessory sex glands. Even in the presence of high serum concentrations of corticosterone, stimulation of testicular testosterone secretion by prolactin was observed. J. Endocr. (1987) 113,111–116


Drug Research ◽  
2018 ◽  
Vol 68 (07) ◽  
pp. 410-414 ◽  
Author(s):  
Xiao-Jia Jiang ◽  
Fu-Xi Wu ◽  
Jian-Ping Zhang ◽  
Lei Shi ◽  
Jin-Qing Hu ◽  
...  

Abstract Objective To evaluate the effects of treatment with risperidone and aripiprazole on serum prolactin, testosterone and estradiol levels in female patients with schizophrenia in China. Methods In the retrospective study, Data were collected and included prolactin, testosterone and estradiol levels of 30 female patients with risperidone monotherapy. In the prospective study, Another 30 female schizophrenic patients were randomized to receive risperidone or adjunctive aripiprazole for six weeks. Serum prolactin, testosterone and estradiol levels were measured. Results Serum prolactin, testosterone and estradiol levels in both studies were significantly decreased after risperidone treatment compared with baseline (P<0.05), and prolactin levels remained at a high level. Serum prolactin levels in the adjunctive aripiprazole group were significantly decreased after treatment compared with baseline in the prospective study (P<0.05). Doses of 5 mg and 10 mg of adjunctive aripiprazole achieved the same efficacy at the end of treatment. Conclusions Risperidone treatment decreased serum testosterone and estradiol levels. Adjunctive aripiprazole relieved hyperprolactinemia, but had no effect on testosterone or estradiol levels. Adjunctive aripiprazole at a dose of 5 mg is recommended for clinical use.


1990 ◽  
Vol 122 (1) ◽  
pp. 121-126 ◽  
Author(s):  
Alia Cohen ◽  
Lia Savu ◽  
Roger Vranckx ◽  
Michelle Maya ◽  
Emmanuel A. Nunez

Abstract The response of pregnant rat corticosteroid binding globulin to maternal adrenalectomy was studied as a function of the stage of pregnancy. Non-pregnant or pregnant rats were deprived of their adrenal glands during 4 days. In non-pregnant animals, adrenalectomy led to undetectable corticosterone levels and to the doubling of corticosteroid binding globulin. In pregnant rats adrenalectomized at 12 days and studied at 16 days, the serum corticosterone was likewise undetectable and the corticosteroid binding globulin was doubled as compared with pregnant rats of the corresponding age. In contrast, adrenalectomy from day 14 to 18 or from day 16 to 20 did not deplete the maternal serum corticosterone and the corticosteroid binding globulin remained unchanged. Under these conditions neither fetal corticosteroid binding globulin nor fetal corticosterone were modified. However, when the pregnant rats adrenalectomized from day 16 to 20 also received an injection of 30 mg of metyrapone on days 19 and 20 in order to inhibit fetal adrenal secretion, the maternal response was again a depletion of serum corticosterone together with an increase in corticosteroid binding globulin. Under these conditions, the fetus also reacted by a fall of corticosterone and a rise of corticosteroid binding globulin. Our results suggest that the maternal response of corticosteroid binding globulin to adrenalectomy depends on the pregnancy stage inasmuch as it may be influenced by a supply of corticosterone from the fetus during late pregnancy. Moreover, they show that in this late period, fetal corticosteroid binding globulin is regulated independently.


Reproduction ◽  
2003 ◽  
pp. 371-382 ◽  
Author(s):  
MB Hapon ◽  
M Simoncini ◽  
G Via ◽  
GA Jahn

Thyroid dysfunctions can produce reproductive problems. Untreated maternal hypothyroidism has serious consequences on development of offspring, resulting in stunted growth and mental retardation. The effects of propylthiouracyl-induced hypothyroidism (0.1 g l(-1) in drinking water starting 8 days before mating, or given to virgin rats for 30 or 50 days) on the serum profiles of hormones related to reproduction and mammary function (prolactin, growth hormone (GH), progesterone, corticosterone, oestradiol, insulin-like growth factor I (IGF-I), thyroid-stimulating hormone (TSH), triiodothyronine and tetraiodothyronine), and on mammary function in virgin, pregnant and lactating rats, were investigated. Propylthiouracyl treatment severely decreased circulating triiodothyronine and tetraiodothyronine concentrations, and increased serum TSH concentrations. Virgin rats showed prolonged periods of vaginal dioestrus, increased circulating progesterone concentrations and afternoon peaks of prolactin concentration, which are indicative of prolactin-induced pseudopregnancy. Propylthiouracyl-treated virgin rats had mammary development comparable to that of midpregnancy, and half of these rats had increased mammary casein and lactose concentrations. Serum prolactin concentrations were decreased on the afternoon of day 5 of pregnancy, increased during late pregnancy (days 15-21) and were normal during lactation. Circulating GH concentrations decreased on days 15-21 of pregnancy, whereas progesterone concentrations increased during late pregnancy and early lactation. Circulating oestradiol (measured in late pregnancy and in virgin rats), IGF-I and corticosterone concentrations were decreased. Although assessment of mammary histology showed no differences in extent of development, casein content was increased in propylthiouracyl-treated rats on day 21 of pregnancy; litter growth was severely reduced and at day 20 of age the pups were hypothyroid, with decreased GH serum concentrations. An acute suckling experiment was performed on days 10-12 of lactation to determine whether some impairment in mammary function or the suckling reflex might account for these differences. After an 8 h separation of mothers from their litters and 30 min of suckling, circulating prolactin values were not affected by propylthiouracyl treatment, but serum oxytocin concentration and milk excretion were reduced. In conclusion, hypothyroidism induces various alterations in the hormone profiles of virgin and pregnant rats, and induces pseudopregnancies and mammary development in virgin rats. These alterations do not appear to have an overt impact on the outcome of pregnancy and on mammary function during lactation, with the exception of the milk ejection reflex, which may account at least partially for the reduced litter growth.


1976 ◽  
Vol 160 (3) ◽  
pp. 663-670 ◽  
Author(s):  
D H Smith ◽  
N J Kuhn

1. The previously reported induction of luteal 20α-hydroxy steroid dehydrogenase by administration of aminoglutethimide to late-pregnant rats was shown to be unaffected by prior removal of the foetuses. Aminoglutethimide therefore does not act via the foetuses in this context. 2. The ability of injected oestrogen to prevent the above induction was lost by delaying the injection for 12h after aminoglutethimide, although the increase in enzyme activity begins only after 24h. 3. Induction of 20α-hydroxy steroid dehydrogenase by foetoplacental removal on day 18 of pregnancy was inhibited by human choriogonadotropin, lutropin (luteinizing hormone) and pregnant-mare serum gonadotropin, but not by somatotropin (growth hormone), thyrotropin or follitropin (follicle-stimulating hormone) 4. Indomethacin blocked the normal induction of 20α-hydroxy steroid dehydrogenase in late pregnancy and that caused by aminoglutethimide. It partially blocked that caused by human choriogonadotropin given on days 19-20 and that caused by 2-bromo-α-ergocryptine on days 5-6, but failed to block that caused by human choriogonadotropin on days 15-16 or by foetoplacental removal on day 18 of pregnancy. 5. These findings, and the control of progesterone synthesis in late pregnancy, are interpreted in terms of a sequence of hormonal or enzymic syntheses, each of which is inhibited by the product of the preceding synthesis.


2008 ◽  
Vol 294 (3) ◽  
pp. H1156-H1163 ◽  
Author(s):  
Ran Reshef ◽  
Doron Schwartz ◽  
Merav Ingbir ◽  
Alexander Shtabsky ◽  
Tamara Chernichovski ◽  
...  

While a specific role for nitric oxide (NO) in inducing the hemodynamic alterations of pregnancy is somewhat controversial, it is widely accepted that excess NO is generated during pregnancy. l-Arginine is the sole precursor for NO biosynthesis. Among several transporters that mediate l-arginine uptake, cationic amino acid transporter-1 (CAT-1) acts as the specific arginine transporter for endothelial NO synthase. The present study was designed to test the hypothesis that, during pregnancy, when arginine consumption by the fetus is significantly increased, compensatory changes in maternal arginine uptake affect the endothelium. Uptake of radiolabeled arginine (l-[3H]arginine) by freshly harvested maternal aortic rings from pregnant rats decreased by 65 and 30% in mid- and late pregnancy, respectively, compared with those obtained from virgin animals. This decrease was associated with a significant increase in endothelial protein nitration (the footprint of peroxynitrite generation), as shown by both Western blotting and immunohistochemistry utilizing anti-nitrotyrosine antibodies, reflecting endothelial damage. Northern blot analysis revealed that steady-state aortic CAT-1 mRNA levels did not change throughout pregnancy, whereas CAT-1 protein abundance was significantly increased, peaking at mid-pregnancy. Protein content of protein kinase C (PKC)-α, which was previously shown to decrease CAT-1 activity, increased significantly in the pregnant animals and was associated with a significant increase in CAT-1 phosphorylation. Intraperitoneal injection of α-tocopherol, a PKC-α inhibitor, prevented the decrease in arginine transport and attenuated protein nitration. In conclusion, aortic arginine uptake is reduced during pregnancy, through posttranslational modulation of CAT-1 protein, presumably via upregulation of PKC-α. The aforementioned findings are associated with an increase in protein nitration and, therefore, in selected individuals, may lead to the development of certain forms of endothelial dysfunction, like preeclampsia.


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