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Biomedical subjects

F Cassorla

Publications and source records attributed to F Cassorla.

70 records · Page 4Linked to original sources
PubMed1984

The effects of prolactin on rat ovarian function.

Hyperprolactinemia has been associated with several reproductive disorders. To investigate whether hyperprolactinemia directly affects rat ovarian function, we examined the ovarian histopathology and the activities of the four ovarian enzymes 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), 17-hydroxylase (17-OH), 17,20-desmolase (17,20-D) and aromatase in hyperprolactinemic rats and controls. Hypophysectomized, gonadotropin-treated Fisher rats were made hyperprolactinemic by isografting pituitary glands under the kidney capsule. The control animals received skeletal muscle. The ovaries were resected, pooled according to prolactin levels and microsomal enzyme activities were measured from each pool. Prolactin (PRL) levels were 344 +/- 23 ng/ml in the hyperprolactinemic rats and 18 +/- 5 ng/ml in the controls (p less than 0.001). Estradiol concentrations were 609 +/- 47 pg/ml in the hyperprolactinemic animals and 56 +/- 13 pg/ml in the controls (p less than 0.001). Ovarian and uterine weights were significantly higher in the hyperprolactinemic rats (p less than 0.02). Ovarian histopathology demonstrated benign polycystic transformation in the hyperprolactinemic animals. Hyperprolactinemia had no effect on 3 beta-HSD, but was associated with significant decreases in the 17-OH, 17,20-D and aromatase activities when compared to controls (p less than 0.001). We conclude that prolactin has a direct effect on rat ovarian function which appears to be independent of changes in gonadotropin secretion.

3-Hydroxysteroid Dehydrogenases↗
PubMed1984

Direct effect of the luteinizing hormone releasing hormone analog D-Trp6-Pro9-Net-LHRH on rat testicular steroidogenesis.

The luteinizing hormone releasing hormone analog D-Trp6-Pro9-Net-LHRH (LHRHa) inhibits rat testicular testosterone secretion. To determine whether LHRHa decreases serum testosterone concentrations solely by inhibiting gonadotropin secretion or, in addition, by influencing directly testicular testosterone biosynthesis, we examined the effects of LHRHa on the activities of 5 key testicular steroidogenic enzymes. Thirty hypophysectomized, hOG treated rats were given either LHRHa (1 micrograms sc/day) or saline during 7 days. The LHRHa treated animals exhibited a significant decrease of serum testosterone when compared to the control group (498 +/- 37 ng/dl vs 2044 +/- 105 ng/dl, mean +/- SEM, P less than 0.001). 17-Hydroxyprogesterone serum levels were also decreased in the LHRHa treated rats (61 +/- 6 ng/dl vs 93 +/- 7 ng/dl, P less than 0.005), while serum progesterone levels were similar in both groups of animals. These changes in steroid concentrations were associated with decreases in the microsomal enzyme activities of 17-hydroxylase (37 +/- 9 vs 654 +/- 41 pmol/mg protein/min, P less than 0.001), 17,20-desmolase (103 +/- 9 vs 522 +/- 47 pmol/mg protein/min, P less than 0.001), 3 beta-hydroxysteroid dehydrogenase (1.7 +/- 0.02 vs 4.1 +/- 0.1 nmol/mg protein/min, P less than 0.001), aromatase (95 +/- 7 vs 228 +/- 6 pmol/mg protein/min, P less than 0.001) and 17-ketosteroid reductase (167 +/- 9 vs 290 +/- 18 pmol/mg protein/min, P less than 0.01) in the LHRHa treated animals. These findings indicate that LHRHa can inhibit directly rat testicular testosterone biosynthesis.

17-alpha-Hydroxyprogesterone↗
PubMed1984

Effects of the luteinizing hormone-releasing hormone (LHRH) analog D-Trp6-Pro9-NEt-LHRH on the pituitary-gonadal axis of prepubertal rhesus monkeys.

To elucidate whether the luteinizing hormone-releasing hormone (LHRH) analog D-Trp6-Pro9-NEt-LHRH (LHRHa) decreases plasma testosterone levels in male primates solely by inhibiting gonadotropin secretion or, in addition, by inhibiting testicular testosterone biosynthesis, we have investigated the effects of this drug on 6 infant male rhesus monkeys. Three animals received LHRHa (12 micrograms . kg . day s.c., experimental group), and 3 animals received saline injections (control group) during the first 2 mo of life. Mean plasma testosterone was significantly lower in the experimental group compared to the control group (54 +/- 7 ng/dl vs. 501 +/- 52 ng/dl, P less than 0.001). The experimental group also had significantly lower mean follicle-stimulating hormone (FSH; 5.1 +/- 0.2 microgram/ml vs. 9.6 +/- 0.7 microgram/ml, P less than 0.001), and bioactive luteinizing hormone (LH; 2.0 +/- 0.08 microgram/ml vs. 3.5 +/- 0.2 microgram/ml, P less than 0.001). To study whether LHRHa influences testicular function directly, all animals were treated with human chorionic gonadotropin (hCG; 100 mIU . kg . day i.m.) for 28 days beginning at 8 mo of age. During Days 15 through 28 we administered LHRHa 12 micrograms . kg . day s.c. to the experimental animals and saline injections to the control group. Plasma testosterone increased to 5827 +/- 557 ng/dl in the experimental group and 4440 +/- 897 ng/dl in the control group after 14 days of hCG treatment. Plasma testosterone concentrations decreased in both groups of animals from Days 15 to 28 fo the study. All steroid intermediates were similar in both groups of animals on Days 14 and 28.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

True precocious puberty complicating congenital adrenal hyperplasia: treatment with a luteinizing hormone-releasing hormone analog.

Congenital adrenal hyperplasia (CAH) is a recognized cause of precocious pseudopuberty. Some children with CAH also develop true precocious puberty with early maturation of the hypothalamic-pituitary-gonadal axis. We have seen four such children (three boys and one girl) who had the diagnosis of CAH made between the ages of 3 and 6 yr. These patients were treated with standard doses of hydrocortisone and fludrocortisone. A diagnosis of true precocious puberty was made because of testicular enlargement in the boys, breast development in the girl, progressive pubic hair development, rapid growth, and rapid bone age maturation. Plasma steroid levels were elevated for age, and gonadotropin levels were within the normal pubertal range, both basally and in response to LHRH stimulation. We treated these children with daily sc injections of a LHRH analog (LHRHa) for 6-18 months in addition to the standard hydrocortisone and fludrocortisone therapy for CAH. LHRHa significantly decreased basal plasma LH and FSH, peak LH and FSH responses to native LHRH, and testosterone levels. Testis size decreased in the males, and breast development regressed in the female. LHRHa therapy led to significant decreases in linear growth rate, ulnar growth rate, and rate of bone age advancement. These results suggest that LHRHa is an effective adjunct to hydrocortisone and fludrocortisone in the treatment of true precocious puberty complicating CAH.

Adrenal Hyperplasia, Congenital↗
PubMed1984

Dose-response relationships for the effects of growth hormone-releasing factor-(1-44)-NH2 in young adult men and women.

Human GRF-(1-44)-NH2 (GRF-44) was administered iv in graded doses of 0.01-10 micrograms/kg to 35 normal young adult men and 38 women. GRF-44 stimulated the release of GH in a dose-dependent fashion, although the individual responses varied widely. The ED50 values for this effect were 0.4 micrograms/kg in men and 0.2 micrograms/kg in women in the midfollicular phase of the menstrual cycle. Maximal responses in men and women were not significantly different, and a dose of 1 micrograms/kg was sufficient to produce a maximal response. There was, likewise, no difference between responses of women tested in the midfollicular and midluteal phases of the cycle. There were no changes in PRL, LH, FSH, TSH, ACTH, beta-endorphin, or cortisol at doses up to 1 microgram/kg; at 10 micrograms/kg, PRL increased by an average of 7.6 ng/ml in the women. Side effects occurred in approximately 20% of both men and women at 1 microgram/kg and in nearly all subjects given 10 micrograms/kg; these consisted primarily of flushing and a sense of warmth. Thus, a dose of 1 microgram/kg GRF-44 is safe and effective, and would appear to be a reasonable choice for use in studying GH responses in normal subjects of other ages and in patients with disorders of GH secretion.

Adolescent↗
PubMed1984

Steroid and gonadotropin secretion in a patient with a 30-year history of virilization due to lipoid-cell ovarian tumor.

A 36-year-old woman with a 30-year history of undiagnosed virilizing lipoid-cell ovarian tumor is described. The tumor was localized by the NP-59 scan. Data of extensive investigations of steroid and gonadotropin secretion are provided. The preoperative dynamics of serum dehydroepiandrosterone sulfate and its decrease after the removal of the tumor suggested that dehydroepiandrosterone sulfate was being secreted by the ovarian tumor. Ovarian-peripheral venous gradients for plasma delta 5 and delta 4 steroids were correlated with the in vitro measurements of various steroidogenic enzymatic activities in the tumor tissue. The proposed metabolic pathway of the tumor is as follows: Pregnenolone----17-hydroxypregnenolone----dehydroepiandrosterone---- androstenedione----testosterone----estradiol. Low basal gonadotropin levels with no discernible pulsatility and no response to gonadotropin-releasing hormone were observed preoperatively, and a gradual normalization in both parameters was observed during the six months after removal of the tumor.

Adosterol↗
PubMed1983

Effects of a growth hormone releasing factor in man.

The effects of the 44-amino acid growth hormone releasing factor (GRF-44) were tested in normal adult men and women. At a dose of 1 microgram/kg, intravenous boluses of GRF-44 stimulated prompt elevations of plasma GH, which in 5 men reached maximum levels of 34 +/- 28 (S.D.) ng/ml, and in 3 women in the mid-follicular phase, 53 +/- 10 ng/ml. The action of GRF was highly selective; there were no changes in plasma PRL, LH, FSH, TSH, or cortisol at this dose level. Side effects, mostly flushing and a sense of warmth of the face and chest, were mild and occurred only in a minority of subjects.

Adult↗
PubMedDate not supplied

Serum 21-deoxycortisol and 17-hydroxypregnenolone in parents of patients with congenital adrenal hyperplasia.

The response of serum 21-deoxycortisol (21-DF), 17-hydroxypregnenolone (17-OHPE), 11-deoxycortisol and cortisol to iv ACTH, was compared in 14 adult controls ane and post stimulation concentrations of hormones were similar in controls and parents, except for those of 21-DF, which were significantly greater in heterozygotes 30 min (p less than 0.005), 60 min (p less than .0025) and 90 min (p less than 0.005) after stimulation with ACTH. When rates of increase were determined, those of 21-DF at 30, 60 and 90 min were significantly higher in the parents. Sixteen of the 26 parents (62%) had a rate of increase of 21-DF from 0 to 60 min greater than the mean plus two standard deviations of the control group. Using this same criteria, 11 of the 13 mothers (85%) of affected children could be identified as heterozygotes. The rate of increase of 21-DF from 0 to 60 min following ACTH provides a method for the detection of some heterozygote carriers of congenital adrenal hyperplasia and may be useful particularly in the identification of female carriers.

17-Hydroxycorticosteroids↗
PubMedDate not supplied

GH-IGF axis during catch up growth in small for gestational age (SGA) infants.

The hormonal profile in 47 small for gestational age (SGA) term newborns during their first year of life was studied. The newborns had a mean birth weight of 2290 +/- 230 g and a length of 45.5 +/- 2.0 cm, and they were followed up every month. Serum IGF-I, IGF-II, and urinary growth hormone (u-GH) concentrations were measured at 3 days of age and every 3 months during one year. Serum IGFBP-3 levels were measured at 3 and 6 months of age. Catch up growth (CUG) was defined as an increase in length z score greater than 1 SD between birth and 6 months of age. According to this definition, 27 infants (57.4%) experienced CUG. We compared the hormonal profile of the infants who demonstrated evidence of CUG [CUG(+)] with those who did not [CUG(-)]. Serum IGF-II levels were significantly higher in CUG(+) infants compared to CUG(-) infants at 3 months of age. We did not find any differences in serum IGF-I, IGFBP-3 and urinary GH between CUG(+) and CUG(-) infants at any time during the study.

Birth Weight↗
PubMedDate not supplied

Gps mutations in Chilean patients harboring growth hormone-secreting pituitary tumors.

Hypersecretion of GH is usually caused by a pituitary adenoma and about 40% of these tumors exhibit missense gsp mutations in Arg201 or Gln227 of the Gs, gene. We studied 20 pituitary tumors obtained from patients with GH hypersecretion. One tumor was resected from an 11 year-old boy with a 3 year history of accelerated growth, associated with increased concentrations of serum GH and IGF-I, which were not suppressed by glucose administration. The remaining 19 tumors were obtained from adult acromegalic patients, who had elevated baseline serum GH levels that did not show evidence of suppression after administration of glucose. The gsp mutations were studied by enzymatic digestion of the amplified PCR fragment of exon 8 (Arg201) and exon 9 (Gln227) with the enzymes NlaIII and NgoAIV, respectively. The tumors obtained from the boy and from nine of the 19 patients with acromegaly exhibited the gsp mutation R201H. None of the tumors had the Gln227 mutation. The gsp positive patients tended to be older, had smaller tumors, and had preoperative basal serum GH levels which were significantly lower (21 +/- 6 vs 56 +/- 16 microg/l, p<0.05) than the gsp negative patients. In this study, we documented the presence of a gsp mutation in Arg201 in a boy with gigantism and in approximately half of 19 Chilean adult patients with acromegaly, similar to other populations.

Adenoma↗
PubMedDate not supplied

Relationship between serum growth hormone binding protein levels and height in young men.

The biochemical mediators responsible for variations in stature among normal subjects are largely unknown. To obtain some initial information about potential endocrine factors, we measured the serum concentrations of GH, IGF-1, IGFBP-3 and GHBP in healthy young men shorter than 159 cm and taller than 187 cm. We studied 14 volleyball and basketball players (tall group), and 14 jockey students from a horse racetrack (short group). A careful medical history was taken, including dietary intake, and physical examination with special attention to the possible presence of genetic stigmata was performed. Serum prealbumin was determined as an index of nutritional status. A buccal smear was performed to exclude Klinefelter's syndrome. The BMI and serum prealbumin levels were comparable in both groups of individuals. The nutritional survey, however, revealed that the tall subjects had a higher intake of calories (42.2+/-11.2 vs. 30.1+/-15.15 kcal/kg, p<0.05), and protein (1.5+/-0.6 vs. 0.8+/-0.4 mg/kg, p<0.01). Serum concentrations of GHBP did not differ in the two groups (0.95+/-0.37 nmol/l in the tall, and 0.95+/-0.53 nmol/l in the short group), and did not correlate with height, serum IGF-I levels, or BMI. We observed a significant difference in the serum concentrations of IGF-I in the two groups of individuals (42.02+/-9.37 nmol/l in the tall and 31.79+/-3.18 nmol/l in the short group, p<0.05), and this growth factor showed a positive correlation with height (r = 0.5, p<0.01). These preliminary findings suggest that final height differences in young men do not appear to be mediated by variations in GHBP concentrations.

Body Height↗
PubMedDate not supplied

Trace minerals in human growth and development.

Trace mineral deficiencies may affect several biological functions in humans, including physical growth, psychomotor development and immunity. We have reviewed the mechanisms whereby several trace mineral deficiencies may affect these biological functions at different ages (fetal life, infancy, childhood and adolescence), as well as the evidence supporting this association. We describe the effects of zinc deficiency on the hormonal regulation of growth and sexual development in both humans and animal models. We provide data regarding the effects of iron deficiency on growth and psychomotor development. We mention the effects of copper, manganese, selenium and iodine deficiencies on growth and development. We conclude that iron deficiency may affect psychomotor development, but does not appear to affect growth. Zinc deficiency may cause growth retardation and psychomotor delay.

Child↗