Influence of corticotrophin and prolactin on the steroid sex hormones and their precursors in postmenopausal women.
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Adrenocorticotropic Hormone↗
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Effect of antiepileptic drug monotherapy on endogenous sex hormonal profile in men and women with epilepsy.
OBJECTIVE: To assess the alterations of endogenous sex hormone profiles in patients with epilepsy (PWE) on different antiepileptic drug (AED) monotherapies compared to healthy controls and drug naïve PWE (DNPWE). METHODS: Four databases MEDLINE, EMBASE, SCOPUS, and CENTRAL were searched for analytical observational/intervention studies on the assessment of endogenous sex hormones in PWE compared to healthy controls and DNPWE. Two researchers reviewed the title/abstract, and full-text articles for the selection of the studies independently. Extracted data included information on study details, participant demographics, interventions, method of assessment and study results. The study outcomes were used to calculate the standard mean differences (SMD) and 95% confidence interval (CI) as effect size for assessing differences in the endogenous sex hormone levels between the treatment group and control/DNPWE. RESULTS: Among 5888 publications retrieved, 33 studies were included. Enzyme-inducing AEDs (EIAEDs) such as phenytoin (men: SMD = 1.36; 95%CI = 1.06,1.66) and carbamazepine (men: SMD = 0.71; 95%CI = 0.39, 1.04 and women: SMD = 0.54; 95%CI = 0.25, 0.83) and weak-EIAED oxcarbazepine (men: SMD = 0.62; 95%CI = 0.26,0.99) increased the SHBG levels in PWE compared to control. The same trend was observed when comparing it to DNPWE. No significant changes in SHBG were observed for non-EIAEDs valproic acid, lamotrigine and levetiracetam in men. Lamotrigine significantly reduced SHBG in women (SMD = -0.50; 95%CI = -0.85, -0.16) compared to controls. Testosterone (T) levels were significantly reduced for both carbamazepine (SMD = -0.39; 95%CI = -0.67, -0.11) and valproic acid (SMD = -0.48; 95%CI = -0.74, -0.21) treated men compared to control. SIGNIFICANCE: Our findings emphasize the importance of screening the endogenous sex hormonal profile in PWE on AED monotherapies to evaluate the associated endocrine-related perturbations which may impact reproductive functions.
Humans↗
[Role of the adrenal glands and the testes in the formation of the sex steroid pool in the peripheral blood of male monkeys].
A study was made of formation of the pool of sex steroid hormones and their precursors in the blood plasma of male Paio hamadryas. Cannulation and simultaneous recovery of the blood from the adrenal, testicular, left iliac veins and the aorta were carried out under nembutal anesthesia. Thirteen steroid hormones and their precursors were determined by the radioimmunological method in all the blood portions. Steroid function was tested on columns with celite. Pregnenolone, 17alpha-oxypregnenolone, and 17alpha-oxyprogesterone were secreted chiefly by the adrenal glands. Dihydroepiandrosterone was produced by the adrenal glands and utilized by the testes. Androstendion and dihydrotestosterone were mostly of adrenal, and testosterone--testicular origin. Estron is secreted by the adrenal glands only, whereas estradiol is produced by the testes in larger quantities than by the adrenal glands. The sulfate forms of pregnenolone and dihydroepiandrosterone are produced chiefly by the adrenal glands.
Adrenal Glands↗
Hypercalcemia and neoplasia. Biologic, biochemical, and ultrastructural studies of a hypercalcemia-producing Leydig cell tumor of the rat.
A localized, transplantable testicular tumor of the Fischer rat regularly produces hypercalcemia and increased phosphorus clearance in host animals. Light and electron microscopic examinations of the tumor indicate that it is of Leydig origin. There is no evidence that the tumor secretes any biologically active sex steroids, judges by weights of target tissues, when the tumor is grown in castrated or spayed rats. No radioactive steroid hormone formation in vitro was detected using 1-14C-acetate as a precursor although 14C was incorporated into the "C27" sterol fraction. Mass (micrograms) amounts of sex steroids were not detected after purifying large amounts of tumor extracts. The phytosterols, beta-sitosterol, stigmasterol, campesterol, were tentatively identified in tumor extracts but were also found in other tissues and in tumors not associated with hypercalcemia. Administered in vivo, human chorionic gonadotropin caused an acute rise in serum calcium in 3 to 5 hours in tumor-bearing hypercalcemic rats. Only trophic hormones with luteinizing hormone activity were found to compete with 125I-human chorionic gonadotropin for binding to the tumor homogenate in vitro indicating the tumor possessed luteinizing hormone receptors. When the tumor was transplanted intrasplenically, hypercalcemia did not occur unless adhesions formed, suggesting that the tumor hormone was rapidly metabolized by the liver and was probably of small molecular weight. Secretory granules, usually thought to be associated with peptide hormone secretion, were not detected at the ultrastructure level. Cortisol, conjugated estrogen, and an inhibitor of sterol biosynthesis (AY-9944) were effective in lowering the elevated serum calcium. Definitive identification of the agent causing lethal hypercalcemia has not been accomplished. The available data suggest it is not parathyroid hormone or vitamin D. The Leydig cell origin of the tumor, its response to human chorionic gonadotropin in vivo, the lack of secretory granules at the ultrastructural level, and biologic characteristics, all lead to the speculation that the secretory product of the tumor is a new hormonal substance, possibly a steroid precursor or related substance not previously described or is a known substance of small molecular weight whose calcium-mobilizing properties have not been fully characterized. This transplantable tumor may represent a model for one form of neoplastic hypercalcemia occurring in man and may have important implications in the general area of calcium and phosphorus homeostasis.
Animals↗
[In-vitro studies on the effect of D-norgestrel and norethisterone acetate on the formation of sex steroids in the human ovary].
In vitro incubations with slices of four normal human ovaries and 4-(14)C-pregnenolone as precursor were carried out to study the possibility of a direct influence of D-norgestrel and norethisterone acetate on the metabolism of pregnenolone. In agreement with our previous studies the in vitro-synthesis of progesterone, 17 alpha-hydroxyprogesterone, estrone and estradiol represents the characteristic profile of steroids of the ovaries from the corpus luteum phase. The in vitro-synthesis of 17 alpha-hydroxypregnenolone, DHA, androstenediol (basic metabolites) and androstenedione represents the characteristic profile of steroids of the ovaries from the follicle phase. The addition of D-norgestrel and norethisterone acetate to the incubation medium influences these steroid profiles in the same way. The metabolites of these characteristic profiles were inhibited by the progestogens, whereas the basic metabolites increased. In previous studies the same influence was found by addition of chlormadinone acetate. The influence of these progestagens on the two different profiles of steroids indicate that D-norgestrel and norethisterone acetate exert an inhibitory effect on the 3 beta-hydroxysteroiddehydrogenase-delta 5-4-isomerase system and the aromatase system of the human ovary. These results suggest that these progestogens act directly upon ovarian function, an action which may be assumed to be operative in their contraceptive effect.
17-alpha-Hydroxypregnenolone↗
A study of the endocrine manifestations of hepatic cirrhosis.
The clinical features and hormonal abnormalities were surveyed in 117 men with cirrhosis of the liver. Compared with healthy men of similar ages, the patients had significantly lower metabolic clearance rates, plasma production rates and total and free levels of testosterone, reduced testosterone responses to human chorionic gonadotrophin stimulation, higher oestradiol, luteinizing hormone and follicle stimulating hormone levels and higher binding capacities of sex steroid binding globulin. The peripheral conversion of testosterone to oestradiol was also found to be significantly increased. However, the metabolic clearance and plasma production rates of oestradiol were not significantly different from those of healthy men. Patients who were severely ill with liver failure and one with haemochromatosis had low levels of luteinizing hormone and follicle stimulating hormone and sub-normal responses to clomiphene and luteinizing hormone-releasing hormone. Higher plasma oestradiol levels were found in patients with gynaecomastia and spider naevi than in those without these signs. However, the clinical features of androgen deficiency--that is, testicular atrophy, impotence and loss of secondary sex hair--were only poorly related to the low testosterone levels, and production rates and longtitudinal studies indicated that the hormonal levels, endocrine features and severity of the liver disease could change independently. It is concluded that the clearance of oestradiol from plasma is not limited by liver disease in all patients, and that reduced degradation of oestrogens is not the initial event in the sequence leading to the hormonal abnormalities of cirrhosis. While gonadotrophin deficiency occurs with liver failure and in some patients with haemochromatosis, the more usual findings are of elevated gonadotrophin levels and a poor Leydig cell response to chorionic gonadotrophin. These suggest that the hypogonadism is primary in most patients with cirrhosis. The causes of the high oestradiol levels were not discovered. Increased peripheral conversion of precursors to oestradiol or increased testicular secretion of oestradiol are possibilities. The high binding capacities of sex steroid binding globulin were not significantly correlated with either the low testosterone or high oestradiol level and the cause of this abnormality remains uncertain. The low metabolic clearance rates of testosterone appeared to result from the increased plasma protein binding of testosterone. The discrepancies in the expected relationships between the hormone and clinical changes suggest that factors other than those studied are also involved in the genesis of the endocrine features of hepatic cirrhosis.
Adult↗
Radioimmunoassay of steroids produced by chick embryo gonads cultured in the presence of some exogenous steroid precursors.
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Androstenedione↗
Steroid sex hormones and prolactin in postmenopausal women with generalized mammary carcinoma during prolonged dexamethasone treatment.
The endocrine response to prolonged dexamethasone treatment was investigated in six postmenopausal women with generalized mammary carcinoma. Plasma cortisol levels decreased rapidly and became undetectable whereas significant concentrations of plasma dehydroepiandrosterone and androstenedione persisted throughout the study, even in two ovariectomized patients, indicating a certain degree of autonomy or a greater resistance of adrenal 'androgens' to the inhibition of ACTH secretion. Except in the ovariectomized patients, plasma testosterone did not fall significantly whereas the plasma oestrogens tended progressively towards undetectable concentrations. A similar response was found in six normal postmenopausal women although the disappearance of their oestrogens was relatively rapid. This indicates that much of the testosterone present after the menopause could still be produced by the ovaries whereas the ovarian production of oestrogens becomes negligible. The delayed disappearance of oestrogens in the patients with mammary carcinoma indicates that the persisting adrenal 'androgens' remained efficient precursors of oestrogen synthesis within the peripheral tissues and presumably within the mammary tumour itself. Plasma dihydrotestosterone behaved like the plasma oestrogens. Despite the fall in plasma oestrogens, plasma gonadotrophins did not increase further but plasma prolactin rose progressively. The persistance of steroid sex hormones and the rise of plasma prolactin might explain the poor response to dexamethasone treatment in mammary carcinoma.
Aged↗
Gonadal function in chronic alcoholic men.
Alcoholism affects nine million individuals in the United States according to United States Government estimates. As many as 80% of hard-core alcoholic men show evidences of feminization including impotence, testicular atrophy, sterility, gynecomastia and changes in bodily hair. The causes of feminization of male alcoholics have remained obscure until recently. Largely as a result of advances in the techniques of measurement of sex hormones, it has become possible to begin to examine the pathogenesis of feminization. The results of initial studies suggest that alcoholics become feminized through the secondary effects of alcohol-induced liver disease, and also through primary effects of alcohol on the endocrine system. It can be shown that liver disease permits the peripheral escape of steroid precursors and their conversion to estrogenic substances. These substances are then inadequately cleared by the liver. In addition, however, alcohol alters testicular steroidogenesis and testosteronogenesis. Hypothalamic-pituitary function also is diminished in chronic alcoholics, and this change contributes to the syndrome of feminization.
Alcoholism↗
The occurrence of C19 steroids in testicular tissue and submaxillary glands of intersex pigs in relation to morphological characteristics.
Five true hermaphrodite pigs and two male pseudohermaphrodite pigs were studied. A 38XX sex chromosome constitution was found in peripheral leucocytes of three true hermaphrodites and in one male pseudohermaphrodite; XX/XY mixoploidy was present in the leucocytes of the remaining male pseudohermaphrodite. The occurrence of C19 steroids, including 16-androstenes, in the testicular tissue and submaxillary gland of intersex pigs was of a similar pattern to that found previously in mature boars, and masculinization of the genital tract was related to the amount of testicular tissue present. It is postulated that in the absence of germ cells in the testicular tissue of intersex pigs the Sertoli cells may be involved in the metabolism of dehydroepiandrosterone to 5-androstenediol, a possible testosterone precursor in the pig. The high levels of 16-androstenes found in the submaxillary gland of intersex pigs indicates that these steroids are responsible for 'boar taint' in these animals. In contrast to the boar, no consistent relationship was found between the occurrence of C19 steroids and the degree of masculinization of the submaxillary gland; it is postulated that the predominantly female genetic constitution may have affected the response of the salivary gland to androgen.
Androstenediols↗
Origin of estrogen in isosexual precocious pseudopuberty due to a granulosa-theca cell tumor.
The purpose of the present study was to quantify the rates of production and to define the mechanism(s) or origin of sex steroid hormones in a 3 1/2-year-old girl with isosexual precocious pseudopuberty caused by a granulosa-theca cell tumor of the ovary. The results suggest that the hyperestrogenism occurs principally due to the secretion of estradiol-17beta synthesized de novo by the tumor, but that the tumor in vivo was also capable of aromatizing C19 plasma precursor hormones to estrogen.
Child, Preschool↗
Sex hormone production and action.
The mechanisms of the production of estrogens and androgens in women and men are reviewed. Extraglandular estrogen formation from circulating androgens is the principal source of estrogen in men and postmenopausal women. The amount of estrogen formed is dependent upon precursor availability and metabolic factors, such as obesity and hepatic disease. Both androgens and estrogens in the circulation of humans are bound to sex hormone binding globulin which limits their availability to target cell receptors.
Adrenal Glands↗
Endocrine studies in a pubertal male pseudohermaphrodite with 17-ketosteroid reductase deficiency.
UNLABELLED: A 12 year old child (46,XY) with 17-ketosteroid reductase deficiency was investigated. The patient, reared as a female, was first noted to have clitoromegaly at 10 years of age. Increased facial hair, deepening of the voice, acne, increased body hair and minimal breast development were noted at 12 years. delta4-Androstenedione (delta4) in peripheral blood was markedly elevated (1913 ng/100 ml) whereas testosterone (T) was in the male range of Tanner III puberty (240 ng/100 ml). Thus, delta4/T in this patient was 9.4, compared to a normal ration of 0.15 to 0.25. T/DHT was normal (10.5). Oestrone (Oe1) level was slightly elevated (6 ng/100 ml, normal: 2.5-4.5 ng/100 ml). Oestradiol (Oe2) was normal (1.7 ng/100 ml, normal: 1.5-3 ng/100 ml. Oe1/Oe2 was slightly elevated (3.6, normal: 1-2). At laparotomy, testes were found and spermatic vein blood was obtained prior to castration. Androgen determinations of spermatic vein blood demonstrated extremely high delta4 levels (283 microgram/100 ml) and low levels of T (16 microgram/100 ml). delta4/T in spermatic vein was 17, higher than in the peripheral blood, suggesting intact peripheral conversion of delta4 to T. Incubation of testes slices with delta4 demonstrated severely impaired conversion to T. Conversion of Oe1 to Oe2 was impaired to a lesser degree. CONCLUSION: 17-ketosteroid reductase deficiency was documented in vivo by impaired conversion of precursor hormones resulting in higher than normal delta4T and Oe1/Oe2 ratios in blood. In vitro studies with testes slices confirmed the enzymatic defect.
17-Hydroxysteroid Dehydrogenases↗
Factors affecting the excretion of common neutral steroids in urine.
After a brief summary of the biosynthesis, production rates, metabolism and elimination of the pertinent adrenocortical and gonadal precursors for the common urinary neutral steroids, a survey is presented of the general, disease related and hormonal factors that can affect the excretion of neutral steroids in urine.
Adrenal Cortex Hormones↗
Interconversion between 17 beta-hydroxy-5alpha-androstan-3-one (5alpha-dihydrotestosterone) and 5alpha-androstane-3alpha, 17 beta-diol in rat kidney: heterogeneity of 3alpha-hydroxysteroid oxidoreductases.
3alpha-Hydroxysteroid oxidoreductases catalyzing the interconversion between 17 beta-hydroxy-5alpha-androstan-3-one (5alpha-dihydrotestosterone) and 5alpha-androstane-3alpha, 17 beta-diol (3alpha-androstanediol) have been studied in rat kidney. Three enzymes can be distinguished: a soluble NADPH-dependent oxidoreductase, a microsomal NADPH-dependent enzyme and a microsomal NADH-linked enzyme. Traces of the microsomal enzymes are consistently observed in the 108 000 X g supernatant. Studies on crude preparations reveal that these enzymes differ not only in subcellular localization and co-factor requirement, but also in optimum pH, kinetic characteristics, sensitivity to potential steroidal inhibitors and sensitivity to detergents, ionic strength and temperature. Moreover, salient sex differences exist in the activity of all three kidney enzymes. The soluble NADPH-dependent enzyme is more active in female rats whereas both microsomal enzymes are considerably more active in male animals. The microsomal NADH-dependent oxidoreductase displays favorable characteristics to catalyze the 3alpha-dehydrogenation of 3alpha-androstanediol. Evidence is presented that it is mainly this enzyme that enables the kidney to use 3alpha-androstanediol as an efficient precursor for the local formation of 5alpha-dihydrotestosterone.
Androstane-3,17-diol↗
The metabolism in man of (3H)-5alpha-16-androsten-3alpha-ol and of (3H)-5alpha-16-androsten-3-one.
The in vitro metabolism in man of two 16-androstene steroids, 5alpha-16-androsten-3-one and 5alpha-16-androsten-3alpha-ol, has been studied using 3H-labelled tracers. 4 healthy subjects (2 of each sex) were chosen, and each labelled steroid was administered, by a single injection, to 1 man and 1 woman. Disappearance of (3H)-3alpha-androstenol in the subjects receiving this compound followed a curve which indicated a two-pool distribution in both cases; metabolic clearance rates for these subjects were found to be 3,790 1/24 h in the man and 3,120 1/24 h in the woman. Blood production rates calculated for the 3alpha-androstenol-treated subjects were 875 microgram/24 h in the man and 1,780 microgram/24 h in the woman. Recovery of 3H in the urine of all 4 subjects was very low, between 28 and 42%. Conversion of the injected precursors to urinary 3alpha-androstenol was 13.5 and 12.7% in the 2 men and 6.1 and 5.9% in the 2 women. The male subjects were found to have a lower 24-hour urinary 3alpha-androstenol output (570 and 387 microgram/24 h) than the average for men of their age. The urinary 3alpha-androstenol output in the women was 225 and 276 microgram/24 h, and was within the normal range for women. The urine production rates of 3alpha-androstenol were 2,470 and 4,090 microgram/24 h in the male and female subjects, respectively; the difference between the blood and urine production rates of this compound are thought to indicate the direct secretion of conjugates. Urine production rates of 5alpha-androstenone (measured as 3alpha-androstenol) were 2,370 and 4,340 microgram/24 h in the male and female subjects, respectively.
Adult↗
The effect of progesterone on brain and body growth of chick embryos.
It has been suggested that in the embryo hormonal steroids may act also as control factors for the growth of neural systems. In the present work progesterone was introduced onto the chorioallantoic membrane of the chick embryo on day 7 or days 7 and 10 of incubation. The embryo, dissected at day 10, showed significant increases in body weight and cerebral hemispheres weight. The response at day 13 was less pronounced; male embryos responded to progesterone more than the female embryos. Progesterone is a precursor to other corticosteroids, but corticosterone itself had a significant harmful effect on embryonal growth. Several possible explanations of these results have been offered. It appears that progesterone itself promotes the growth of the early embryo, but the effect depends on its age and sex.
Animals↗
The effects of gonadectomy on monoamine metabolism in three regions of mouse brain.
The concentrations 5-hydroxytryptamine, noradrenaline, their precursors and metabolites have been determined in three regions of mouse brain following gonadectomy; the rates of depletion of 5-hydroxytryptamine and noradrenaline following synthesis blockade have also been examined. Previous investigations have shown that gonadectomy results in changes in hypothalamic catecholamine metabolism; this report shows that changes are not confined to the hypothalamic area and suggests that the effects in other areas of the brain may contribute to the increased incidence of mental disturbances in man when hormone levels are drastically altered. Gonadectomy results in reduced 5-hydroxytryptamine and 5-hydroxyindoleacetic acid concentrations in all regions of the mouse brain. Normetanephrine concentrations are significantly increased and the rate of depletion of noradrenaline from the brain following synthesis blockade is markedly accelerated following gonadectomy; this suggests that circulating steroid sex hormones may exert a stabilising effect on brain catecholamine stores.
Animals↗