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Biomedical subjects

M G Forest

Publications and source records attributed to M G Forest.

At least 91 records · Page 5Linked to original sources
PubMed1984

[Kinetics of the testicular steroidogenic response to stimulation with placental gonadotropin in the prepuberal boy].

The kinetics of the plasma level responses of steroid hormones to a single injection of human chorionic gonadotrophin (hCG) (100 Ul/kg) was studied for one week in 7 prepubertal boys. Plasma testosterone levels progressively increased up to 8.22 +/- 1.33 nmol/l, usually at the 100th hour. The kinetics of dihydrotestosterone was quite similar. On the other and, progesterone, 17 alpha-hydroxyprogesterone and delta 4-androstenedione did not change significantly; 17 beta-estradiol slightly increased 5 to 7 days later. This profile of response is deeply different from those observed in adults, in whom are observed an early response (24 hrs) of 17 alpha-hydroxyprogesterone and estradiol and a two-phase response of testosterone. These results show that the hCG-induced steroidogenic desensitization is present only in patients previously exposed to a certain level of gonadotrophic stimulation (endogenous or exogenous).

Adolescent↗
PubMed1983

Role of androgens in fetal and pubertal development.

During fetal development, androgens exert long-term effects which are either organizational on specific organs during a critical phase of morphogenesis (e.g. sexual differentiation of external genitalia), or programming neural functions or enzyme activities expressed later in life. At all stages of development, which extends from fetal and neonatal stages to pubertal accomplishment, androgens also have activational effects that are immediate, multiple, reversible and dose dependent. Both types of actions are intricate during human development. This review will focus (1) on the intricate morphological and activational roles of androgens on sexual differentiation and pubertal development of the genital tract, external genitalia and mammary glands, and (2) on the organizational effects of androgens on four central nervous system functions: pituitary regulation of liver metabolism, gonadotropin secretions, sex dimorphic behavioral patterns, and 'sexualization of the brain'. If the molecular basis of the immediate androgenic action is known, depending of androgen receptor's availability and affinity, little is known of the way androgens exert their influence on either so various morphological processes or neuroendocrine imprinting.

Androgens↗
PubMed1983

[Aggravation of salt loss due to hydrocortisone in the first days of treatment of congenital adrenal hyperplasia caused by 21-hydroxylase deficiency].

The longitudinal study of five infants affected with congenital hyperplasia (CAH) due to 21-hydroxylase deficiency illustrate the aggravation of the salt losing syndrome during the initial period of replacement therapy with hydrocortisone alone, associated or not with salt supplementation as demonstrated by weight loss or failure to thrive, hyponatremia and rise in plasma renin activity. Concomitantly, the plasma levels of both ACTH and aldosterone decreased monkedly. The sodium loss was rapidly normalized following the association of small doses (25 gamma/day) of 9 alpha fluorohydrocortisone to the same glucocorticoid replacement dosage. Initial treatment of infants affected with CAH should therefore include both mineral and glucocorticoid hormones.

Adrenal Hyperplasia, Congenital↗
PubMed1982

[Plasma androgens and testosterone binding globulin levels in hirsute women. Effects of dexamethasone and oestrogen-progestagen administration (author's transl)].

In a group of 19 women with idiopathic hirsutism plasma levels of testosterone binding globulin were significantly lowered, and plasma levels of total and unbound testosterone were significantly raised. After administration of dexamethasone or oestrogenprogestagen combination, the concentrations of free testosterone returned to the normal range for non hirsute women. This suggests that both the ovary and the adrenal cortex were responsible for the high plasma testosterone levels observed in these patients.

Adolescent↗
PubMed1982

Pitfalls in the etiological diagnosis of congenital adrenal hyperplasia in the early neonatal period.

The plasma levels of 8 steroid hormones were studied longitudinally in 20 newborns affected with either 21-hydroxylase (21-OH), 11-hydroxylase (11-OH) or 3 beta-hydroxysteroid deshydrogenase (3 beta-ol) deficiencies during the first month of life. Comparison was also made between the patterns observed according to age at first examination (n = 13 before 8 days of age) and the type of the enzymatic block. The most striking findings were the variability in hormone levels and/or evolution with age and the difficulties in making a definite positive or etiological diagnosis at first examination. In some newborns with untreated 21-OH deficiency, 17 alpha-hydroxyprogesterone levels may start off within the normal range or not so far above it. Also, levels of unconjugated dehydroepiandrosterone and other delta 5 steroids may be so high during the first week of life in all 3 forms that an erroneous diagnosis of 3 beta-ol deficiency could easily be considered. In several cases the etiological diagnosis was only ascertained by multiple steroid determination and/or dynamic tests. These discrepancies were not found in infants studied later on in life. It thus appears that a peculiar steroid pattern is observed in the immediate postnatal period in babies with various enzyme defects, which might be related to the morphological changes occurring in the adrenal cortex at this age.

3-Hydroxysteroid Dehydrogenases↗
PubMed1982

[Does adrenarche really play a determining role in pubertal development? A study of the dissociations between adrenarche and gonadarche. The failure of dehydroepiandrosterone sulfate treatment in delayed adrenarche].

The temporal events of adrenarche (prepubertal shift in adrenal androgen biosynthesis) are described. The mechanisms responsible for the initiation and maintenance of the adrenal secretion of androgens are poorly understood. The hypotheses put forward to explain it are reviewed. The transectional or longitudinal study of the plasma levels of dehydroepiandrosterone, its sulfate (DHAS), delta 4-androstenedione, testosterone, and 170H-progesterone in 121 children with a variety of clinical disorders in which adrenarchal and gonadal maturations are dissociated (precocious adrenarche, precocious or delayed puberty, adrenal insufficiency, gonadal dysgenesis, hypogonadotropism hypogonadotrophic) is presented. Treatment of a group of 10 children, with delayed or absent adrenarche and growth failure, with DHAS at physiological dose, for a mean of two years, failed to induce any change in growth rate, bone maturation, growth of sexual hair, or genitalia, or to advance puberty. A physiological role for adrenal androgens remains to be discovered. The author's concept is that adrenarche represents a "marker of body maturation".

Adolescent↗
PubMed1982

Evidence of excessive androgen secretion by both the ovary and the adrenal in patients with idiopathic hirsutism.

Fifteen patients with idiopathic hirsutism, who had no attenuated adrenal hyperplasia, obesity, enlarged ovaries, or amenorrhea, were studied. Excessive androgen secretion by adrenal tissue was suggested by the finding of increased levels of dehydroepiandrosterone sulfate, which decreased after dexamethasone administration but did not change after human chorionic gonadotropin (hCG) injection. Excessive androgen secretion by ovarian tissue was suggested by the finding that testosterone and androstenedione levels were elevated, correlated significantly with the levels of luteinizing hormone, decreased with administration of estrogen-progestagen, and increased after hCG injection. Notably, free testosterone levels, which were significantly increased, were only partially suppressed during dexamethasone or estrogen-progestagen administration. These results provide further evidence that both the adrenals and the ovaries secrete androgens excessively in patients with idiopathic hirsutism.

Adrenal Glands↗
PubMed1981

Prenatal diagnosis of congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency by steroid analysis in the amniotic fluid of mid-pregnancy: comparison with HLA typing in 17 pregnancies at risk for CAH.

Amniotic fluid (AF) levels of 17-hydroxyprogesterone (17OHP) and testosterone (T) were determined at 16-17 weeks in 17 pregnancies at risk for CAH and results compared to 75 normal controls. The fetus was predicted to be unaffected in 12 cases on the findings of normal AF levels of both 17OHP and T and the latter allowed a correct prediction of fetal sex in all instances. HLA typing confirmed normality in 12 cases revealing 5 carriers, 5 homozygous normal and 2 indeterminate. Steroid levels of the 2 groups were similar. Three fetuses were predicted to be CAH affected on unambiguously high levels of 17OHP and T (in female only). HLA typing was in agreement, and the diagnosis was confirmed in 2 abortuses and a female newborn by physical and hormonal studies. In the last 2 cases AF levels of OHP and T were normal but HLA (A/B/C) genotypes were identical to the CAH affected siblings. Normal physical and hormonal findings in the 2 aborted fetuses would exclude the possibility of an in utero virilizing form of CAH. The discrepancy could be explained on the basis that the fetuses had an allelic form of 21-hydroxylase deficiency or on the basis of recombination (not fully tested). It is concluded that a fully informative prenatal diagnosis of CAH should not rely entirely on HLA typing but on hormonal studies.

Adrenal Hyperplasia, Congenital↗
PubMed1981

Synthesis and stereochemistry of 7 beta- and 7 alpha-amino-, acetamido-, hemisuccinamido- and terephthalamido derivatives of testosterone.

The reduction of 3-ethylenedioxy-7-oximino-5-androsten-17 beta-yl acetate and of its 17 beta-tetrahydropyranyl ether analog with sodium in ethanol, followed by thin-layer chromatography, allowed the isolation of the corresponding 17 beta-hydroxy- and 17 beta-tetrahydropyranyloxy-5-en-7 beta- and 7 alpha-amines which were also characterized as 7-acetamides. The acylation of the two epimeric 17 beta-hydroxy-5-en-7-amines with succinic anhydride followed by selective saponification of the 17 beta-hemisuccinate group and diazomethane esterification, gave the corresponding 17 beta-hydroxy-5-en-7 beta- and 7 alpha-hemisuccinamido methyl esters characterized also as 17 beta-acetates. On the other hand, the acylation of the two 17 beta-tetrahydropyranyloxy-5-en-7-amines with the acid chloride of terephthalic acid monomethyl ester led to the more rigid 7 beta- and 7 alpha-terephthalamido methyl ester side-chains. The acidolysis of the 3-ethyleneketal protecting group of the preceding 5-en-7-N-acyl derivatives regenerated the 4-en-3-oxo function while the 17 beta-tetrahydropyranyl ether group was cleaved simultaneously into the 17 beta-alcohol. The four desired 7 beta- and 7 alpha-hemisuccinamido- and terephthalamido carboxylic side-chain derivatives of 17 beta-hydroxy-4-androsten-3-one (testosterone) were finally obtained by saponification of the corresponding methyl esters.

Stereoisomerism↗
PubMed1981

Perinatal activity of the hypothalamic-pituitary-gonadal axis in the lamb. III. LH, testosterone and prolactin secretory pattern in newborn lambs.

Crossbred male and female lambs from Suffolk rams and Dorset-Finnish ewes born in January and February were studied at 1, 3, 7, 21 and 28 days of age and female lambs at 14 days. Ultradian variations in plasma luteinizing hormone (LH), prolactin (PRL) and testosterone were studied at 30-min intervals during a 4-hour period. In female lambs LH secretory peaks were observed at 7 days of age the amplitude of LH peaks increasing 8-fold between 7 and 14 days and 2-fold between 21 and 28 days. The number of secretory peaks also increased with age. Ultradian variations in PRL were observed from 1 day of age, the amplitude of the PRL peaks increasing also with age. In male lambs, LH and testosterone peaks were observed at 3 days of age, the testosterone peak being preceded by or concomitant with LH peaks. The amplitude of LH peaks increased with age together with basal testosterone levels although the amplitude of testosterone peaks was unchanged. This study demonstrates pulsatile secretion of LH and PRL in lambs of both sexes and of testosterone in male lambs in the first week of postnatal life. In addition, since the ovine testis is responsive to endogenous gonadotropic stimulation at this period, it is suggested that the hypothalamic-pituitary-gonadal axis is already operative at this age. It can be concluded that the hypothalamic activity concerned with pulsatile LH and prolactin secretion is present very early in the lamb neonate.

Animals↗
PubMed1981

Perinatal activity of the hypothalamic-pituitary-gonadal axis in the lamb. IV. Testicular responsiveness to hCG from 1 through 28 days of life.

Previous studies in this laboratory have shown the existence of an early postnatal activation of the hypothalamic-pituitary-gonadal axis (HPGA) in the male lamb which was present at 2 and 4 weeks of age. In order to define more precisely the time sequence of HPGA activity, we have studied the in vivo and in vitro testicular responsiveness to human chorionic gonadotropin (hCG) of the immature lamb at 1, 3, 7, 14, 21 and 28 days of life. Plasma testosterone (T) increments (delta) after hCG were lower in 1-day-old animals than in other age groups. Testicular concentrations of T, dehydroepiandrosterone and 17-hydroxyprogesterone increased from 1 to 14 days. Testicular 17, 20 lyase activity rose significantly with age but was not influenced by hCG. hCG and dibutyryl cyclic AMP increased significantly the T production by enriched interstitial cell preparation at 1, 3, and 7 days, the greatest response being found at 7 days. hCG also increased significantly the T production at 14 days. These data suggest that the lamb testis has the capacity to respond to hCG in vivo and to various stimuli vitro from the 1st day of life and that the response reaches a plateau from 2 to 4 weeks after birth.

Androstenedione↗
PubMed1981

Effects of chronic intermittent immobilization stress on rat testicular androgenic function.

In rats, chronic intermittent immobilization stress induced a drastic fall in the plasma concentration and testicular content of testosterone (T) without detectable changes in plasma LH values. In vitro basal T production by interstitial cell-enriched preparations from stressed rats and the responses to hCG, dibutyryl cAMP, or choleratoxin were suppressed, while cAMP production was not modified. The increase in plasma T concentrations in control animals was identical after the in vivo injection of 5, 10, or 50 IU hCG, while stressed rats failed to respond to 5 IU, but showed a response similar to that of control animals with 10 and 50 IU. These results suggest that chronic intermittent immobilization stress decreases Leydig cell sensitivity to gonadotropins.

Animals↗
PubMed1980

[Variations of testosterone uptake by gonadotropic cells of the adenohypophysis of the rat].

Testosterone (T) could be detected by immunocytochemistry after cryoultramicrotomy and T is likely bound on a binding site of a high affinity. Castration and adrenalectomy involve a swift disappearance of T in the gonadotropic cells. Synthesis of new binding sites was induced by daily T injection in the castrated and surrenalectomized Rat from 90 days. This synthesis is inhibited by cycloheximide. These data suggest that binding sites are proteins. The captation of T by the gonadotropic cells was diminished similarly at the diminution of T, afterwards, T captation was stabilized at a weak level which became stable for several weeks. It seems that immunocytochemistry permits the study of the variation of T captation by Rat pituitary gonadotropic cells.

Adrenalectomy↗