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Query: UMLS:C0848255 (female puberty)
 121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The growth curves of the endocrine glands in female puberty are described. Adrenarche with an elevated production of adrenal dehydroepiandrosterone marks the beginning of prepuberty. By decrease of hypothalamic sensitivity to sexual steroids begins the deviation of FSH and LH levels. Significant increases of gonadotrophins and prolactin occur during sleep. There is a good correlation between bone age, Tanner-stages of breast and pubic hair development and steroid hormone levels. Criteria of maturity for young girls including menarche and ovulation are given.
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PMID:[Hormonal regulation and hormone therapy in childhood and adolescence. Part 1: development of endocrine glands, hormone production, menarche and secondary sex characteristics]. 21 73

Experiments were performed in rats to study the role played by ovarian estrogens, the hypothalamus, the medicortical amygdala, and the ventral hipopcampus in the neurohormonal control of female sexual maturation. The results obtained demonstrated that the ovulation-inducing effect of a single administration of estradiol benzoate (EB) to immature female rats is not tantamount to the induction of precocious puberty. Long-term treatment with very low doses of EB, however, can accelerate sexual maturation, although it was established that the endogenous ovarian estrogen secretion during prepuberal life is not essential for the maturation of the cyclic ovarian function. Implantation of very low quantities of EB into the mediobasal hypothalamus of ovariectomized immature and postpuberal female rats revealed that the hypothalamic sensitivity to the LH-inhibiting effect of estrogen exhibits a gradual decrease that begins some days prior to the onset of puberty. It may be responsible for a temporary elevation of the LH level in the blood triggering final maturation of the ovarian follicles and an increase of estrogen secretion. - Studies on the influence of the limbic system on female sexual maturation lead to the following conclusions: 1. The mediocortical amygdala has an essential function in the maturation of the positive estrogen feedback. 2. An LH-inhibiting activity not related to the negative estrogen feedback is exerted by this nuclear region during critical periods of sexual maturation. It may form an additional protective mechanism against precocious stimulation of the ovaries. 3. By means of its stimulatory action on growth hormone and FSH secretion, the ventral hippocampus may be involved, by cholinergic mechanisms, in the interrelationships between metabolism and the onset of female puberty. The results which suggest a significant role of the limbic system in the control of female sexual maturation will be discussed with regard to recent data obtained in girls and women.
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PMID:Experimental studies on the neurohormonal control of female puberty. 53 37

The rate at which girls progress through the stages of puberty in relation to body fat mass and body fat distribution and its relation to their hormonal profiles was studied. Sixty-eight schoolgirls participated in a longitudinal study during 3 yr. The girls were divided into subgroups with increasing skinfold thicknesses and waist-hip ratio. They were also grouped depending on Tanner's breast development classification (M2 and M3). The age at M2 was only marginally correlated with the menarcheal age, but the age at M2 and the time interval from that age to menarche was negatively correlated. Age at the onset of puberty was not related to body fat mass or distribution. The rate of pubertal development after pubertal stage M3 was negatively related to the body fat mass. Age at M2 was only correlated with estrone (E1), while the rate of pubertal development was associated with higher FSH, E1, estradiol (E2), the fraction of E2 that was not bound to sex-hormone-binding globulin (non-sex-hormone-binding globulin bound E2) and androstenedione plasma levels at the onset of puberty. Body fat distribution, rather than body fat mass was related to the total and the non-sex-hormone-binding globulin bound plasma levels of E2 and testosterone at the onset of puberty. Changes in body fat distribution in early female puberty were chiefly related to the waist circumferences. We found no evidence that body fat mass or body fat distribution triggers the onset of puberty. Body fat distribution was related to early pubertal endocrine activity. Body fat mass was negatively related to the rate of pubertal development toward menarche, but no clear indications for an endocrine-related process is found. We conclude that onset of puberty and menarche are not parallel pubertal events, and that early pubertal plasma E1, E2 and androstenedione levels are predictors for the rate of pubertal development toward menarche. We propose that the control of the onset of puberty and maturation of the hypothalamic-pituitary gonadal axis, with regard to negative feedback control, are at least partially independent. This induces on the average a "catch up" pubertal maturation in girls with a late onset of puberty.
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PMID:Body fat mass, body fat distribution, and pubertal development: a longitudinal study of physical and hormonal sexual maturation of girls. 163 45

The increases in serum immunoreactive (RIA) LH and FSH concentrations during puberty are small and of limited value in the evaluation of pubertal development. We, therefore, used highly sensitive time-resolved immunofluorometric assays to evaluate the changes in LH and FSH during female puberty. The sensitivity of the LH assay was 0.02 IU/L, and that of the FSH assay was 0.01 IU/L. Fifty normal premenarcheal girls, 7-12 yr old, 15 postmenarcheal girls, 16 to 17 yr old, and 15 adult women, 24-29 yr old, were studied. In postmenarcheal women, the blood samples were taken on cycle days 4-7. Serum estradiol concentrations were measured by RIA, and pubertal stages were graded. Serum LH levels in prepubertal girls were very low; the mean concentration was 0.05 IU/L. All girls less than 10 yr of age had serum LH concentrations below 0.2 IU/L, while FSH levels varied from 0.3-2.0 IU/L. The earliest significant changes in serum LH, FSH, and estradiol levels took place simultaneously at 9-10 yr of age. The increase in serum FSH was gradual, but the increase in serum LH was sudden and very steep, coinciding with the increase in serum estradiol and the onset of physical puberty. The increase in the mean LH concentrations between the 7-yr-old and the adult group was 116-fold, that for estradiol was 12-fold, and that for FSH was 6.7-fold. These results suggest that the increase in serum LH is important at the onset of puberty, and LH concentrations are a sensitive indicator of pubertal development.
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PMID:Serum luteinizing hormone concentrations increase 100-fold in females from 7 years to adulthood, as measured by time-resolved immunofluorometric assay. 249 66

This study assessed the effect of a dietary deficiency in the essential fatty acids (EFA) linoleic and linolenic acids on the onset of female puberty. EFA deficiency was produced in female rats by means of a semipurified diet and was biochemically documented by analyzing serum and erythrocyte fatty acid levels of more than 30 fatty acids, including all members of the n-6 and n-3 series. Levels of linoleic acid (18:2 n-6) and all n-6 derivatives, particularly arachidonic acid, were strikingly reduced. A less pronounced but clear-cut decrease in n-3 fatty acids, including docosahexaenoic acid (22:6 n-3) was also found. The times of puberty and first ovulation, as assessed by the ages at vaginal opening and first diestrus, were significantly delayed in EFA-deficient rats. The mechanisms underlying this delay appear to reside at both hypothalamic and ovarian sites. Simulation of preovulatory plasma estradiol (E2) levels via implantation of E2-containing Silastic capsules evoked a LH surge 30 h later in control juvenile rats, but not in EFA-deficient animals, indicating a delay in the development of the hypothalamic component of E2-positive feedback in the latter group. This delay appears to be due at least in part to reduced prostaglandin E2 (PGE2) synthesis, as the ability of the neurotransmitter norepinephrine to induce PGE2 release from median eminence nerve terminals was markedly reduced in EFA-deficient rats compared with that in controls. The decrease in hypothalamic PGE2 release was related to the EFA deficiency and not to reduced PG synthase activity, as determined by HPLC analysis of PG synthase products derived from exogenous [14C]arachidonic acid. Basal and hCG-stimulated PGE2 synthesis was also compromised in ovaries from EFA-deficient rats. Depressed gonadal function resulting from the EFA deficiency was further evidenced by a reduced gonadotropin receptor content, a blunted E2 response to hCG in vitro, and an increase in mean serum FSH levels. These results suggest that the delay in puberty resulting from EFA deficiency is due to a reduced availability of arachidonic acid for synthesis of bioactive metabolites. This results in delayed development of both the hypothalamic and ovarian components of the reproductive axis.
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PMID:Essential fatty acid deficiency delays the onset of puberty in the female rat. 275 37

Ovaries of 23- and 35-day-old rats were transplanted under the kidney capsules of 31- and 23-day-old females, respectively. The recipient rats were ovariectomized on the fourth day after transplantation, and the onset of puberty was recorded. Neither the age and body weight at vaginal opening and first ovulation nor the length of the first ovarian cycle differed significantly between the experimental rats and sham-transplanted or untreated controls. Estimation of the serum FSH an LH concentrations before and after ovariectomy provided no evidence that different gonadotropic responses had masked puberty-delaying or puberty-advancing effects of the implanted immature and prepuberal ovaries, respectively. The results suggest that the developmental stage of the ovaries is not a decisive factor in the control of the onset of female puberty.
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PMID:Failure to demonstrate a significant influence of ovarian maturity on the onset of puberty in female rats. 679 8

Studies in female rats have shown that transforming growth factor alpha (TGF alpha) stimulates release of luteinizing hormone-releasing hormone (LHRH), the neuropeptide controlling sexual maturation, and that expression of the TGF alpha gene in the hypothalamus increases during both the initiation of normal puberty and after hypothalamic lesions that induce sexual precocity. Since blockade of epidermal growth factor receptors (EGFR), which mediate TGF alpha actions, delayed the normal timing of puberty, it was postulated that TGF alpha/EGFR contributes to the neuroendocrine process that underlies the initiation of normal female puberty. The present study was undertaken to examine the hypothesis that hypothalamic expression of the TGF alpha gene and its receptor changes in relation to the stage of sexual development in nonhuman primates, and to determine whether these changes are accompanied by corresponding alterations in LHRH gene expression. DNA fragments complementary to the coding regions of the rhesus monkey TGF alpha, EGFR and LHRH genes were cloned by reverse transcription-polymerase chain reaction (RT-PCR), sequenced and used to prepare monkey-specific antisense RNA probes. A quantitative RT-PCR was developed in which the cloned sequences were utilized to prepare RNA standards for the quantitation of tissue mRNA levels. Both TGF alpha and EGFR mRNA levels in the medial basal hypothalamus and preoptic area of female monkeys were elevated during neonatal life (1 week to 6 months of age), when FSH secretion is also high, decreased during juvenile development (8-18 months of age), when secretion of both FSH and LH is low, and markedly increased during the expected time of puberty (30-36 months of age). No such changes were observed in either the cerebellum or the cerebral cortex, two brain regions irrelevant to neuroendocrine reproductive control. In contrast to the pronounced alterations in hypothalamic TGF alpha/EGFR gene expression observed during sexual development, LHRH mRNA levels did not vary significantly during this time. Hybridization histochemistry revealed the presence of both TGF alpha and EGFR mRNAs in cells scattered throughout the hypothalamus, but more predominantly in the median eminence, suprachiasmatic nuclei, optic chiasm and cells along the wall of the third ventricle. These results demonstrate that increases in TGF alpha and EGFR gene expression, specific to the neuroendocrine brain, occur during developmental phases in which gonadotropin output is also elevated--most noticeably at the time of puberty.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Developmental expression of the genes encoding transforming growth factor alpha and its receptor in the hypothalamus of female rhesus macaques. 754 71

Concentrations of LH and FSH are known to increase during normal pubertal development, but changes in the isoforms of the gonadotropins at this time have not been investigated in depth. We examined the median charge of serum LH and FSH using agarose suspension electrophoresis in 81 normal children at pubertal stages I-V. In pubertal girls there were no significant (P > 0.05) differences in the median charge of LH, but there was a small (P = 0.05) shift to more acidic FSH isoforms between pubertal stages I and IV. In boys there was a significant (P < 0.01) shift to more acidic isoforms for both LH and FSH by pubertal stage II. Further changes were not found later in puberty. Except for LH at pubertal stage I, where the median charge was similar (P > 0.05) for both sexes, the median charge was more basic (P < 0.001) for both LH and FSH in girls compared with boys at all five pubertal stages. The degree of charge heterogeneity of FSH, estimated as the peak width at half the peak height, was significantly (P < 0.01) larger at pubertal stage I than at pubertal stages III-V in both boys and girls. The charge heterogeneity of LH was similar for all pubertal stages in both sexes. In conclusion, there were few qualitative changes in the gonadotropins during normal female puberty, whereas in the male there was a dramatic shift to more acidic isoforms of LH and FSH early in puberty. This information may assist our understanding of normal and pathological processes during puberty and may be of clinical relevance in detecting the initiation of puberty in boys.
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PMID:Changes in the isoforms of luteinizing hormone and follicle-stimulating hormone during puberty in normal children. 928 52

To investigate hormonal changes before the onset of female puberty, we measured LH and FSH in serum samples drawn every 20 min for 24 h and measured testosterone and estradiol hourly for 24 h. Seventeen girls (13 prepubertal and 4 early pubertal) of short stature, from 5.1-11.4 yr of age, participated in this study. LH and FSH were measured using a time-resolved immunofluorometric assay, and testosterone and estradiol were measured using a sensitivity RIA capable of detecting testosterone and estradiol concentrations of 10 and 2 pg/mL, respectively. Diurnal rhythms of LH, FSH, and testosterone were apparent in all subjects, including those aged 5-6 yr. Serum LH and FSH concentrations showed night-day variation in a pulsatile fashion. The serum testosterone concentration was elevated in the early morning in all subjects. The serum estradiol concentration was elevated in the early morning in 4 of 13 prepubertal subjects and all 4 early pubertal subjects. The diurnal pattern of the serum estradiol concentration was similar to that of the serum testosterone concentration. Mean 24-h LH and testosterone concentrations in prepubertal subjects who did not attain puberty for at least 1 yr were 0.07 U/L and 65 pg/mL, respectively, whereas those in prepubertal subjects who attained puberty within 1 yr (0.14 U/L and 106 pg/mL, respectively) were significantly higher. Furthermore, mean 24-h LH, FSH, testosterone, and estradiol concentrations increased with the onset of puberty. In conclusion, the diurnal rhythms of LH, FSH, and testosterone already exist at 5-6 yr of age, and serum LH and testosterone levels increase before the onset of puberty. These results suggest that preparation for the onset of female puberty may begin in 5- to 6-yr-old girls.
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PMID:Diurnal rhythms of luteinizing hormone, follicle-stimulating hormone, testosterone, and estradiol secretion before the onset of female puberty in short children. 1072 42

In recent years, animal models of puberty in children have focused on factors responsible for the developmental increase in gonadotropin secretion independent of gonadal negative feedback. Although the testis may play little if any role in timing the initial increase in gonadotropin secretion in the male, the situation may be different for the female. The present study tested the hypothesis that removal of endogenous estradiol by ovariectomy would produce an immediate increase in nocturnal but not daytime LH and FSH concentrations, an effect reversed by estradiol replacement. Morning (1000 and 1030 h) and evening (2200 and 2230 h) concentrations of bioactive LH and, in selected samples, immunoreactive FSH were evaluated in young juvenile female rhesus monkeys (n = 7) before and after ovariectomy at 13 months of age. Evening but not morning concentrations of gonadotropins were significantly increased within 2 wk of ovariectomy, whereas estradiol replacement returned these to presurgical levels and to those observed in age-matched, gonadally intact females (n = 7). By 145 d after ovariectomy, or approximately 17 months of age, evening as well as morning concentrations of LH were significantly higher than concentrations seen immediately after surgery. Estradiol replacement at approximately 18 months of age suppressed both morning and evening LH but not to the degree seen during a similar treatment after ovariectomy. These data support the hypothesis that, for the female, the developmental rise in diurnal gonadotropin secretion is controlled by a gonad-independent mechanism as well as a gonadal negative feedback inhibition. The importance of gonadal restraint on gonadotropin secretion in young juvenile females is evident only in samples obtained during the evening. These data underscore the notion that, for the female puberty, onset, at least in terms of gonadotropin secretion, is a misnomer and that puberty reflects a progression in multiple control mechanisms that ultimately time the attainment of fertility.
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PMID:Estradiol negative feedback regulates nocturnal luteinizing hormone and follicle-stimulating hormone secretion in prepubertal female rhesus monkeys. 1529 35


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