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PubMed2006

Effects of genotype and feed allowance on plasma luteinizing hormones, follicle-stimulating hormones, progesterone, estradiol levels, follicle differentiation, and egg production rates of broiler breeder hens.

The aim of this study was to compare and relate plasma hormone levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone (P4), estradiol (E2), and the in vitro P4 production capacity of the largest yellow (F1) follicle granulosa cells with the laying performance of 2 genotypes (a standard S line and a dwarf cross-experimental E line) maintained under ad libitum (SA, EA) or restricted (SR, ER) feeding regimens. Age-related hormone changes were determined from 4 to 50 wk, hormone changes during the ovulatory cycle were determined during lay, and changes in follicle granulosa cell P4-producing capacity in response to LH with or without growth factors were measured in vitro at different ages. The mean laying rate was similar for SR, EA, and ER but were lower for the SA. Plasma LH and FSH concentrations increased with age in all groups and peaked at puberty. Restricted feeding delayed puberty in both genotypes. Concentrations of E2 and P4 increased after puberty in all groups but delayed in restricted hens. Plasma levels of LH, FSH, P4, and E2 before and after puberty were not correlated with egg-laying performance, but peak E2 levels were. Luteinizing hormone and P4 concentrations during the ovulatory cycle showed differences that may be associated with the different laying performances of the 2 genotypes under ad libitum and restricted feeding. The increase in plasma LH concentration (from basal) during the preovulatory surge was higher in the SR than in the SA but was similar for EA, ER, and SA. The increase in P4 was also higher in SR than in the SA with no difference between EA and ER. In vitro P4 production by granulosa cells in response to LH with insulin-like growth factors, and bone morphogenetic protein-7 was different among the SA, SR, EA, and ER; the EA, SR, and ER had greater responses, and the SA had less response. The presence of insulin-like growth factors and bone morphogenetic protein-7 enhanced LH effects depending on the feeding regimen and age of hen. This finding suggests that differences in laying performances among genotypes fed at different nutritional levels may be partly due to differences in processes associated with follicular maturation modulated by gonadotropins and growth factors. It is concluded that the age at puberty is determined mainly by feed allowance, irrespective of genotype, and that differences in laying performance may be due to a combination of factors that include changes in the levels of gonadotropins or ovarian hormones and growth factors, BW, and the condition of the different genotypes under different feeding allowances.

Aging↗
PubMed1990

Relationship between chronic raised intracranial pressure and empty sella presenting hormonal disturbances.

The role of intracranial pressure in the development and maintenance of the primary empty sella has been pointed out in the literature previously. The hormonal changes and clinical features have been evaluated in a 30 year-old female patient examined for a convexity meningioma and a 20 year-old patient examined for chronic hydrocephalus caused by cured meningitis. Histories and investigations revealed an empty sella turcica associated with primary amenorrhoea and delayed puberty. The removal of the convexity meningioma resulted in loss of amenorrhoea and a rise in plasma gonadotrophins. The establishment of a ventriculo-peritoneal shunt did not bring about any changes in hormonal values and clinical features except the subjective headache disappeared. The importance of consideration of intracranial causes in patients who have delayed puberty or absence of menstrual history is briefly emphasized in light of the literature. Our data also demonstrated a correlation between an increase in intracranial pressure and a deficiency of hormonal secretion by the hypophysis.

Adult↗
PubMed1982

Evaluation of pituitary gonadotropic function in men: value of luteinizing hormone-releasing hormone response versus basal luteinizing hormone level for discrimination of diagnosis.

We examined the serum LH response to LRH in 40 normal men and 38 men with various forms of gonadal dysfunction in an attempt to determine whether the LH response to LRH was more useful than the basal LH level alone for categorizing pathophysiological subgroups of gonadal dysfunction. The subgroups studied included hypogonadotropic hypogonadism, delayed puberty, idiopathic oligospermia, and primary hypogonadism. Log transformation of all values was done in order to normalize the data. Spearman's correlation analysis showed that increased basal LH was associated with increased incremental LH responses. However, our preliminary analysis of LRH response data suggested that the changes in LH were smaller in the secondary hypogonadal and delayed puberty groups then could be accounted for by the differences in basal LH level. Accordingly, we used various statistical techniques to test whether, and under what conditions, LRH testing provides information beyond that evident from examination of basal LH values. We found that the relationship between basal LH and the LH response to LRH differs in men with and without hypothalamic-pituitary dysfunction and that this difference can be exploited to improve the discrimination of men with pituitary hypogonadism from normals.

Adolescent↗
PubMed1986

Relationship of plasma growth hormone-releasing hormone levels to pubertal changes.

Basal plasma GH-releasing hormone (GHRH) concentrations were measured by RIA in 180 normal subjects (93 boys and 87 girls between the ages of 8 and 18 yr). Every subject was in good health and between -2 and +2 SD for height. Fourteen boys with delayed puberty also were studied. Plasma GHRH concentrations were higher during puberty than before it. At midpuberty, the mean GHRH levels in girls was 159.1 +/- 28.5 (+/- SEM) pg/ml, approximately 5-fold higher than the level in prepubertal girls (30.3 +/- 4.3 pg/ml). The mean plasma GHRH in midpubertal boys (101.4 +/- 11.5 pg/ml) was approximately 2-fold higher than the level in prepubertal boys (48.1 +/- 5.2 pg/ml). The GHRH levels in boys with delayed puberty more closely resembled those in boys at a similar pubertal stage than those in boys of similar chronological age. The dramatic rise in plasma GHRH levels during puberty suggests a role for this peptide in the adolescent growth spurt. Moreover, these data indicate that GHRH levels during adolescence may be a marker of the patient's pubertal development.

Adolescent↗
PubMed1988

Gonadal function in patients with beta thalassaemia major.

Endocrine studies were made on 23 female patients aged 13 to 29 years, with delayed puberty or primary amenorrhoea and beta thalassaemia major, and 12 healthy controls, of whom six were prepubertal and six were in Tanner's stage 3-4. Each patient and control received a single intravenous dose of 100 micrograms gonadotrophin releasing hormone (GnRH), and one week later, 10 U/kg body weight of human menopausal gonadotrophin (hMG) to stimulate ovarian function. The patients had decreased gonadotrophin reserves when compared with those of normal controls, only one of 23 patients had an intact luteinising hormone and follicle stimulating hormone response. Most of the thalassaemic patients with delayed puberty showed normal gonad response to human menopausal gonadotrophin (hMG), but three had very low responses, when compared with that of controls. The gonadal failure was even more severe in four of six patients with primary amenorrhoea. It is important to assess hypothalamic-pituitary-gonadal function in young women with beta thalassaemia major, so that those with glandular dysfunction may be started on replacement therapy.

Adolescent↗
PubMed1995

Bone mineral content of young female former gymnasts.

Intense physical exercise and diet restriction could result in delayed puberty and have a negative influence on the acquisition of peak bone mass during puberty. Nineteen young women who had been in elite gymnastic training during their prepubertal and pubertal years were investigated with regard to their health, menstrual data and bone mineral areal mass (BMA). Twenty-one women of comparable age served as controls. The age of menarche of the "former" gymnasts and the controls was 14.8 +/- 1.8 and 12.1 +/- 1.4 years, respectively. Fourteen of the gymnasts had been or were using oral contraceptives (OCs) and most of the non-users now had regular menstrual periods. During the years preceding the study, physical activity among the "former" gymnasts had gradually declined. Although the gymnasts had had a delayed puberty, no difference was found in total body or spinal BMA compared to the healthy controls. Their normal BMA in early adulthood could reflect a catch-up due to a combination of decreasing athletic activity, normal menstrual cycles and intake of OCs.

Adolescent↗
PubMed1997

X-linked ichthyosis with hypogonadism: not always Kallmann's syndrome.

We describe two males with congenital ichthyosis secondary to steroid sulphatase deficiency who also manifested delayed puberty with biochemical features of hypogonadotrophic hypogonadism. In the first patient a history of cryptorchidism and the clinical findings of anosmia, micropenis and bimanual synkinesis suggested a contiguous gene syndrome, comprising X-linked Kallmann's syndrome and X-linked ichthyosis. An X-Y chromosomal translocation involving the Xp22.3 locus was identified; deletions of the STS locus and of exons 10-14 of the KAL locus were subsequently demonstrated. The second patient was euosmic and, although the STS locus was deleted in association with a pericentric inversion involving Xp22.3, no deletions were detected at the KAL locus. Clinically, he was felt to have constitutionally delayed puberty rather than hypogonadotropic hypogonadism and this diagnosis was substantiated by his subsequent development.

Adolescent↗
PubMed1988

Pulsatile luteinizing hormone-releasing hormone treatment of male hypogonadotropic hypogonadism.

Luteinizing hormone-releasing hormone (LH-RH) secretion from the hypothalamus follows a rhythmic pattern, inducing pulsatile luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion from the pituitary gland. Consideration of this physiologic principle led to the introduction of pulsatile LH-RH therapy via infusion pump for the treatment of different forms of hypogonadotropic hypogonadism. We report on 10 male patients, 16 to 28 years of age, suffering from idiopathic hypogonadotropic hypogonadism (IHH) including Kallman's syndrome (n = 2) and delayed puberty (n = 2). All presented with complete eunuchoidism and had undergone no treatment for their conditions during the previous 2 years. LH-RH was administered in subcutaneous pulses of 4 to 16 micrograms, with a portable infusion pump (ZYKLOMAT, Ferring Corp., Kiel, FRG); treatment periods ranged from 6 to 24 months. With therapy, the subjects improved secretion of LH, FSH and testosterone. Testicular volumes and penis size increased; all patients developed normal secondary sexual characteristics. Spermatogenesis was induced in all patients. The time to onset of spermatogenesis ranged from 3 to 15 months. No major side effects were observed, and no patient dropped out of the study. The results indicate that pulsatile LH-RH therapy is an highly effective treatment for IHH and delayed puberty.

Adolescent↗
PubMed1999

X-linked adrenal hypoplasia congenita: a mutation in DAX1 expands the phenotypic spectrum in males and females.

X-linked adrenal hypoplasia congenita (AHC) is a disorder associated with primary adrenal insufficiency and hypogonadotropic hypogonadism (HH). The gene responsible for X-linked AHC, DAX1, encodes a member of the nuclear hormone receptor superfamily. We studied an extended kindred with AHC and HH in which two males (the proband and his nephew) were affected with a nucleotide deletion (501delA). The proband's mother, sister, and niece were heterozygous for this frameshift mutation. At age 27 yr, after 7 yr of low dose hCG therapy, the proband underwent a testicular biopsy revealing rare spermatogonia and Leydig cell hyperplasia. Despite steadily progressive doses of hCG and Pergonal administered over a 3-yr period, the proband remained azoospermic. The proband's mother, sister (obligate carrier), and niece all had a history of delayed puberty, with menarche occurring at ages 17-18 yr. Baseline patterns of pulsatile gonadotropin secretion and gonadotropin responsiveness to exogenous pulsatile GnRH were examined in the affected males. LH, FSH, and free alpha-subunit were determined during 12.5-24 h of frequent blood sampling (every 10 min). Both patients then received pulsatile GnRH (25 ng/kg) sc every 2 h for 6-7 days. Gonadotropin responses to a single GnRH pulse iv were monitored daily to assess the pituitary responsiveness to exogenous GnRH. In the proband, FSH and LH levels demonstrated a subtle, but significant, response to GnRH over the week of pulsatile GnRH therapy. Free alpha-subunit levels demonstrated an erratic pattern of secretion at baseline and no significant response to pulsatile GnRH. We conclude that 1) affected males with AHC/HH may have an intrinsic defect in spermatogenesis that is not responsive to gonadotropin therapy; 2) female carriers of DAX1 mutations may express the phenotype of delayed puberty; and 3) although affected individuals display minimal responses to pulsatile GnRH, as observed in other AHC kindreds, subtle differences in gonadotropin patterns may nevertheless exist between affected individuals within a kindred.

Adolescent↗
PubMed1988

Hormonal responses in pubertal males to pulsatile gonadotropin releasing hormone (GnRH) administration.

Twenty-two boys (9 with delayed puberty and 13 with short stature) ages 12.3 - 17.8 yr, and 10 adult males with idiopathic hypogonadotropic hypogonadism (ages 17.3 - 41.1 yr) have been studied following pulsatile, sc GnRH therapy (240 ng/kg/pulse) over 6 days. Mean pre- and post-therapy LH and FSH concentrations were estimated by 15 min blood sampling over 3-h periods immediately before and at the end of the treatment period. There were significant correlations between the mean pre- and posttreatment LH and FSH concentrations (r = 0.82, p less than 0.001 and r = 0.51, p less than 0.02, respectively) for the 2 groups of peripubertal boys when assessed together. Nine of the 10 adults with hypogonadism showed proportionately greater gonadotropin increments following pulsatile therapy when compared with the peripubertal boys. Standard bolus GnRH tests (100 micrograms iv) did not differentiate between the three groups of patients before pulsatile GnRH therapy. Bolus GnRH tests could predict the subsequent response to pulsatile therapy in the peripubertal boys only. There was no significant change in LH increments following the GnRH bolus tests in either group, after pulsatile GnRH administration (p greater than 0.1). Early response to pulsatile GnRH administration is dependent upon the maturity of the hypothalamic-pituitary-testicular axis in males with delayed puberty or short stature. Patients with hypogonadotropic hypogonadism do not show this relationship.

Adolescent↗
PubMedDate not supplied

[Effects of body weight changes on menarche and menstrual cycles in a group of adolescents].

In Italian girls (7-17 years-old) the effects of body weight on the onset of menarche and on menstruation were studied on the basis of measurements performed in 86 normally developed healthy girls (group 1), in 5 girls affected by precocious puberty (group 2), and in 9 girls with delayed puberty (group 3). Height and weight were evaluated at menarche in all groups, as well as 2 years later in groups 2 and 3. The results were transferred on the graphs proposed by Frisch for the American girls: at menarche 20% of group 1 girls were out of range; in group 2 all girls were in range; 33% of group 3 were below the 10th percentile. Two years later, all groups 2 and 3 girls but one were in range. These data do not confirm the role of body fat in determining the onset of the puberal process, while they support it in the maintenance of menses.

Adolescent↗
PubMed1976

Spironolactone stimulation of gonadotropin secretion in boys with delayed adolescence.

Spironolactone (Aldactone) acts as an antiandrogen by blocking testosterone synthesis and competing with testosterone for the androgen receptor. These properties of the mineralcorticoid antagonist were used in an attempt to interrupt the gonadal-pituitary-hypothalamic negative feedback axis and thereby stimulate LH and FSH in 7 boys with delayed puberty. Following administration of aldactone (5 mg/kg) daily for one week, there was a significant (P less than .01) mean increase in serum LH of 60%. In all 7 boys an absolute rise in LH was observed, but these changes were statistically significant in only 5 individuals. While mean FSH levels increased by 60% in this group of boys, the individual responses were variable. No rise in gonadotropin levels occurred in 2 patients with Kallmann's syndrome, who also received 5 mg/kg of spironolactone daily for 1 week. Large doses of the drug appeared necessary to stimulate gonadotropin secretion since a dose of 3 mg/kg per day did not cause LH or FSH increments in 2 additional patients with delayed puberty. Progesterone and 17alpha-hydeoxyprogesterone levels increased to a greater extent than LH and FSH in response to spironolactone, reflecting either adrenal or testicular enzyme inhibition. Spiornolactone is the first drug shown to be capable of stimulating gonadotropin secretion by interrupting negative feedback inhibition in boys with delayed puberty.

Adolescent↗
PubMedDate not supplied

Puberty is delayed in male growth hormone receptor gene-disrupted mice.

The role of insulin-like growth factor-I (IGF-I) in the initiation of puberty and testicular function is poorly understood. Growth hormone (GH) receptor (R) gene-disrupted mice or GHR gene "knockouts" (GHR-KO) are GH resistant and IGF-I deficient. To assess whether the age of sexual maturation is affected by the absence of IGF-I, various parameters of sexual development including testicular and accessory reproductive organ weights, balanopreputial separation, germ cell development, and intratesticular testosterone levels were determined in normal and GHR-KO mice between the ages of 25 and 60 days. In addition, at 36 days of age, the testosterone response to luteinizing hormone (LH) treatment was assessed in these mice. The results indicate that the balanopreputial separation was delayed 5 days, and a significant increase in the weights of the seminal vesicles (SV) occurred later in GHR-KO mice than in normal animals (between 30 and 35 days and between 35 and 40 days, respectively). Also, the weights of testes and epididymii were significantly reduced in GHR-KO mice. The intratesticular testosterone levels and the testosterone response to LH treatment were attenuated in GHR gene-disrupted mice. Furthermore, elongated spermatids appeared later in the testes of GHR-KO mice than in the testes of normal mice. These results suggest that the absence of IGF-I secretion delays the normal course of sexual maturation in male GHR-KO mice, indicating that IGF-I plays an important role in the initiation of puberty in male mice.

Animals↗
PubMed2006

The cystic fibrosis transmembrane conductance regulator (Cftr) modulates the timing of puberty in mice.

BACKGROUND: Delayed puberty is common among individuals with cystic fibrosis (CF) and is usually attributed to chronic disease and/or poor nutrition. However, it has recently been recognised that pubertal delay can occur even in the setting of good nutritional and clinical status. This finding, along with evidence that Cftr is expressed in rat brain, human hypothalamus, and a gonadotropin releasing hormone secreting cell line, raises the possibility that some of the pubertal delay in CF could stem directly from alterations in Cftr function that affect the hypothalamic-pituitary-gonadal axis. METHODS: To examine this hypothesis, we investigated pubertal timing (as assessed by vaginal opening (VO)) in a mouse model of CF (Cftr(tm1Unc)) engineered to produce a truncated Cftr mRNA and referred to as S489X. Homozygous knockout, heterozygote, and wild type (WT) female mice were examined. RESULTS: As expected, the S489X-/S489X- knockout mice, which have chronic inflammation and gastrointestinal disease, grew more slowly and had later onset of puberty than WT animals. We anticipated that the S489X-/S489X+ heterozygotes, which have no clinical CF phenotype, might display an intermediate timing of puberty. Surprisingly, however, these mice had earlier VO than WT. These findings were confirmed in a second, independent model of CF engineered to generate the deltaF508 mutation in mice. Again, the homozygotes displayed later pubertal timing, while the heterozygotes displayed earlier VO than the WT animals. CONCLUSIONS: These data provide further evidence that Cftr can directly modulate the reproductive endocrine axis and raise the possibility that heterozygote mutation carriers may have a reproductive advantage.

Animals↗
PubMed1980

[Puberty in congenital hypothyroidism (author's transl)].

Puberty was studied in 95 patients with congenital hypothyroidism treated between 1953 and 1977 from the first months or first year of life. Pubertal abnormalities were observed in 13 cases: 1. Delayed puberty in 11 cases (late diagnosis in 6 cases, insufficient treatment in 2 cases, delayed puberty in the family in 1 case). 2. An amenorrhea-galactorrhea syndrome was observed in two cases with insufficient treatment. In the other cases, the outcome of puberty seemed within the normal range. However a careful study showed: 1st. A delay of every stage of puberty, 2nd. The absence of the peak of high velocity in some cases. 3rd. The age of menarche was 13 years 8 months (9 years 1 month-16 years 6 months) (normal girls: 13 years). Final height was dependent upon an early and efficient treatment, and upon a fast catch up of growth and bone maturation.

Adolescent↗
PubMed2005

Regulation and disorders of pubertal timing.

Disorders of pubertal timing are common and challenging problems for pediatric endocrinologists. Early or late puberty can have immediate effects on a child's psychosocial well-being and may have long-term effects on adult stature. Much is known about the regulation of the hypothalamic-pituitary-gonadal axis, but the triggers of pubertal onset in the general population remain elusive. This article reviews recent data suggesting a possible shift in the age of pubertal onset; current knowledge regarding factors that regulate the onset of puberty; and the etiologies, diagnosis, and treatment of precocious and delayed puberty.

Humans↗
PubMed2001

Disorders of growth and puberty in children with non-tumoral hydrocephalus.

Hydrocephalus may cause disorders of growth and puberty. 31 patients (25 girls) with non-tumoral hydrocephalus were seen at 8.5 +/- 3.1 (SD) years for short stature (8 patients), overweight (8 patients), central early puberty (onset before 9 years, 21 patients), premature pubarche (1 patient) and/or delayed puberty (2 patients). Among the patients with short stature, 4 had meningomyelocele and one had untreated early puberty. Only 1/11 patients evaluated had growth hormone deficiency. Among the overweight patients, 5 had early puberty. The plasma leptin concentrations were positively correlated with the body mass index (r = 0.65, p < 0.01, n = 14). Free thyroxin, cortisol, prolactin and concomitant plasma and urinary osmolalities were normal in all cases evaluated, except one who had low free thyroxin. The 7 patients with early puberty and who were given gonadotropin releasing hormone analog for over 2 years had mean predicted adult height of -2.45 +/- 1.9 SD before treatment and -2.46 +/- 1.4 SD afterwards. Ventriculocisternostomy performed on 2 girls seen for delayed puberty was followed by breast development and menarche. In conclusion, in children with hydrocephalus, short stature is frequently due to meningomyelocele and rarely to GH deficiency. Central early puberty is the most frequent endocrine disorder.

Body Height↗
PubMed1989

Prolactinomas presenting as primary amenorrhoea and delayed or arrested puberty: response to medical therapy.

Fourteen patients presented with arrested pubertal development associated with prolactin-secreting pituitary tumours; serum prolactin ranged from 4000-104,300 mU/l in the ten females and 920-68,000 in four males. Skull X-ray showed a markedly expanded pituitary fossa in eight patients. CT scan and/or air encephalography showed macroadenomas in nine, of whom seven had large suprasellar extensions to their tumours, yet only five had complained of headache and only two had visual field defects. All were treated with bromocriptine (7.5-60 mg/day) which lowered prolactin substantially in all and into the normal range in 11 (range less than 60-3090, median 105 mU/l). Puberty thereafter progressed spontaneously in 13, but in one patient, whose prolactin did not suppress completely, menarche could be induced only with clomiphene. Anterior pituitary function improved on bromocriptine. In seven patients with macroadenomas, tumour shrinkage into the pituitary fossa was complete and in two others incomplete shrinkage was followed by transsphenoidal hypophysectomy. Seven patients received pituitary irradiation, six after bromocriptine-induced shrinkage and one after transsphenoidal surgery. At follow-up 6 months to 10 years (median 5 years) after presentation, ten remain on bromocriptine with a suppressed serum prolactin, one has a normal prolactin after surgery, and three are off bromocriptine with residual hyperprolactinaemia (418-4680 mU/l). To date, four females have become pregnant and one male has fathered two children. Prolactinomas are an important, albeit rare, cause of arrested puberty and should therefore be sought. Most patients respond well to bromocriptine, with or without pituitary irradiation.

Adolescent↗