PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Progesterone--side effects”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Effects of progesterone on some enzymes of fat and carbohydrate metabolism in rat liver.

The known effect of progesterone on carbohydrate metabolism prompted a study of some of the hepatic "lipogenic" and "gluconeogenic" enzymes in rats treated with progesterone. Several enzymes providing lipid precursors (phosphofructokinase, malic enzyme, glucose-6-phosphate dehydrogenase, and citrate cleavage enzyme) showed increased specific activity. These changes may represent insulin effects. Specific activity of phosphoenolpyruvate carboxykinase, usually associated with control of gluconeogenesis, was also increased. The latter is compatible with increased capability for glycogenesis, which is recognized as a progesterone effect.

ATP Citrate (pro-S)-Lyase↗

[Neurohumoral influences of steroid hormones on sexual responsiveness in women (author's transl)].

An analysis has been carried out on the basis of endocrinological and psychosomatic studies of the influence of steroid hormones, acting via probable transmitter substances, on the sexual response in women. From a review in the literature it can be concluded that among other factors the endocrine state of the women determines her sexual response and behaviour. However, the present lack of specific psychological tests is pointed out, as well as the absence of relevant hormonal data to the sexual sphere, both normal and pathological.

Aging↗

Interference of gestagens and androgens with rat uterine oestrogen receptors.

The inhibitory effect of some gestagens and calusterone on the binding of oestradiol-17beta to its specific uterine receptors has been investigated in intact rats. Progesterone, medrogestone, clogestone, medroxyprogesterone acetate and calusterone reduce the specific oestradiol-receptor interaction in vitro; this effect is dose-dependent and does not differ significantly from one drug to the other. A more relevant decrease in the amount of oestradiol-17beta bound to specific receptors has been observed with calusterone. Progesterone, clogestone, medrogestone, medroxyprogesterone acetate and calusterone given orally induce a marked decrease (between 30 and 70% depending on the dose) in the binding capacity of oestradiol-17beta to specific uterine receptors in vivo. Results from a Scatchard plot analysis suggest that the interference with the binding of oestradiol-17beta caused by both progestogens and calusterone is due to a non-competitive interaction.

Animals↗

[Histochemical and histological investigations on the human fallopian tube under different hormonal influences. I. Demonstration of ATPase with special reference to reactive ciliated cells (author's transl)].

The localization of the Mg++-activated adenosine triphosphatase (ATPase) in the human Fallopian tube has been studied by means of histochemical methods. The samples were obtained from 18 women in the age from 23--62 years. Some of them were treated by various steroid hormones. Endosalpinx ciliary ATPase-activity represents dynein and is therefore an indicator of ciliary motility. Estrogens and gestagens have a different influence on the ATPase-activity. All cilia of one ciliated cell react in the same manner and may be regarded as a reaction unit. The relation of negative to positive ciliary borders differs characteristically in the tubal isthmus, ampulls and infundibulum and coincides with commonly known phenomena of egg transport through the oviduct. Postovulatory, reaction units increase in ampulla and infundibulum compared with the proliferative phase. The oviducts of postmenopausal women possess but a scanty outfit of reaction units. Short-time treatment with estrogen in the early secretory phase results in a great number of reaction units in all tubal segments; a similar treatment in the proliferative phase diminishes the reaction units in the ampulla. Midcycle progesterone treatment activates the ciliary ATPase in the isthmus. Low doses of lynestrenol (minipill) in the proliferative phase leads to a decrease of reaction units in all tubal segments; the pattern of ciliary reaction under low doses of lynestrenol at the time of ovulation coincides with that of the proliferative phase. Treatment with a contraceptive steroid (0,05 mg ethinylestradiol and 0,25 d-norgestrel) causes a considerable activation of the ciliary ATPase in all portions of the oviduct.

Adenosine Triphosphatases↗

Mammary tumors and serum hormones in the bitch treated with medroxyprogesterone acetate or progesterone for four years.

After 4 years of a long-term contraceptive steroid safety study, the incidence and the histologic types of mammary dysplasia produced are shown to be similar in beagles treated with medroxyprogesterone acetate (medroxyprogesterone) or progesterone. Serum insulin, thyroid-stimulating hormone (TSH), triiodothyronine, growth hormone, prolactin, 17 beta-estradiol, progesterone, and cortisol were determined by radioimmunoassay on samples collected after 45 months of treatment. Serum growth hormone and insulin concentrations were elevated in a dose-related manner in both treatment groups. Levels of triiodothyronine, cortisol, and 17 beta-estradiol (medroxyprogesterone only) were lowered. TSH and prolactin concentrations were not changed. Pituitary-gonadal hormone interaction in the pathogenesis of mammary neoplasia of the dog is discussed. Prolonged treatment of beagles with doses of progesterone or medroxyprogesterone 1 to 25 times the human contraceptive dose or luteal phase (dog) levels, respectively, results in a dose-related incidence of mammary nodules.

Adenoma↗

Embryo mortality and altered uterine luminal proteins in progesterone-treated rabbits.

This study was undertaken to elucidate the location, time, and nature of embryo mortality induced by preovulatory progesteron administration. Progesterone was injected into rabbits on days -2, -1, and 0 (the day of mating) at doses of 0.5, 1.0, and 1.0 mg, respectively. Normal fertilization rates resulted, but embryonic death occurred by day 4. Embryos residing in progesterone-treated does for up to 3 days survived normally when transferred to normal recipients, whereas day 4 embryos from treated does exhibited a reduced ability to implant. Uterine fluid (UF) protein pattern was examined on days 1 to 7 after mating. Total UF protein levels were significantly greater in treated animals on day 4 than in controls. Uteroglobin secretion was significantly advanced in the treated animals by day 3. Examination of the time of the arrival of embryos into the uterus revealed a delay in the progesterone-treated rabbits. This delay, coupled with the earlier secretion of uteroglobin in the treated rabbits, indicated a possible asynchrony of approximately 1 day between embryo arrival in the uterus and certain uterine proteins. To determine whether UF could be etiologically implicated in the progesterone-induced embryonic death, embryonic development in vitro and in vivo was examined after exposure to UF collected at different gestational stages. More normal day 3 morulae placed in UF from day 3 control and day 2 progesterone-treated rabbits developed than similar morulae placed in UF from day 2 controls and day 3 progesterone-treated does. Hence, partial physiologic synchrony was achieved. This was interpreted to mean that "asynchronous" UF can be embryotoxic. Infertility was transient. Ability of the does to produce young at a pregnancy immediately following a progesterone-treated pregnancy was not impaired.

Albumins↗

Mechanism of oestrogen and progesterone effects on lipid and carbohydrate metabolism: alteration in the insulin: glucagon molar ratio and hepatic enzyme activity.

As in women receiving oestrogens the administration of 17beta-oestradiol to ovariectomized female rats caused a rise in fasting plasma triglycerides and a fall in plasma glucose. Progesterone, on the other hand, had no significant effects. In the oestradiol treated rats, the portal vein basal insulin levels were slightly reduced. Oestradiol, however, had a marked suppressive effect on the alpha cells of the pancreas resulting in a greater reduction in basal glucagon and impaired glucagon response to alanine infusions. The relative insulin to glucagon (I/G) molar concentration ratio in portal vein blood was increased. Oestradiol also produced a dose dependent increase in the activity of the liver lipogenic enzymes, acetyl CoA carboxylase and fatty acid synthetase. On the other hand, the activity of the gluconeogenic rate limiting enzyme phosphoenol-pyruvate carboxykinase (PEPCK) was inhibited. The cross-over pattern of gluconeogenic intermediates confirmed inhibition of gluconeogenesis at this step, an effect which is similar to that induced by relative insulin 'excess'. Progesterone produced an increase in the portal vein insulin concentrations. Both the basal and the alanine-stimulated glucagon levels were also increased. The I/G molar ratio in portal vein blood of progesterone treated rats remained unaltered and the hepatic lipogenic and gluconeogenic enzyme activities were similar to control animals. These data suggest that insulin activity is increased relative to glucagon in the liver of oestradiol-treated rats due to the rise in portal vein I/G ratio. The changes in liver lipogenic and gluconeogenic enzymes and the alterations in fasting plasma triglycerides and glucose in response to oestrogens could be secondary to this effect.

Acetyl Coenzyme A↗

Effect of progestins on glucose and lipid metabolism.

Gestamimetic amounts of progesterone enhance basal and glucose-stimulated insulin production. Contraceptive doses of synthetic progestins cause a moderate increase or no change in glucose-stimulated insulin production, depending on route of administration and species tested. Estrogens potentiate the insulinotropic effects of progesterone and the synthetic progestins. Basal serum triglyceride concentrations are generally unaffected by progesterone or 17 alpha-acetoxyprogesterone treatment but may decrease during 19-nortestosterone administration. Glucose tolerance does not change during treatment with gestamimetic doses of progesterone alone but may improve in rats and monkeys during concurrent estrogen administration. By contrast, deterioration of glucose tolerance is observed in women treated concurrently with synthetic estrogen plus 19-nortestosterone derivatives and, occasionally, with 19-nortestosterone derivatives alone. No consistent changes in glucose metabolism have been observed after treatment with 17 alpha-acetoxyprogesterone derivatives alone. The cause of the species-related differences in glucose metabolism during 19-nortestosterone treatment is obscure.

Animals↗

Enzymatic responses of transplanted tumour cells towards estrogen, progesterone and testosterone.

The influence of estrogen, progesterone and testosterone on the activities of alkaline and acid phosphatases, adenosine triphosphatase and succinate dehydrogenase were determined by cytochemical methods in sarcoma 180 and Ehrlich's carcinoma cells transplanted in male and female Swiss mice. The results revealed differential effects of the sex hormones on different enzymes which seemed to depend on the type of tumour cell studied and the sex of the host mice.

Acid Phosphatase↗

The mechanism of action of the copper intrauterine device.

The effects of copper ions on the binding of steroids to receptors revealed that the inhibitory effect of Cu++ was apparent at 10(-6)M, ANd the binding capacities decreased to 10% at 10(-2)M Cu++. The kinetic study demonstrated that Cu++ was a competitive inhibitor of steroid hormone-receptor binding (Ki divided by 2.7 X 10(-5)M to estrogen receptor; Ki divided by 5.1 X 10(-6)M to progesterone receptor). These results indicate that copper ions interfere at the steroid-binding site of receptor and that progesterone receptor is more affected by copper ions than is estrogen receptor. The sedimentation pattern showed the dissociation and aggregation of receptor macromolecules by copper. These phenomena may indicate the biologic inactivation of receptor. In fact, morphologically, progestational proliferation was severely inhibited and estrogenic action seemed to be inhibited. The Timm stain showed copper uptake by endometrial epithelium and superficial stromata. The copper content apparently increased in the cytoplasm of uteri bearing a copper intrauterine device, compared with controls. In vivo, the concentration of cytoplasmic copper was approximately 1.4 X 10(-6)M, which was obviously inhibitory to steroid hormone-receptor interaction. However, complete morphologic suppression of the progestational effect by copper cannot exclude the coexistence of some other mechanism in these phenomena.

Animals↗

Postnidatory effects of luteinizing hormone releasing hormone (LHRH) in hamsters.

Whereas the administration of LHRH to pregnant hamsters has no effect during the prenidatory period, the hormone is effective in terminating pregnancy when given after implantation (days 6-10). The ED50 for pregnancy termination over this period approximates a dose of 0.35-0.4 mg b.i.d. When given to pregnant females in a second study, the effects of LHRH at this dose were completely reverse by minute doses of progesterone (30 microgram and above). Finally, administration of LHRH at 1.5 mg b.i.d., from days 6-10 was followed by daily sacrifice through day 12; bloods were sampled at autopsy for progesterone evaluation. Autopsies on days 7 and 8 showed few differences between controls and LHRH-treated hamsters, although decreased weights of the uterine/conceptus units signaled the initation of resorption. Significant LHRH-induced decreases in circulating progesterone were seen by day 9. Fetal resorption continued and was essentially complete by day 11, while progesterone levels continued depressed through the end of the study.

Animals↗