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PubMed1994

Effects of recombinant bovine somatotropin and dietary energy intake on growth, secretion of luteinizing hormone, follicular development, and onset of puberty in beef heifers.

The effects of dietary energy and recombinant bovine somatotropin (bST) on pattern of LH release, follicular development, and onset of puberty were studied in 40 Angus heifers. At 7 mo of age, heifers were assigned to a 2 x 2 factorial experiment; the main effects were dietary energy (high [HDE]: 14.15 Mcal of ME/d or moderate [MDE]: 10.84 Mcal of ME/d) and somatotropin (bST; 350 mg every 2 wk or vehicle). Beginning at 9 mo of age, heifers were observed twice daily for estrous activity. From 10.5 to 12 mo of age, five heifers from each treatment group were selected for weekly ultrasound examination of ovarian structures and biweekly sequential blood sampling to determine concentrations of LH. Somatotropin treatment altered intermediary metabolism in a manner consistent with enhanced accretion of lean tissue and decreased deposition of fat. The HDE heifers were younger (P < .001) at puberty than the MDE heifers, but BW at puberty was not different among treatment groups. Age and body weight at puberty were not affected by bST. Frequency of LH pulses increased within the 10.5 to 12 mo of age sampling window in HDE-treated heifers but not in MDE heifers (dietary energy x month of age; P < .02). Secretion of LH was unaffected by bST. Ovaries of bST-treated heifers tended (P < .09) to have fewer follicles > 5 mm in diameter than those of vehicle-treated heifers. We conclude that chronic treatment with bST did not alter age at puberty or pattern of LH release in heifers and that even modest differences in energy intake influence the timing of the prepubertal increase in pulsatile LH release.

Animals↗
PubMed1997

Lack of a nocturnal rise in serum concentrations of melatonin as gilts attain puberty.

Twenty prepubertal crossbred gilts (Yorkshire x Hampshire x Duroc) weighing 98.1 +/- 4.2 kg at 5 mo of age were placed in an environmentally controlled room having a temperature of 18 degrees C and light:dark cycle of 12 h:12 h. Light intensity measured 700 lx at eye level to the gilts. Three mature ewes were penned adjacent to the gilts to serve as positive controls for the light-dark cycles. After a 30-d acclimation period, 10 gilts from the pool determined to be prepubertal (serum progesterone < 500 pg/mL) were fitted with surgically implanted jugular catheters. Blood samples were drawn at 1100 (4 h after onset of light), 1130, 1200, 2300 (4 h after onset of darkness), 2330, and 2400 for 4 d. On d 5 of sampling, gilts were transported in an open-bed truck for 15 min, returned to their original environment, and exposed to boars for 20 min. Boar exposure was repeated every day throughout the remainder of the experimental period. Blood samples were drawn from each gilt until 7 d after estrus or for 12 d in those gilts that did not exhibit estrus. Blood samples were drawn by venipuncture from the ewes during the entire experimental period. For each sampling day, within an individual gilt or ewe, means of serum concentrations of melatonin (MEL) for night (scotophase) and day (photophase) samples were calculated. After three replications were conducted, four classes of animals were obtained: ewes (n = 9); nonpubertal gilts (n = 10); and two classes of gilts that ultimately reached puberty (prepubertal [n = 16] and postpubertal [n = 16]). Across all gilts, only 65 of 406 bleeding periods (16.0%) had a nocturnal (scotophase) rise in serum MEL. The proportion of gilts expressing a nocturnal rise in serum MEL did not differ as gilts approached puberty (P > .05). Incidence of nocturnal rises of MEL was similar (P > .05) in gilts that attained puberty and gilts that did not attain puberty. Nocturnal rises in MEL were observed in 86.2% of the bleeding periods of ewes housed in the same environment. These data indicate clearly that nocturnal rises in serum MEL are not necessary for a gilt to attain puberty.

Animals↗
PubMed1999

Effects of active immunization against growth-hormone releasing factor on puberty and reproductive development in gilts.

Hormones within the somatotropin cascade influence several physiological traits, including growth and reproduction. Active immunization against growth hormone-releasing factor (GRFi) initiated at 3 or 6 mo of age decreased weight gain, increased deposition of fat, and delayed puberty in heifers. Two experiments were conducted to investigate the effects of GRFi on puberty and subsequent ovulation rate in gilts. Crossbred gilts were actively immunized against GRF-(1-29)-(Gly)2-Cys-NH2 conjugated to human serum albumin (GRFi) or against human serum albumin alone (HSAi). In Exp. 1, gilts were immunized against GRF (n = 12) or HSA (n = 12) at 92 +/- 1 d of age. At 191 d of age, antibody titers against GRF were greater (P < .05) in GRFi (55.5 +/- 1.3%) than in HSAi (.4 +/- 2%) gilts. The GRFi decreased (P < .05) BW (86 +/- 3 vs 104 +/- 3 kg) by 181 d of age and increased (P < .05) backfat depth (15.7 +/- .4 vs 14.8 +/- .4 mm) by 130 d of age. At 181 d of age, GRFi reduced the frequency of ST release (1.0 +/- .5 vs 5.0 +/- .5, peaks/24 h; P < .0001) and decreased (P < .01) ST (1.1 +/- .06 vs 1.7 +/- .06 ng/mL), IGF-I (29 +/- 2 vs 107 +/- 2 ng/mL), and insulin concentrations (3.5 +/- .2 vs 6.3 +/- .2 ng/mL). The GRFi decreased (P < .05) feed conversion efficiency but did not alter age at puberty (GRFi = 199 +/- 5 d vs HSAi = 202 +/- 5 d) or ovulation rate after second estrus (GRFi = 10.7 +/- .4 vs HSAi = 11.8 +/- .5). In Exp. 2, gilts were immunized against GRF (n = 35) or HSA (n = 35) at 35 +/- 1 d of age. The GRFi at 35 d of age did not alter the number of surface follicles or uterine weight between 93 and 102 d of age, but GRFi decreased (P < .05) ovarian weight (.41 +/- .08 vs 1.58 +/- .4 g) and uterine length (17.2 +/- 1.1 vs 25.3 +/- 2.3 cm). Immunization against GRF reduced (P < .05) serum IGF-I (GRFi = 50 +/- 4 vs HSAi = 137 +/- 4 ng/mL) and BW (GRFi = 71 +/- 3 vs HSAi = 105 +/- 3 kg) and increased (P < .05) backfat depth (GRFi = .38 +/- .03 vs HSAi = .25 +/- .02 mm/kg). Age at puberty was similar in GRFi and HSAi gilts, but ovulation rate was lower (P < .05) after third estrus in GRFi (11.3 +/- .8) than in HSAi (13.8 +/- .8) gilts. Thus, GRFi at 92 or 35 d of age decreased serum ST, IGF-I, and BW in prepubertal gilts without altering age of puberty. However, GRFi at 35 d of age, but not 92 d of age, decreased ovulation rate. These results indicate that alterations in the somatotropic axis at 1 mo of age can influence reproductive development in pubertal gilts.

Animals↗
PubMed2004

Chronic administration of recombinant ovine leptin in growing beef heifers: effects on secretion of LH, metabolic hormones, and timing of puberty.

Serum concentrations of leptin increase linearly from approximately 16 wk before until the week of pubertal ovulation in beef heifers. To test the hypothesis that exogenous leptin can hasten the onset of puberty in heifers, we examined the effects of chronic administration of recombinant ovine leptin (oleptin) on timing of puberty, pulsatile and GnRH-mediated release of LH, and plasma concentrations of GH, IGF-I, and insulin. Fourteen fall-born, prepubertal heifers (Brahman x Hereford, 12 to 13 mo; 304.7+/-4.12 kg) were used. Heifers were stratified by age and BW and assigned randomly to one of two groups (seven animals per group): 1) Control; heifers received s.c. injections of saline twice daily (0700 and 1900) for 40 d; and 2) Leptin; heifers received s.c. injections of oleptin (19.2 microg/kg) twice daily at 0700 and 1900 for 40 d. Blood samples were collected at 10-min intervals for 5 h on. d 0, 5, 10, 20, 30, and 40, and twice daily, just before each treatment injection, throughout the study. On d 41, heifers received i.v. injections of GnRH at 0 (0.0011 microg/kg) and 90 min (0.22 microg/kg), with additional sampling for 5.5 h to examine releasable pools of LH. Diets promoted a gain of 0.32+/-0.09 kg/d, which did not differ between groups. Plasma concentrations of leptin increased markedly in leptin-treated heifers and were greater (P < 0.001) than controls throughout (27.8+/-0.8 vs. 4.9+/-0.12 ng/mL). None of the heifers reached puberty during the experiment, but did so within 45 d of its termination. Mean concentrations of plasma LH, GH, IGF-I, and insulin were not affected by treatment, nor was there an overall effect on the frequency of LH pulses. However, a treatment x day interaction (P = 0.02) revealed that the frequency of LH pulses (pulses/ 5 h) was greater (P = 0.03) in controls (3.6+/-0.36) than in leptin-treated heifers (1.7+/- 0.28) on d 10. Characteristics of GnRH-induced release of LH were not affected by treatment. In summary, chronically administered leptin failed to induce puberty or alter endocrine characteristics in beef heifers nearing the time of expected puberty.

Animals↗
PubMed1986

Effect of energy intake after weaning on the sexual development of beef bulls. II. Age at first mating, age at puberty, testosterone and scrotal circumference.

Simmental and Hereford bulls were individually fed varying levels of the same diet to determine the effect of energy intake after weaning on rate of sexual development. For 200 d, 29 Simmentals were fed an average of 14.6, 19.2 or 23.8 Mcal and 27 Herefords were fed 13.4, 17.5 or 22.2 Mcal metabolizable energy per bull daily. Higher energy did not hasten sexual development, as measured by serum testosterone, age at first mating or age at puberty. As energy level increased, weight at puberty increased (P less than .05) for both breeds, and scrotal circumference at puberty increased (P less than .05) for Simmentals. When adjusted for breed and energy level, bulls that were heavier at 1 yr of age had larger scrotal circumference (P less than .05) and were younger at puberty (P less than .01). Bulls that had higher serum testosterone at 1 yr of age reached puberty earlier (P less than .01). At a constant age there was no relationship between testosterone and scrotal circumference. Although higher levels of energy increased scrotal circumference of Simmentals, it did not hasten sexual development for either breed.

Age Factors↗
PubMed2006

Onset of puberty and duration of seasonal cyclicity in Lipizzan fillies.

REASONS FOR PERFORMING STUDY: The onset of puberty and duration of seasonal cyclicity in Lipizzan fillies and young mares have been determined mostly by empirical data, but very little is known about the hormonal changes at puberty and during the seasonal cyclicity in this breed. OBJECTIVES: To determine the onset of puberty and the course of the cyclicity in young Lipizzan mares from age 1-4 years. METHODS: Blood samples were collected twice a month for 2 years from 46 Lipizzan fillies age 1-4 years. Progesterone concentrations, indicating ovarian activity, were measured using an EIA kit. Values above 6.4 nmol/l were taken to indicate luteal phase and those below 3.4 nmol/l, oestrus. RESULTS: Fifty percent of Lipizzan fillies entered puberty during the first spring after their birth at mean +/- s.e. age 15.25 +/- 0.31 months and 50% during the second spring, at age 25.2 +/- 0.57 months. For several fillies of all ages, manifesting anoestrus during the winter months, the oestrus started in March and reached a peak in June to September. The duration of the oestrus activity was age-dependent, at 2.37 +/- 0.62 months in yearlings and 8.56 +/- 0.46 months in fillies age 4 years. In December, >50% of fillies age 2-4 years still exhibited oestrus activity and some entered anoestrus in January the following year. A small proportion of fillies age 3-4 years remained cyclic during the whole year, indicating that factors other than photoperiod can be involved in regulating seasonal cyclicity. CONCLUSIONS AND POTENTIAL RELEVANCE: Our results demonstrate the influence of seasonal factors on the onset of puberty and on the course of oestrus activity in the majority of Lipizzan fillies. However, certain exceptions were also demonstrated but reasons for the prolonged periods of oestrus activity in some Lipizzan fillies were not identified, and the role of the hormone leptin should be studied in future investigations.

Age Factors↗
PubMed1986

Histological assessment of puberty in dogs in the Zaria area of northern Nigeria.

The ages of puberty and sexual maturity were histologically determined in 300 dogs, comprising 115 local Nigerian dogs and 185 crosses of local with exotic breeds. The ages ranged from six months to eight and a half years. The age at puberty was estimated to be seven to eight months and the age of sexual maturity to be 10 to 11 months for all the dogs, both local and exotic. Testicular and epididymal dimensions and weights, on average, increased progressively from before puberty until sexual maturity. The same trend was observed in the diameters of seminiferous tubules, the percentage of spermatogenesis and the epididymal sperm reserves. At puberty an average of 51.8 per cent of the caudal epididymal sperm cells of the local dogs had morphological defects compared with 54.5 per cent in the exotic cross breeds. The defects were mostly coiled tails and proximal cytoplasmic droplets. These defects had decreased to an average of 12.8 per cent in all breeds by the time the dogs had attained a mean age of one and a half years. In general the post-pubertal pattern of spermatogenesis in the dogs resembled that of the bull, and the ages at onset of puberty and sexual maturity fall within the range determined for exotic breeds of dogs. There were no significant differences between the local Nigerian dogs and the local cross exotic breeds in the parameters studied.

Aging↗
PubMed2000

New reference for the age at childhood onset of growth and secular trend in the timing of puberty in Swedish.

UNLABELLED: The objectives of the present work were to present a new reference for the age at childhood onset of growth and to investigate the secular trend in the timing of puberty in a community-based normal population in Sweden. A total of 2,432 children with longitudinal length/height data from birth to adulthood were used to determine the two measures by visual inspection of the measured attained length/height and the change in growth velocity displayed on a computer-generated infancy-childhood-puberty (ICP) based growth chart. The series represents a sample of normal full-term children born around 1974 in Göteborg, Sweden. We found about 10% of children were delayed (>12 mo of age) in the childhood onset of growth based on the previous reported normal range, i.e. 14% in boys and 8% in girls. Distribution of the age at childhood onset of growth was skewed. The medians were 10 and 9 mo for boys and girls, respectively. After natural logarithmic transformation, the mean and standard deviation (SD) were 2.29 (anti-log 9.9 mo) and 0.226 for boys, 2.23 (anti-log 9.3 mo) and 0.220 for girls, respectively. The 95% normal ranges were 6.3-15.4 and 6.0-14.3 for boys and girls, respectively. The distribution of the timing of PHV was close to the normal distribution. The mean values were 13.5 y for boys and 11.6 y for girls with 1 y SD for both sexes. CONCLUSION: A downward secular trend in the onset of puberty was clearly shown in the population. The age at childhood onset of growth did not correlate with the timing of puberty (r = -0.01 and 0.05, p > 0.7 and 0.1 in boys and girls, respectively). Normal ranges of the age at childhood onset of growth are in need of revise, as this study indicates. The new reference presented here could be a reliable indicator in further studies.

Adolescent↗
PubMed2025

Steroid hormone-mediated epigenetic programming during puberty: uncovering links to depression.

DNA methylation (DNAm) is a key epigenetic modification that dynamically regulates eukaryotic development over time. DNAm has been found to influence a variety of biological processes in both normative and pathological states, such as depression. Since DNAm can serve as an interface between environmental influence and gene expression, it is a mechanism studied in the context of many pathologies, including psychiatric. Depression is a complex and heterogeneous disorder strongly influenced by puberty, as evidenced by increased rates in both sexes after sexual maturation. However, this effect is more pronounced in females, contributing to its twofold increased lifetime prevalence compared to males. Additionally, depression is consistently associated with altered DNAm at specific genomic sites. In this review, we discuss how DNAm programming can affect functional pathways during puberty and in turn, influence disease outcomes. Here, we highlight the bidirectional relationship of steroid hormone surges during this sensitive period and DNAm, adding a layer of complexity and insight into the pathophysiology of depression. Specifically, we explore the extent of DNAm change throughout puberty, how it contributes to individual and sex-specific differences in puberty, and how it may influence the risk for depression.

Humans↗
PubMed2006

The pubertal timing controversy in the USA, and a review of possible causative factors for the advance in timing of onset of puberty.

Previously used standards for the diagnosis of precocious puberty in girls no longer appear to be appropriate in the USA, in that a significant number of girls are being seen in paediatricians' offices with breast budding before 8 years of age. The timing of menarche, however, has changed little over the past few decades. Early maturing girls are more likely to become obese in adolescence and adulthood than normal or late maturing girls. Early maturing white girls are heavier at the onset of puberty, but this is not the case for African-American girls or boys of either race. Boys and girls with premature pubarche may be more hyperinsulinaemic than normal children, and girls with premature pubarche more likely to develop functional ovarian and adrenal hyperandrogenism. Early menarche is preceded by prepubertal hyperinsulinaemia. It is proposed that pubertal onset, although not necessarily the tempo of puberty, is influenced by hyperinsulinaemia and insulin resistance. If this hypothesis is correct, insulin resistance may be more prevalent in US children than previously recognized. An advance in timing of onset of puberty has not been noted in other countries, although it is likely that this phenomenon may become more prevalent as other countries adopt a more American lifestyle and diet.

Adolescent↗
PubMed2003

The effects of manipulation of puberty on growth.

Short stature in adulthood can be considered as a disability because it can be associated with many difficulties including those of a psychological and social nature. Many factors can influence final adult height such as genetics, the magnitude of growth hormone (GH) secretion, height before puberty, and the onset and duration of puberty. A crucial factor affecting final adult height, however, is the total height achieved during puberty. The combination of GH and gonadotropin-releasing hormone analogues greatly enhances growth and their separate and combined use for the treatment of GH deficiency, central precocious puberty and other diagnoses in children and adolescents is discussed in this article.

Adolescent↗
PubMed1975

Responsivity of pituitary gonadotropes to luteinizing hormone-releasing factor in idiopathic precocious puberty, precocious thelarche, precocious adrenarche, and in patients treated with medroxyprogesterone acetate.

One hundred micrograms synthetic luteinizing hormone-releasing factor (LRF) were administered to 13 girls and 2 boys with idiopathic precocious puberty, 3 girls with precocious thelarche, 2 girls with precocious adrenarche, and 5 children treated with medroxyprogesterone acetate (MPA). Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and sex steroid responses were assessed. The mean readily releasable LH rose to a peak of 8.4 plus or minus 1. 8 ng/ml (LER 960) in the children with idiopathic precocious puberty and was significantly greater than in normal prepubertal (1.8 plus or minus 0.14) or pubertal children (4.9 ng/ml) (LER 869) was higher in precocious puberty but not significantly greater than in normal prepubertal (5.3 plus or minus 1.9) or pubertal girls (6.0 plus or minus 1.2). The mean concentration of plasma estradiol rose significantly above resting levels after LRF in the girls with idiopathic precocious puberty. The LH response in girls with precocious the larche was in the prepubertal range. In 4 of 5 children with sexual precocity treated with MPA, the LH release evoked by LRF was diminished.

Child↗
PubMed1996

The role of luteinizing hormone-beta gene polymorphism in the onset and progression of puberty in healthy boys.

An immunologically anomalous LH with two point mutations in its beta-subunit gene (Trp8Arg and Ile15Thr) has recently been described. This polymorphism is common in Finland; 28% of the population are homo- or heterozygous for the variant allele. To assess the effect of the LH variant on LH action, we correlated its presence in a group of 49 healthy boys with the onset and progression of puberty. This group was followed-up longitudinally from a mean age of 11.7 +/- 0.1 yr for 3 yr at 3-month intervals. In addition, we studied the prevalence of the variant LH in boys with constitutional pubertal delay (testicular volume < or = 4 mL after 13.5 yr of age). The LH beta gene status of each subject in this study was judged from a single venous blood sample using two immunofluorometric LH assays with different combinations of monoclonal antibodies: one detecting both the variant and wild-type LH, and the other detecting only wild-type hormone. Of the boys with pubertal onset at a normal age, 36 (74%) were homozygous for the wild-type LH beta allele, 12 (24%) were heterozygous, and 1 (2%) was homozygous for the variant LH beta allele. Clear differences in pubertal parameters were found between the boys with normal and mutated (homo- or heterozygous) LH genotypes. During the follow-up, the boys with the mutated genotype had smaller testicular volumes (P < 0.03), were shorter (P < 0.02), had slower growth rates (P < 0.04), and had lower serum insulin-like growth factor I-binding protein-3 levels (P < 0.03) than the boys with the normal LH genotype. In the boys with delayed onset of puberty, the frequency of the variant LH beta allele did not differ from that in the reference population, indicating that the variant LH is not associated with conditions due to disturbed control of the reactivation of GnRH secretion. We conclude that during the progression of puberty, the variant LH may be less active in stimulating testicular growth than wild-type LH. Thus, the gene may affect tempo, contributing to the wide normal variation in pubertal progression in healthy boys. Our results also suggest that the variant LH not only affects the course of puberty, but is already involved in the regulation of the GH-insulin-like growth factor I axis during childhood.

Adolescent↗
PubMed1999

Unsustained or slowly progressive puberty in young girls: initial presentation and long-term follow-up of 20 untreated patients.

A small number of young girls with unsustained or slowly progressive puberty have been described, but few data regarding their final heights and adult reproductive function have been reported. We have conducted a study that delineates the initial presentation and 12-yr follow-up of 20 patients who initially presented with unsustained or slowly progressive puberty as young girls. The patients were first seen between 1984-1987. They all underwent extensive clinical and hormonal studies, including frequent blood sampling and pelvic ultrasound to characterize pituitary-gonadal function. Twelve years later, we were able to locate 17 of the patients, and 16 of these agreed to participate in a questionnaire-based follow-up study. Follow-up data about the other patients were gleaned from available medical records as were corroborative data regarding the 16 study participants. Our results indicate that this form of early puberty is a benign entity. Seventy percent of our patients experienced cessation of their early pubertal development, whereas the remainder reported a slowly progressive course. Those with a slowly progressive course were older than those with an unsustained course [mean age of the larche, 6.1 vs. 3.4 yr (P < 0.01); age of pubarche, 6.0 vs. 4.0 yr (P = 0.02); age at our evaluation, 7.1 vs. 5.2 yr (P = 0.02)]. They also had more advanced skeletal maturation (bone age, 10.2 vs. 7.3 yr; P = 0.04) at the time of our evaluation. Both groups, however, had similar outcomes with respect to linear growth and young adult reproductive function. On the average, the study patients reached their genetic targets for final height (mean final height, 165.5 +/- 2.2 cm; mean genetic target height, 164.0 +/- 1.1 cm; P = NS). The average age of menarche was 11.0 +/- 0.4 yr. Twenty-three percent of our patients have evidence of anovulatory menstrual cycles, which is comparable to the 28% found in normative studies of similarly aged women. Two of the patients have become pregnant to date. Unsustained or slowly progressive puberty in young girls does not warrant therapy with GnRH agonists. Thus, when evaluating patients with early pubertal development, one should ensure that sexual maturation is continually progressive before initiating potentially unnecessary therapy.

Adult↗
PubMed1994

Growth at puberty: interaction of androgens and growth hormone.

Puberty is characterized by the onset and continued development of secondary sexual characteristics and an abrupt onset of linear growth. Growth in boys occurs due to the rising levels of androgens and also indirectly mediated by growth hormone (GH) and the insulin-like growth factors. Data are presented to show marked androgen-dependence of GH increases at puberty. The mode of this increase is through an augmentation in the amplitude of the pulses rather than in their frequency. Shortly after the maximal rate of growth, the pattern of GH release reverts toward that of the prepubertal child. To investigate the neuroendocrine mechanism through which androgens increase the mean circulating GH level, deconvolutional analysis has been applied. At mid-puberty the maximal rate of GH release per secretory burst and the total amount released per burst were increased. There were no significant alterations in the duration or frequency of the GH secretory burst or in the serum half-life reflecting the metabolic clearance of the hormone. Thus, the pubertal growth spurt in boys is likely subserved by the altered neurosecretory dynamics for GH. These altered hormone levels likely produce the equally profound changes in body composition, regional fat distribution, and muscular strength that occur during puberty in boys.

Adolescent↗
PubMed2001

Multiple pituitary hormone deficiency: management of puberty for optimal auxological results.

The overview in this paper focuses on ways of achieving optimal auxological results in puberty, principally in idiopathic and congenital multiple pituitary hormone deficiency (MPHD), suggested by the co-authors. We agreed that diagnosing gonadotrophin insufficiency/deficiency is difficult in young children and should be repeated in late prepuberty, but a firm diagnosis of MPHD helps avoid endocrine re-testing at the end of growth. The hypothalamic-pituitary axis must be reassessed periodically in evolving endocrinopathies, though current practice varies widely. Optimum age to induce puberty is 11-12 years in girls and 13-14 boys, and sex steroids are the preferred agents. Short-course testosterone to increase micropenis size is advantageous, but inducing early testicular maturation is not known to improve later fertility. There is also little evidence for increasing the dose of GH during puberty, though therapy should continue to final height, and possibly until peak bone mass is achieved. Delaying puberty is an option in septo-optic dysplasia, and minimising the dose of hydrocortisone is crucial in treating ACTH/cortisol insufficiency. Many unresolved questions remain in this difficult area.

Adolescent↗
PubMedDate not supplied

Final height outcome in both untreated and testosterone-treated boys with constitutional delay of growth and puberty.

The present retrospective study is based on a historical follow-up of 49 boys with constitutional delay of growth and puberty (CDGP) who went into puberty spontaneously (27 cases) or induced by depotestosterone treatment, 50 mg/ month for 6 months (22 cases). At the time of puberty the two groups of boys were similar in bone age, height deficiency, target height (TH) and had similar predicted final heights (FH). Their FH was measured and compared with TH calculated from measured parents' heights. FH did not significantly differ between the untreated boys and those treated. In the two groups of patients FH was similar and corresponded to both TH and height predicted at puberty onset. This study confirms that most boys with CDGP spontaneously attain a FH within the target range (24/27 cases). A short-term and low dose course of depotestosterone can be used without adverse effects on FH. The Bayley-Pinneau method can be generally considered accurate for predicting FH in CDGP, although significant discrepancies between FH and predicted height have been recorded in a fair number of both untreated and treated boys.

Adolescent↗
PubMed2002

The role of sex steroids in the regulation of insulin sensitivity and serum lipid concentrations during male puberty: a prospective study with a P450-aromatase inhibitor.

OBJECTIVE: Our purpose was to study the sex steroid-mediated changes in serum insulin and lipid concentrations in boys during puberty. DESIGN AND METHODS: We treated boys with constitutional delay of puberty either with testosterone plus placebo or with testosterone plus an aromatase inhibitor, letrozole, which inhibits the conversion of androgens to oestrogens. We demonstrated previously that during treatment with testosterone plus letrozole the increase in testosterone concentration was more than 5-fold higher than during treatment with testosterone plus placebo. The concentrations of 17beta-oestradiol, IGF-I and IGF-binding protein-3 increased during testosterone-plus-placebo treatment, but during testosterone-plus-letrozole treatment the concentrations remained unchanged. These divergent changes in the two groups enabled us to study the effects of sex steroids and GH on insulin sensitivity and lipid concentrations. RESULTS: The insulin concentration in the testosterone-plus-placebo-treated group did not change. In contrast, in the testosterone-plus-letrozole-treated group, the concentration decreased during letrozole treatment, indicating improved insulin sensitivity. Changes in insulin and IGF-I concentrations within 12 and 18 months were correlated. In the testosterone-plus-placebo-treated group, the high-density lipoprotein cholesterol concentration did not change but in the testosterone-plus-letrozole-treated group the concentration decreased. The concentrations of low-density lipoprotein cholesterol (LDL-cholesterol) and triglycerides did not change in either of the groups. CONCLUSIONS: The findings indicate that androgens do not directly alter insulin sensitivity in boys during puberty. In contrast, the observations suggest tight regulation of glucose--insulin homeostasis by GH in boys at this stage. Furthermore, our findings indicate that sex steroids do not significantly participate in the regulation of serum concentrations of LDL-cholesterol or triglycerides in boys during early and mid-puberty.

Adolescent↗