Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating levels of FSH, LH, prolactin (Prl), estradiol (E), and progesterone (P) were determined by RIA in four intact and four monkeys luteectomized (CLX) at parturition in order to a) characterize the patterns of these hormones during the puerperium, and b) examine a possible inhibitory role of the "rejuvenated" corpus luteum (CL) on the resumption of follicle growth post partum. In both groups during the first four weeks, FSH and LH were at tonic levels typical of ovulatory cycles. Recurrent puerperal "surges" of FSH, but not LH, unaccompanied by increments in serum E, were observed in both intact and CLX monkeys. No consistent pattern of serum Prl was apparent. CLX was followed by a prompt fall in serum P levels, which were elevated above typical follicular phase levels into the second week post partum in intact monkeys. Menstrual cycles resumed 2-4 months after delivery. Hormonal patterns during the first menstrual cycle post partum were indistinguishable from those observed in pregravidic ovulatory cycles. The findings indicate that in nonsuckling cynomolgus monkeys a) although it secretes progesterone, the puerperal CL does not inhibit the resumption of the ovarian cycle post partum, b) the puerperal ovary is not absolutely refractory to gonadotropins, since initial trials with Pergonal + hCG stimulated ovarian function, and c) ovarian activity during the puerperium may be limited by factors other than the tonic supply of gonadotropins.
Steroids 1978 May
PMID:Post partum patterns of circulating FSH, LH, prolactin, estradiol, and progesterone in nonsuckling cynomolgus monkeys. 9 8

Hypophysectomy of immature rats results after 5 days in a loss of LH responsiveness of Leydig cells. LH responsiveness can be partly maintained by treatment with FSH for 5 days. When estradiol benzoate was administered together with FSH to hypophysectomized rats the maintenance of LH responsiveness was not observed. The loss in LH responsiveness after hypophysectomy in terms of testosterone production could not be explained by either a change in the amount of Leydig cells present in the Leydig cell preparation or to a higher conversion of testosterone. The LH-stimulated cAMP production in cells from hypophysectomized rats was very low compared to cells from intact rats. There was no difference between cAMP production of Leydig cells from untreated, FSH-treated or FSH plus estradiol benzoate treated hypophysectomized rats. During the first 2 days after hypophysectomy LH responsiveness in both untreated and FSH-treated rats showed a comparable decrease. From day 2 after hypophysectomy LH responsiveness remained at a constant level in cells from rats treated with FSH, but declined further in cells from untreated rats. A single injection of estradiol benzoate to hypophysectomized rats treated with FSH counteracted the effect of FSH on LH responsiveness, but only when estradiol was administered at that time after hypophysectomy, when the effect of FSH on LH responsiveness was clear.
Steroids 1978 Jan
PMID:Further characterization of the effects of hypophysectomy, FSH and estrogen on LH stimulation of testosterone production in Leydig cells isolated from immature rats. 20 98

Cultures of Sertoli cells isolated from testes of 18-and 36-day-old Long Evans rats were used to investigate their capacity to metabolize testosterone and the effect of FSH on such metabolism. Three different approaches were used: 1) investigation of the metabolism of radiolabeled testosterone under saturating substrate conditions; 2) study of the metabolism of radiolabeled testosterone utilizing trace amounts of high specific activity substrates; 3) the utilization of radioimmunoassay for measurement of estradiol-17 beta. The following steroids were isolated and identified by recrystallization to constant specific acitvity from the control and FSH-treated cultures; testosterone (unconverted substrate), androstenedione, dihydrotestosterone, 3 alpha-hydroxy-5 alpha-androstan-17-one and 5 alpha-androstane-3 alpha, 17 beta-diol. Radioimmunoassay data suggests that the Sertoli cells produce an estradiol-17 beta-like compound from unlabeled testosterone and that this production is stimulated by FSH. However, the radioactive metabolite from all our studies that behaved chromatographically like estradiol--17 beta failed to crystallize to constant specific activity, while in each experiment, authentic radiolabeled estradiol-17 beta added as recovery tracer did. The data demonstrate that : 1) cultures of Sertoli cells from immature rats have 5 alpha-reductase, 3 alpha- and 17 beta-hydroxysteroid oxidoreductase activities; 2) these enzymes may be affected by FSH; 3) based on radiolabeled metabolic techniques, Sertoli cells were unable to biotransform testosterone to estradiol-17 beta even in the presence of FSH.
Steroids 1979 May
PMID:In vitro metabolism of testosterone by cultured Sertoli cells and the effect of FSH. 31 14

The effects of glucocorticoids on the steroidogenesis of ovarian granulosa cells were investigated. Cortisol and dexamethasone inhibited the increase in aromatase activity induced by FSH in cultured rat granulosa cells. In the same cultures progesterone production was stimulated to a maximum of 167% of the control level. This differential effect of glucocorticoids on estrogen and progesterone production by the granulosa cells indicates that glucocorticoids exert specific inhibition of the induction of aromatase by FSH and do not cause a general suppression of granulosa cell activity. In contrast to their inhibition of the FSH induction of aromatase enzymes, glucocorticoids did not interfere with the activity of pre-existing aromatase enzymes. In granulosa cells containing full aromatase activity, treatment with cortisol and dexamethasone did not inhibit aromatization of androstenedione to estrogens whereas two known aromatase inhibitors (dihydrotestosterone and 4-androstene-3, 6, 17-trione) were effective. These results indicate that the glucocorticoids exert a selective inhibition of the FSH-induction of aromatase activity in rat granulosa cells by a mechanism other than directly interfering with the aromatization reaction.
Steroids 1978 Dec
PMID:Glucocorticoid inhibition of FSH-induced estrogen production in cultured rat granulosa cells. 73 98

Immature rat ovaries increase their secretion of estradiol (E2) when stimulated by gonadotropins but only after a lag period of several hours. Once established, estrogen secretion can be maintained, or increased, by the continued presence of gonadotropin. A combination of ovine FSH+LH given at 2 hr intervals stimulated the estrogen synthesizing system (ESS) of the ovary and serum E2 showed a pronounced rise between 16 and 20 hrs after the initial injection. When given every 2 hrs for 5 doses (0-8 hrs) serum E2 was undetectable. However, it was increased if 20 IU PMS was injected at the time of the last dose of FSH+LH. Endogenous FSH+LH, increased by hourly injections of LH-releasing hormone for a period of 8 hrs, stimulated the ESS: serum E2 increased at the expected when this treatment was followed by an injection of PMS. Anti-PMS antiserum given 12 hrs after PMS, prevented the expected rise in serum E2 at 24 hrs. However, FSH, LH or a combination of the two given every 2 hrs beginning at the time of the anti-PMS produced an increase in E2 secretion; the combination was more effective than either hormone alone. These results are consistent with the interpretation that a combined FSH-LH action is responsible for induction fo the ESS in the immature rat ovary. The combination of homones is also very effective in maintaining estrogen secretion but some function appears possible with FSH or LH alone.
Steroids 1976 Apr
PMID:Stimulation of the estrogen synthesizing system of the immature rat ovary by exogenous and endogenous gonadotropins. 77 88

Testosterone production in isolated Leydig cells from testes of immature and adult rats was stimulated by addition of LH in a dose dependent way. Hypophysectomy of adult rats had no influence on LH-stimulated testosterone production in isolated Leydig cells after 5 days. In contrast hypophysectomy of immature rats resulted after 5 days in an almost complete loss of LH sensitivity of isolated Leydig cells. Daily adminitration of FSH during 5 days starting immediately after hypophysectomy maintained LH responsiveness of isolated Leydig cells of immature rats. Also FSH administration starting on day 5 after hypophysectomy resulted in a restoration of LH responsiveness. Estradiol benzoate, injected simultaneously with FSH, abolished the FSH-induced LH responsiveness.
Steroids 1976 Dec
PMID:Hormonal regulation of LH stimulation of testosterone production in isolated Leydig cells of immature rats: the effect of hypophysectomy, FSH, and estradiol-17beta. 101 46

The in vitro conversion of 20alpha-hydroxy-4-pregnen-3-one (20alpha-DHP) by medial basal hypothalamus and anterior pituitary was investigated throughout the day of proestrus in the 4-day cyclic rat. Reverse isotopic dilution analysis was utilized to quantitate the substrate remaining and three metabolic products: 20alpha-hydroxy-5alpha-pregnan-3-one, 5alpha-pregnane-3alpha,20alpha-diol and progesterone. Serum levels of 20alpha-DHP, progesterone, LH and FSH were measured by radioimmunoassay. Conversion of 20alpha-DHP to its 5alpha-reduced metabolites (20alpha-hydroxy-5alpha-pregnan-3-one and 5alpha-pregnane-3alpha,20alpha-diol) by the pituitary was constant throughout proestrus except for a significant decrease at 1600 h, near the end of the critical period. Although 5alpha-reduction of 20alpha-DHP by the hypothalamus fluctuated, it was relatively high at 1600 h and was lowest at 1400 h. Small amounts of progesterone (less than2%) were formed but there was not variation with time. The decrease in pituitary enzymic activity coincided with the time when serum levels of LH, FSH and progesterone were increasing but not with later times when the elevated serum levels were maintained. Thus, there may be endogenous regulation of 5alpha-reductase and 3alpha-hydroxysteroid dehydrogenase activity in rat pituitary and perhaps hypothalamus on the afternoon of proestrus. The regulation and subsequent effects of quantitative changes in 5alpha-reduction of 20alpha-DHP by pituitary and hypothalamus remain to be elucidated.
Steroids 1976 Oct
PMID:Quantitative changes in the metabolism of 20alpha-hydroxy-4-pregnen-3-one by rat hypothalamus and pituitary during proestrus. 103 57

The follicle plays a major role in the dual function of the ovary--oocyte maturation and release and steroidogenesis required for regulating its own growth and providing the proper environment in reproductive organs for the transport of gametes and nidation. Some aspects of how follicles attain their functional competence following a series of developmental changes are discussed. The presentation is based on data obtained mainly in rodents in which follicular development occurs postnatally. The peak activity of follicular growth occurs during the 1st week of life, but not until the 5th day is follicular development clearly dependent upon gonadotrophin stimulation. The formation of the theca layer and zona pellucida, differentiation of the vascular system and competence to respond to gonadotrophins are acquired during the 2nd week. FSH alone is primarily responsible for granulosa cell proliferation and the integrity of the granulosa cell membrane, but has little differential effect on steroidogenic enzymes. Synergism of FSH and LH promotes an enrichment of the theca layer, enhancement of vascular development and antrum formation, and induces a marked differential stimulation of 20alpha-hydroxysteroid dehydrogenase, aromatizing and cholesterol side-chain cleavage systems. The number of gonadotrophin receptors on granulosa and theca cells increases with follicular development. Steroids secreted by the ovary seem to modulate follicular growth, not only by effects upon FSH and LH release but also by a local influence within the ovary. A number of physiological events related to follicular function are explained according to these observations.
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PMID:The function of the growing follicle. 120 57

Composite microassays for plasma progesterone (P), 17alpha-OH-progesterone (17P), estrone (E1), 17beta-estradiol (E2), and estriol (E3) were developed. Steroids were extracted from plasma samples with diethyl ether, and were separated from each other through two steps of sephadex LH-20 microcolumn chromatography (benzene:methanol 85:15, and n-hexane: benzene: methanol 80:10:10), prior to assays by radioimmunoassay (P, E1, E1, and E3) and competitive protein binding assay (17P). Steroids were recovered satisfactorily through these procedures (mean recovery; P:107.6%, 17P:102.3%, E1:88.2%, E2:84.1%. E3:78.5%). The detectable range for P, 17P, E1, E2, and E3 were 0.01-2 ng/tube, 0.1-10 ng/tube, 10-2000pg/tube, 10-2000 pg/tube, and 0.5-100 ng/tube. The interassay coefficient of variations were less than 10.7%, 15.2%, 17.8%, 11.4%, and 28.1%, respectively. These steroids were measured daily in 4 menstrual cycles from 4 normally menstruating women. Plasma FSH and LH were quantitated previously. The following results were obtained; 1) Plasma P elevated from around LH surge (Day O), and reached a peak on day +5 approximately +7 with the values of 12.74 +/- 2.34 ng/ml (Mean +/- S.D.). 2) Slight decrease in P levels was noted on day +8 approximately +9. 3) A peak in 17P was observed in the preovulatory phase (day -3 approximately -1) with the values of 0.6 approximately 1.3 ng/ml in three of four cases. 4) Changes of 17P during the luteal phase were paralleled to those of P with a peak of 1.16 +/- 0.31 ng/ml on day +5 approximately +7. 5) No remarkable patterns were found in E1 levels throughout the menstrual cycle. 6) A sharp peak in E2 was detected in the preovulatory phase (day -1 approximately 0) with the values of 709.2 +/- 95.9 pg/ml. 7) The second peak of E2 with 378.6 +/- 140.7 pg/ml was observed in the late luteal phase (day +8 approximately +12). 8)E3 was not detected in all samples. The interrelationship between steroids and the correlation with the morphological changes of the ovaries in the normal menstrual cycle are discussed. In the follicular phase, the theca interna cells around the maturing follicle may be growing under the influence of pitiutary gonadotropins to secrete large amounts of 17P and E2, which may possibly affect the pituitary for LH surge, followed by ovulation. In the luteal phase, both the granulosa cells and theca intera cells are luteinized, which may produce and secrete large amount of P, 17P, and E2.
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PMID:[Composite microassays of plasma progesterone, 17alpha-OH-progestrerone, estrone, 17beta-estradiol and estriol in normal adult women. I. Assay methods and steroid patterns in normal menstrual cycle (author's transl)]. 124 48

Prodynorphin is expressed by neurons of the hypothalamus and gonadotrophs of the anterior pituitary gland (AP) and plays a role in the negative feedback regulation of the reproductive neuroendocrine axis. The present study examined whether gonadal steroid hormones are capable of modulating pituitary prodynorphin expression in immature, female rats. Steroids were administered via subcutaneous Silastic implants and rats were killed at 29 days of age. Northern blot analysis was used to measure AP prodynorphin, luteinizing hormone-beta (LH beta), follicle-stimulating hormone-beta (FSH beta), and common alpha-subunit mRNA levels (normalized to 18S ribosomal RNA). Treatment groups (n = 5-6) consisted of control (CNT; empty implants), estradiol (E2; 4 days), E2 + progesterone (E2 + P4; 8 days and 4 days, respectively), and dihydrotestosterone (DHT; 4 days). Pituitary prodynorphin mRNA was significantly suppressed in only the DHT-treated animals (26 +/- 10% of CNT, p < 0.01). LH beta mRNA was suppressed by all steroid treatments (p < 0.01), FSH beta was lower in only the E2 group, and alpha-subunit was reduced in both the E2 + P4 and DHT groups (p < 0.01). Serum LH was suppressed by all steroid treatments but FSH was reduced in only the E2 and E2 + P4 groups (p < 0.01). Treatment of prepubescent rats with continuous high levels of gonadal steroids is known to severely reduce endogenous hypothalamic gonadotropin releasing hormone (GnRH) release and this is supported by our observation of reduced gonadotropin-subunit gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential regulation of anterior pituitary prodynorphin and gonadotropin-subunit gene expression by steroid hormones. 145 42


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