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

The most important therapeutic problems of female puberty and adolescence are discussed, including high stature, amenorrhoea, oligomenorrhea, pubertas tarda, anovulation, anorexia, anisomastia, hypermastia. Indications for treatment are given and the possibilities for a prophylactic medicine in this age group are stressed.
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PMID:[Hormonal regulation and hormone therapy in childhood and adolescence. Part 2: Therapeutic problems (tall stature, amenorrhea, delayed puberty, oligomenorrhea, precocious puberty, anorexia nervosa, anisomastia, hypermastia, acne etc)]. 15 44

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

Insulin resistance (IR) and polycystic ovarian syndrome (PCOS) appear as linked phenomena, although this is not easy to obviate in common forms of PCOS while it is evident in the rare cases of extreme IR and hyperinsulinism (HI). Experimental data indicate that insulin could interfere with the local insulin-like growth factor systems in ovaries, and presumably in adrenals and in the hypothalamic pituitary system. The female puberty system offers a physiological model to explain the gonadotropic action of insulin. In patients with IR, HI could induce a state of hyperpuberty, leading to the constitution of PCOS during adolescence.
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PMID:Insulin resistance and polycystic ovarian syndrome. 130 14

Although sex education programmes are thought to be useful in teaching people with intellectual disabilities, there is very little evidence that the material taught is retained by clients. This paper reports data which has been collected routinely on a sex education programme. Forty-six subjects were assessed on their level of sexual knowledge in seven areas: parts of the body, masturbation, male puberty, female puberty, intercourse, pregnancy and childbirth, and birth control and venereal disease. They were retested after a 9-month sex education programme and tested again at a 3-month follow-up. A control group of 14 subjects were tested on two occasions, 4 months apart. There were significant and substantial increases in sexual knowledge on all areas for the experimental group. The control group showed no corresponding increases in knowledge.
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PMID:Increases in knowledge following a course of sex education for people with intellectual disabilities. 147 90

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

To determine the effects of prepubertal ethanol (ETOH) exposure on hypothalamic and pituitary hormones known to be involved in the onset of female puberty, we have chronically exposed female rats to either a liquid-diet containing ETOH or an isocaloric control liquid-diet. An additional set of controls consisted of animals maintained on Lab Chow, and water provided ad lib. Our results indicate that the feeding regimen employed produced no differences with regard to body and reproductive organ weights, as well as any of the hormones measured between the two control groups. Conversely, ETOH-treated animals showed significantly lower body and reproductive organ weights than the control animals and although no differences were detected between ETOH-treated and control animals with regard to the hypothalamic content of somatostatin (SRIF), there was a significant increase in the hypothalamic content of growth hormone releasing hormone (GHRH), with a concomitant and significant decrease in the serum concentration of growth hormone (GH). Furthermore, the ETOH-treated animals showed a significant increase in the hypothalamic content of luteinizing hormone releasing hormone (LHRH) with a significant decrease in the serum concentration of luteinizing hormone (LH), but not follicle stimulating hormone (FSH). These results demonstrate for the first time that chronic, prepubertal ETOH administration alters the concentrations of specific hypothalamic and pituitary hormones which are known to be involved in the female pubertal process.
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PMID:Actions of ethanol on hypothalamic and pituitary hormones in prepubertal female rats. 196 48

To assess more closely the physiological mechanism(s) by which ethanol (ETOH) delays the onset of female puberty, we have evaluated its effects on body weight, the vaginal opening (VO)-first diestrus (D1) interval and the serum concentrations of growth hormone (GH), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) throughout the peripubertal period in the rat. Using a specific intragastric feeding regimen, 29-day-old rats began receiving either a liquid diet containing ETOH or an isocaloric control liquid diet. Additional controls consisted of animals maintained on laboratory chow and water provided ad libitum. Animals were either killed between 32 and 37 days of age, categorized with regard to their phase of puberty and their serum hormones measured; or, in some animals, the ETOH liquid diet was administered through day 41 and at that time replaced by the control liquid diet in order to determine if recovery would occur. Our results indicate that ETOH-treated animals showed significantly lower body weights and a significantly longer mean VO-D1 interval than the control animals. Also, serum GH and LH levels were significantly lower in the ETOH-treated animals; however, FSH levels were not affected. Administration of the ETOH liquid diet through day 41 produced varying detrimental effects on the onset of puberty and subsequent removal of ETOH from the diet resulted in rapid growth of the animals, followed by the onset of puberty.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of ethanol during the onset of female puberty. 210 89

The change of fundamental voice frequency in continuous speech in female puberty was analysed in 47 girls by comparison of 2000 consecutive electroglottographic cycles in a reading situation. The results were compared with serum concentrations of androgens (dihydroepiandrosterone, delta-4-androstenedione, testosterone, and sex hormone binding globulin), oestrogens (oestradiol, oestrone, and oestronesulphate), and somatic puberty (weight, height, mamma stages, and pubic hair stages). Fundamental frequency in continuous speech was related only to oestrone r = -0.34, (P less than 0.05). But the tone range in continuous speech and the lowest tone in the phonetogram were found to be significantly correlated with many of the pubertal and hormone parameters. All these correlations could be explained by a common age-dependency. By multiple regression analysis different sets of variables for prediction of speaking fundamental frequency were found before and after menarche.
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PMID:Fundamental voice frequency in female puberty measured with electroglottography during continuous speech as a secondary sex characteristic. A comparison between voice, pubertal stages, oestrogens and androgens. 226 90

We examined whether there is a relationship between body fat mass or body fat distribution and hormonal profiles in the plasma of early pubertal girls. Thirty-five apparently healthy caucasian schoolgirls were selected for Tanner's breast development stage M2; they had all been classified as being stage M1 6 months earlier. Body fat mass had no relationship with the total plasma sex steroid concentration or gonadotropins. However, body fat mass was correlated with the fraction of testosterone that was not bound to sex hormone-binding globulin and considered the fraction available for biological activity. Body fat distribution, rather than body fat mass, was different in relation to the total concentrations of estrone, estradiol (E2), and testosterone as well as the percentage of available E2 or testosterone. Girls with fat localized predominantly on the hips had the highest levels of sex steroids and gonadotropins. It seems likely that this type of fat distribution is a result of ovarian activity. Girls with predominantly abdominal fat were also more obese and showed increased plasma levels of total E2 and a lower androgen/estrogen ratio in plasma, possibly due to increased aromatization, especially in abdominal adipose tissue. The findings suggest a reciprocal relationship among body fat distribution, plasma sex hormone levels, and availability of sex steroids in early female puberty.
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PMID:Body fat mass, body fat distribution, and plasma hormones in early puberty in females. 231 46


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