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PubMed1999

Effects of season of birth on the prepubertal pattern of gonadotropin secretion and age at puberty in beef heifers.

There is an early transient rise in gonadotropin secretion in spring-born prepubertal heifers and there is an indication that this pattern is different in autumn-born heifers. The effect of season of birth on age and weight at puberty is equivocal. This study was designed to compare the temporal patterns of LH and FSH secretion between spring- and autumn-born heifers and to determine the effects of season of birth on age and weight at puberty. Blood samples from 2 groups of heifer calves born in spring (last week of March, n = 5) or autumn (last week of October, n = 5) were collected every other week from birth to puberty and every 15 min for 10 h at 6, 12, 18, 24 and 32 wk of age. Timing of puberty was determined by measuring progesterone in plasma samples collected every 2 to 3 d starting at 42 wk of age. Age and weight at onset of puberty did not differ between the 2 groups of heifers (P > 0.05); however, the autumn-born heifers tended to mature in a wider range of ages and weights. Based on the 10-h sampling periods, mean serum concentrations of LH and LH pulse frequency and amplitude were higher in spring-born heifers at 18 wk of age than in autumn-born heifers (P < 0.05). In spring-born heifers, LH pulse frequency increased over time to 32 wk of age, and LH pulse amplitude was higher at 12 and 18 wk than at 32 wk of age (P < 0.05). Autumn-born heifers had higher LH pulse frequency at 6 wk and showed a decrease in mean concentrations of LH at 12 and 18 wk of age (P < 0.05). The FSH pulse frequency of spring-born heifers was higher at 12 wk of age than in autumn-born heifers (P < 0.05), FSH pulse amplitude in autumn-born heifers decreased from 6 to 32 wk of age. It was concluded that although the mean age and weight at puberty did not differ between spring- and autumn-born heifers, the range in age and weight at puberty was wider in the autumn-born heifers. The patterns of LH secretion differed between spring- and autumn-born prepubertal heifers, with spring-born calves exhibiting an early rise in LH secretion, while mean serum concentrations of LH decreased during this period in autumn-born heifers.

Aging↗
PubMed2004

Effects of feeding maize stover and cottonseed cake on onset of puberty in Bunaji (Bos indicus) heifers.

A study was conducted to determine the influence of maize stover and cottonseed cake supplementation on age and live weight at onset of puberty in Bunaji heifers. A total of 49 pre-pubertal Bunaji heifers approximately 12 months of age were allotted randomly to one of two treatments of feed supplementation: (i) supplementation with maize stover and (ii) supplementation with cottonseed cake. The heifers were monitored for a period of 18 months for first observable oestrus or onset of puberty. The maize stover group were given maize stover (crop residue) supplementation ad libitum during the dry season; in the cottonseed cake group each heifer received 500 g of cottonseed cake per day during the dry season. The heifers supplemented with cottonseed cake attained puberty at an earlier age (23.9+/-1.2 months) than the heifers supplemented with maize stover (28.2+/-1.3 months; p<0.05). Similarly, heifers on the cottonseed cake supplementation attained puberty at a live weight of 270.5+/-3.5 kg; while the heifers on maize stover attained puberty at 237.6+/-5.8 kg (p <0.05). The cottonseed cake-supplemented heifers had higher daily gains than the maize stover-supplemented heifers. It is concluded that provision of cottonseed cake as a supplement for heifers hastened the onset of puberty when compared to the maize stover supplemented heifers. Puberty can be achieved at an early age with improved nutrition and this can in turn reduce the generation interval and thus increase the rate of genetic gain of indigenous animals. Provision of protein supplements in cattle is recommended, especially in the tropics where marked seasonality of rainfall results in extremely poor pastures and herbage and low available protein.

Age Factors↗
PubMedDate not supplied

Effects of bull exposure and body growth on onset of puberty in Bunaji and Friesian x Bunaji heifers.

A total of ninety seven pre-pubertal Bunaji (BJ) and Friesian-Bunaji (FR x BJ) heifers were allotted randomly to two treatments groups for a period of 15 months. The treatment groups consisted of the followings: Mature Bull Exposure (MBE) and No Bull Exposure (NBE). Heifers were body condition scored and their live weights recorded on 28 days consecutive intervals. A heifer tactile stimulation in bull bio-stimulation. was considered to have attained puberty if she displayed oestrus, had a palpable corpus luteum with an associated P4 concentration > 1 ng x mL(-1). The onset of puberty was significantly earlier in MBE heifers (23.1 +/- 0.4 months) than NBE heifers (26.4 +/- 0.4 months). The mean ages at puberty for MBE-BJ, NBE-BJ, MBE-FR x BJ, NBE-FR x BJ were 24.3, 27.8, 22.1 and 25.0 months respectively. More MBE heifers (70.8%) attained puberty between 17 and 24 months of age than NBE heifers (18.3%) and on the same ages, more FR x BJ heifers (62.0%) than BJ heifers (25.5%). The mean live weight of MBE heifers at puberty (224.4 +/- 4.2 kg) was significantly lower than that of the NBE heifers (255.8 +/- 4.2 kg). The FR x BJ heifers attained puberty at a significantly higher live weight (270.2 +/- 4.2 kg) than the BJ heifers (228.6 +/- 4.2 kg). The use of a vasectomised bull especially in some elite farms that rely on artificial insemination services may be an effective management tool that can decrease age at puberty. More work is required to determine the relative contribution of visual, auditory, olfactory, pheromonal and tactile stimulation in bull biostimulation.

Age Factors↗
PubMed1996

Progestin-induced puberty and secretion of luteinizing hormone in heifers.

Two experiments were designed to investigate the endocrine mechanisms by which progestin administration induces puberty in heifers. In experiment 1, prepubertal heifers were randomly assigned by age to receive either a single norgestomet implant for 10 days (NORG; n = 15) or to serve as unimplanted controls (CONT; n = 14). Serial blood samples were obtained on Days -0.5, 8.5, and 10.5 (Day 1 = day of implant insertion) and were analyzed for concentrations of LH. On days 9 and 11, 4 heifers in each treatment were slaughtered, and the reproductive tracts were obtained. Weekly progesterone analyses were performed to estimate the day of puberty in heifers not slaughtered. Puberty was induced in 6 of 7 heifers in the NORG treatment, resulting in an earlier (p < 0.05) day of puberty in the NORG than in the CONT treatment. The frequency of LH pulses was higher (p < 0.05) on Days 8.5 and 10.5 in the NORG as compared to the CONT treatment. Although no difference (p > 0.10) was observed between treatments in follicular development, uterine weight was greater (p < 0.05) in NORG than in CONT heifers on Day 11. In experiment 2, prepubertal heifers (n = 47) were administered either 1 (1NORG; n = 16), 3(3NORG; n = 16), or 0 (CONT; n = 15) norgestomet implants for 10 days, and serial blood samples were obtained as described for experiment 1. Transrectal ultrasonography was used to determine the diameter of the largest follicle on Day 9. Plasma samples were obtained after each serial sample collection period and were analyzed for estradiol concentrations. Puberty was induced in 75% (12 of 16) and 81% (13 of 16) of heifers in the 1NORG treatments, respectively. Four heifers in the 1NORG treatment, from which serial blood samples were collected, ovulated before removal of the progestin implant, and the LH data for this treatment were deleted. In the 3NORG treatment, LH pulse frequency was suppressed (p < 0.05) on Day 8.5, but was greater (p < 0.05) 12 h after removal of the progestin (Day 10.5) than in the CONT treatment. We conclude that progestin administration hastens puberty by increasing LH secretion after progestin withdrawal and propose that progestin administration induces puberty by accelerating the peripubertal decrease of estradiol negative feedback on LH secretion.

Animals↗
PubMed2004

Behavioural and neuroendocrine adaptations to repeated stress during puberty in male golden hamsters.

In adult animals, the consequences of stress are often severe and long lasting. Repeated subjugation in adult male golden hamsters inhibits aggression and increases submissive and avoidant behaviours. By contrast, subjugation during puberty enhances offensive aggression. The goals of this study were to characterize behavioural and neuroendocrine responses of naïve and repeatedly subjugated juveniles to social defeat and to assess potential recovery from social stress. From the onset of puberty on postnatal day 28 (P28) to mid puberty (P42), animals were either socially subjugated or placed in a clean and empty cage for 20 min daily. The subjugated and control groups were further divided into subgroups and sacrificed under basal conditions or after social defeat on P28, P35 (early puberty), P45 (mid puberty) and P70 (early adulthood). On P35 and P45, repeatedly subjugated juveniles showed a complete inhibition of olfactory investigation (i.e. risk assessment) towards aggressive adults. Repeatedly subjugated also animals had lower postdefeat cortisol levels than controls on P45. Interestingly, basal cortisol levels increased gradually during puberty but did not differ between treatment groups at any point. Repeated subjugation was also associated with increased tyrosine hydroxylase immunoreactivity (ir-TH) within the extended medial amygdala. After a 4-week recovery period, none of these variables differed between subjugated and control groups. In an additional experiment, subjugated adults also had increased ir-TH in the medial extended amygdala, suggesting that these neurones are particularly responsive to social stress. In conclusion, puberty may be a developmental period characterized by behavioural and neuroendocrine plasticity in stress responsiveness. Furthermore, peri-pubertal changes in stress hormones may explain why juvenile hamsters are more resilient to social stress than adults.

Adaptation, Physiological↗
PubMed1988

Cessation of long day melatonin rhythms time puberty in a short day breeder.

This study tested the hypothesis that in the female sheep, a short day (SD) breeder, puberty can occur normally in the absence of ambient short days. More specifically, the photoperiod cue timing the transition into adulthood is exposure to and then termination of a long day melatonin rhythm. Control lambs born in the spring were exposed to 5 weeks of long days (LD; 16 h of light, 8 h of darkness; 18-23 weeks of age) and were raised in SD (8 h of light, 16 h of darkness) at other times. As expected from previous studies, this alternating photoperiod sequence (SD-LD-SD) induced puberty at the normal age in autumn [33 +/- 2 weeks (mean +/- SEM); n = 6]. The other three groups were exposed only to LD from birth; the superior cervical ganglia were removed bilaterally at different ages to denervate the pineal gland in order to block transduction of subsequent LD cues. Puberty occurred normally (31 +/- 1 weeks; n = 7) after ganglionectomy at 23 weeks of age, indicating that ambient short days are not required to initiate reproductive cycles. LD are necessary, as evidenced by the results for the other two groups ganglionectomized neonatally at 4 weeks of age. With no further treatment, puberty was either delayed (n = 1) or did not occur during the first year of life (n = 5), after which the study ended. This delay was prevented in the other group of ganglionectomized lambs by a 5-week (18-23 weeks of age) exposure to LD melatonin patterns by means of 8-h melatonin infusions nightly; 12 weeks after melatonin replacement therapy, puberty occurred at the normal time (34 +/- 1 weeks; n = 6). The inference is that for puberty to occur in the female lamb the animal must be exposed to relatively limited periods of LD, followed by the blockade or absence of further LD cues (pineal denervation, termination of LD melatonin infusion, or presence of SD). This supports the concept that the LD of summer, followed by their disappearance in autumn, time puberty in the female sheep.

Animals↗
PubMed2004

Minor involvement of somatic growth in the onset of puberty of Hatano high- and low-avoidance rats.

The present study was planned to examine the effects of somatic growth on the determination of timing of puberty using Hatano high- and low-avoidance rats (HAAs and LAAs); the rats were genetically selected from Sprague-Dawley (SD) rats for good or poor performance in a two-way active avoidance-learning test. Since these two lines were found to have different characteristics, such as body weight at birth, maternal care and timing of male puberty, the present study characterized female puberty in Hatano rats and then compared postnatal growth and timing of puberty between the two lines of rats when they were nursed by foster SD dams. When nursed under biological dams, HAAs became heavier, exhibited vaginal opening at a younger age and first ovulation was accompanied by more oocytes than LAAs. In all of the HAAs, but none of the LAAs, ovulation was induced by a single s.c. injection of 5 IU equine chorionic gonadotropin (eCG) on day 22 after birth. An additional treatment with 10 IU human CG revealed that, in the ovaries of LAAs, a small number of follicles had developed to an ovulable stage as a result of the treatment. The fostering improved somatic growth, and weights of LAAs were sustained at a heavier level than those of fostered HAAs. The fostering, however, did not eliminate the line difference in the timing of puberty of both sexes; it did accelerate the vaginal opening of LAAs but not the balanopreputial separation. Thus, there is a phenotypic difference in the timing of female puberty in Hatano rats exhibiting a different timing of ovarian development in response to gonadotropin. The present study indicates that postnatal somatic growth is not the predominant determinant in the onset of puberty in Hatano rats.

Animals↗
PubMed1995

Body composition and metabolic profiles associated with puberty in beef heifers.

Rapid growth large frame (RL, n = 61) or average growth medium frame (AM, n = 71) biotype heifers fed to achieve either moderate (MOD, .6 kg/d) or high ADG (HI, 1.0 kg/d) were used to determine whether puberty occurs at similar body composition or metabolic status. A heifer was considered pubertal after being detected in estrus and then forming a functional corpus luteum. Live animal estimates of body composition and blood samples for assessment of metabolic status were taken at 13 +/- .2 d after estrus for all heifers. Body composition and metabolic status were assessed every 56 d from 7 mo of age until puberty in a subset of 80 heifers representing all biotype-diet combinations. At puberty, 32 of these 80 heifers were slaughtered and physical and chemical composition of the empty body were determined. High-gain diet heifers were younger, heavier, taller, and more muscular (all P < .01) at puberty than MOD heifers. Slaughter measurements paralleled live animal estimates; bodies of HI and RL heifers contained more (P < .01) carcass and noncarcass components than those of MOD and AM heifers, respectively. Carcasses of RL and HI heifers were more (P < .05) muscular and fatter than AM and MOD heifers. At puberty, HI heifers had a greater (P < .01) mass of moisture, fat, and fat-free organic matter (FFOM) than MOD, whereas RL heifers had more moisture, ash, and FFOM than AM. Percentage of fat was greater (22.1 +/- 1.0 vs 1.0 vs 19.1 +/- 1.0; P < .05) and percentage of moisture was less (55.4 +/- .6 vs 58.1 +/- .6; P < .01) in bodies of HI than in those of MOD heifers. Concentrations of blood urea nitrogen and insulin were greater (P < .05) in HI than in MOD heifers. Diet did not influence concentration of IGF-I or glucose, and metabolic markers were unaffected by biotype. No dramatic changes in body composition or metabolic signals were detected before puberty. Puberty did not occur at similar body composition or metabolic status in all heifers.

Animals↗
PubMed1997

Effect of age and pattern of gain on induction of puberty with a progestin in beef heifers.

Crossbred heifers (n = 75) fed for rapid (R; .82 kg/d) or slow-then-rapid (SR; .41 kg/d for 90 d then .82 kg/d) postweaning gain were used to examine the effects of age or pattern of gain on induction of puberty by a progestin. At 9.5, 11.0, and 12.5 mo of age, 12 prepuberal heifers from each growth treatment received progestin (a 6-mg Norgestomet implant for 10 d) or control treatments. Induction of puberty, LH secretory profiles, and ovarian follicular characteristics were assessed in Norgestomet-treated and control heifers. Body weights of R heifers were greater (P < .01) than those of SR heifers at all ages. At 12.5 mo, more Norgestomet-treated heifers exhibited a puberal estrus within 5 d after implant removal compared with controls (82% vs 9%, respectively), but Norgestomet did not induce puberty at 9.5 or 11 mo of age (progestin x age, P < .05) in heifers of either gain pattern. Norgestomet increased (P < .01) LH pulse frequency at all ages, whereas Norgestomet increased only mean LH concentrations at 12.5 mo of age (progestin x age, P < .03). Norgestomet treatment altered (P < .01) ovarian follicular characteristics at all ages. Gain pattern did not affect (P > .1) LH secretory profiles, ovarian characteristics, or induction of puberty by Norgestomet. We conclude that progestins induce puberty by hastening the normal cascade of endocrine and ovarian events associated with spontaneous puberty. Furthermore, age, but not pattern of gain, seems to be the critical factor influencing the efficacy of progestins to induce puberty in heifers.

Aging↗
PubMed2003

Age at puberty, total fat and conjugated linoleic acid content of carcass, and circulating metabolic hormones in beef heifers fed a diet high in linoleic acid beginning at four months of age.

In the current study, we hypothesized that diets high in linoleic acid would increase conjugated linoleic acid (CLA) tissue content, reduce adiposity and leptin production, and result in an increase in the age at puberty in heifers. Heifers were weaned and blocked by body weight (heavy, n = 10, and light, n = 10) and allocated randomly within block to receive isocaloric and isonitrogenous diets with either added fat (HF, n = 10) or no added fat (C, n = 10) from 4 mo of age until post-pubertal slaughter. Whole sunflower seed (55% oil; 70% linoleic acid) was used as the fat source in HF diets and provided 5% added fat from the start of the study until heifers weighed 250 +/- 8 kg, at which time added fat was increased to 7% of dry matter until slaughter. Body weights were recorded weekly, and blood samples were collected weekly for total cholesterol and hormone analyses. Puberty was confirmed based on serum concentrations of progesterone and ultrasonographic confirmation of corpora lutea. Heifers were slaughtered at 325 +/- 10 d of age, and longissimus muscle between the 9th and 11th rib was collected and analyzed to estimate carcass composition. Subcutaneous and kidney, pelvic, and heart fat were collected at slaughter for fatty acid analyses. The HF heavy group tended (P < 0.10) to reach puberty later than all other groups, and one HF light heifer did not reach puberty during the study. Linoleic acid and cis-9, trans-11 CLA tissue contents were higher (P < 0.03) in HF heifers than controls, but neither total carcass fat nor percentage of dry matter differed by dietary group, although the percentage of protein tended (P < 0.10) to be lower in HF heifers. Mean serum concentrations of leptin did not differ due to diet; however, leptin increased (P < 0.01) linearly as puberty approached. Circulating concentrations of growth hormone and insulin-like growth factor I increased or remained relatively constant between wk 2 to 10 of feeding, and then declined (P < 0.01) until the onset of puberty. Serum IGF-I was lower (P < 0.01) in heifers receiving the HF diet. Mean serum concentrations of insulin and total cholesterol increased (P < 0.01) with time in both groups, but only total cholesterol was increased by the HF diet (P < 0.05). Results indicate that diets high in linoleic acid fed to growing beef heifers beginning early in life have little or no effect on total carcass fat, circulating leptin, or age at puberty despite measurable increases in CLA accumulation.

Adipose Tissue↗
PubMed1986

The effect of confinement on days to puberty in gilts.

In the late fall and winter of 1982 to 1983, 112 crossbred gilts were used in a factorially arranged experiment to determine the effect of confinement on the age at which a gilt reaches first estrus (puberty). Two environments (confinement and non-confinement) and three ages at movement to non-confinement (100, 140, and 180 d) were studied. No differences were detected (P greater than .05) between confinement and non-confinement in the proportions of gilts reaching puberty by 210 d of age. Gilts were older at puberty (P less than .05) in confinement than in non-confinement (192.0 vs 187.7 d) and had a longer interval (P less than .05) from first boar contact to first estrus (12.1 vs 7.8 d). Age at puberty (192.1 vs 187.0 vs 190.5 d) and the proportion reaching puberty (56.4 vs 45.7 vs 65.8%) were not different (P greater than .05) between age-of-movement groups. However, a higher (P less than .05) proportion of the non-confinement gilts reached puberty within 10 d after the beginning of boar exposure than confinement (44.6 vs 26.8%). Moving gilts from confinement to non-confinement (pasture) at 180 d appeared to be the most effective method tested for inducing puberty in gilts.

Animals↗
PubMed1996

Gonadotropin-releasing hormone and NMDA receptor gene expression and colocalization change during puberty in female rats.

During development, an increase in gonadotropin-releasing hormone (GnRH) release occurs that is critical for the initiation of puberty. This increase is attributable, at least in part, to activation of the GnRH neurosecretory system by inputs from neurotransmitters, such as glutamate, acting via NMDA receptors. We examined changes in GnRH and NMDA-R1 gene expression by RNase protection assay of preoptic area-anterior hypothalamic (POA-AH) dissections of female rats undergoing normal puberty or in which precocious puberty was induced by treatment with the glutamate agonist NMA. GnRH mRNA levels increased significantly throughout normal development; this was accelerated by treatment with NMA. NMDA-R1 mRNA levels increased only between P10 and P20. The acceleration of the elevation in GnRH mRNA levels by NMDA suggests that a stimulation of GnRH gene expression may be a rate-limiting factor for the onset of puberty. This is attributable to a post-transcriptional mechanism because GnRH primary transcript levels, an index of proGnRH gene transcription, were not observed to change during puberty. Alterations in the colocalization of GnRH neurons with the NMDA-R1 subunit during puberty also were assessed immunocytochemically. The percentage of GnRH neurons that double-labeled with NMDA-R1 was 2% in prepubertal rats and 3% in pubertal rats; this increased to 19% in postpubertal rats. Taken together, these studies suggest that an increase in glutamatergic input to GnRH neurons plays a role in the increase in GnRH release and gene expression that occurs at the initiation of puberty.

Animals↗
PubMed2004

[Influence of birthweight on the onset and progression of puberty and final height in precocious pubarche].

BACKGROUND: Girls born small for gestational age (SGA), with a birth weight < 1.5 SDS, are at increased risk of early onset and rapid progression of puberty, with reduced final height. In contrast, idiopathic precocious pubarche (PP) does not seem have negative effects on the onset of puberty or final height. OBJECTIVE: We evaluated the relationship between birthweight, the onset and progression of puberty and final height in girls with PP. METHODS: We performed a retrospective study of girls at the onset of puberty with a history of PP (pubic hair before the age of 8 years). RESULTS: A total of 124 girls (37 SGA) were investigated; 61 had presented menarche and 44 had reached final height. The mean ( SD) age was 6.8 0.8 years at pubarche, 9.5 0.9 at the onset of puberty and 11.7 6 0.9 at menarche. No significant differences were found in the correlation between birth weight expressed in SDS and age at presentation of pubarche, bone age at presentation of pubarche, age at telarche or age at menarche. A positive correlation was found between birthweight and height at pubarche, telarche, and menarche and final height. These data suggest that pubertal progression is faster in SGA girls. All patients reached the familial target height but only those with an appropriate birthweight were taller than their mothers. CONCLUSIONS: PP does not seem to modify age of onset or progression of puberty or final height in girls with adequate birth weight. In contrast, in SGA girls, PP is associated with faster puberal development and shorter final height. Therefore, SGA girls with PP require periodic monitoring.

Age of Onset↗
PubMed2000

Changes in serum inhibin, activin and follistatin concentrations during puberty in girls.

Serum concentrations of inhibin A, inhibin B, activin A and follistatin were determined using two-site enzyme-linked immunosorbent assays (ELISA) during pubertal ovarian development in 28 girls and five follicular phase women. Blood obtained every 15 to 20 min overnight was pooled for peptide determination. Serum inhibin A concentrations increased in mid puberty, exhibiting positive correlations with bone age (r = 0.527, P = 0.0016) and oestradiol concentrations (r = 0.581, P = 0.0005). Inhibin B concentrations peaked in mid puberty and declined thereafter, but remained greater than concentrations seen in prepubertal girls, and correlating positively with oestradiol (r = 0.362, P = 0.046) and follicle stimulating hormone (FSH) concentrations (r = 0.369, P = 0.038). Total activin A concentrations did not vary significantly across pubertal stages. Total follistatin concentrations, determined by radioimmunoassay, decreased with advancing puberty, exhibiting negative correlations with bone age (r = -0.634, P = 0.0001) and oestradiol concentration (r = -0.687, P = 0.0001). Follistatin concentrations determined by an ELISA specific for follistatin 288 were greatest in mid-pubertal girls, but concentrations in late puberty were less than those in early puberty. The free follistatin assay indicated that all circulating follistatin was activin-bound. These results suggest that significant changes in serum concentrations of FSH-regulatory peptides accompany the onset of puberty.

Activins↗
PubMed1999

Pubertal growth as a determinant of adult height in boys with constitutional delay of growth and puberty.

In boys with constitutional delay of growth and puberty, adult height may be inconsistent with parental (target) height. We aimed at studying which period of growth was important to account for adult height being above or below target height. In this retrospective study, adult height measured after 20 years in 39 patients was compared with target height and height data obtained at about 6 and 12 years of age and at diagnosis of delayed puberty (mean 14.6 years). Twenty-eight patients were untreated while 11 received testosterone enanthate (50 or 100 mg/month for 6 months). The growth data from both groups were pooled since they were not different. On average, the adult height standard deviation score (-0. 6 +/- 0.8, mean +/- SD) was similar to target height (-0.5 +/- 0.6). There were, however, marked individual differences since adult height varied between 1.7 SD (11 cm) below target height and 1.4 SD (9.5 cm) above target height. Multiple regression analysis showed that the most significant determinant of the difference between adult height and target height was height catch up during puberty (p < 0.002). We conclude that the magnitude of height catch up during puberty is a significant determinant of adult height in boys with constitutional delay of growth and puberty. Thus, optimizing pubertal growth may be a relevant therapeutic aim for adult height in boys with short stature and delayed puberty. Copyrightz1999S. KargerAG,Basel

Adolescent↗
PubMed2006

Metformin treatment to prevent early puberty in girls with precocious pubarche.

CONTEXT AND OBJECTIVE: Girls with precocious pubarche (PP, pubic hair at < 8 yr of age) are at high risk for early onset and rapid progression of puberty, in particular if their prenatal growth was restrained, i.e. low birth weight (LBW), and followed by rapid postnatal catch-up of weight gain. We postulated that insulin resistance contributes to early onset and rapid progression of puberty in LBW-PP girls and thus explored the puberty-delaying effects of insulin sensitization with metformin initiated shortly after PP diagnosis. SETTING, DESIGN, AND PATIENTS: The study population consisted of 38 prepubertal LBW girls with PP attributed to exaggerated adrenarche [mean body weight, 2.4 kg; age, 7.9 yr; body mass index (BMI), 18.4 kg/m(2)]. These girls were randomly assigned to remain untreated (n = 19) or to receive metformin (n = 19; 425 mg/d) for 2 yr. MAIN OUTCOME MEASURES: Pubertal staging, age at menarche, body composition by absorptiometry, fasting insulin, glucose, lipids, leptin, IGF-I, IGF-binding protein-1, testosterone, dehydroepiandrosterone sulfate, and SHBG were the main outcome measures. RESULTS: Metformin treatment was associated with a less adipose body composition (and lower serum leptin levels) and with a 0.4-yr delay in the clinical onset of puberty (Tanner B2; 9.5 vs. 9.1 yr; P < 0.01). These findings were corroborated by a delay of at least 1 yr in the puberty-associated rise of circulating IGF-I (P < 0.01). Available results also point to a metformin-associated delay of menarche (P < 0.02). Gain in height and lean mass was not divergent between study subgroups. CONCLUSION: The efficacy of early metformin treatment in PP girls is here extended to include not only a less adipose body composition after 2 yr but also a less advanced onset of puberty, whereas height gain is maintained. These findings open the perspective that, ultimately, metformin treatment may also prove to heighten the short adult stature of LBW-PP girls.

Adrenarche↗
PubMed1986

Naloxone-induced luteinizing hormone secretion in normal, precocious, and delayed puberty.

The aim of the present study was to evaluate the activity of opiate receptors involved in the control of LH secretion during pubertal development, as determined by the LH response to naloxone. Normal children (n = 28) of both sexes, subdivided according to breast (girls) or testicular (boys) development, and patients with idiopathic precocious puberty (n = 7), delayed puberty (n = 8), or hypergonadotropic hypogonadism (n = 4) were studied. Plasma LH levels were measured after the administration of naloxone (NLX; 0.08 mg/kg BW, iv), GnRH (50 micrograms, iv) or placebo. In healthy subjects, NLX significantly increased plasma LH levels only in girls and boys at the most advanced stage of gonadal maturation. NLX was ineffective in prepubertal and early pubertal children, and it did not significantly alter LH levels in children with delayed puberty or hypogonadism or in most of the children with precocious puberty. GnRH injection consistently increased plasma LH levels in healthy subjects as well as in the children with pubertal disturbances. These results indicate that the LH response to NLX occurs only at the most advanced stages of pubertal maturation when normal or precocious and is absent in early puberty or in children with pubertal disturbances. Furthermore, the results suggest that opioid regulation of LH secretion in humans changes during puberty, reaching an adult-like functional state with maturation of the hypothalamus-pituitary-gonadal axis.

Adolescent↗
PubMed1992

[Disorders of puberty and gonadal disorders in the child].

Normal puberty has a characteristic harmony or consonance between the individual modalities of sexual maturation. Thus, the objective description and detailed knowledge of physical pubertal development is the basis of the clinical analysis of pubertal disorders. An aim of the review is to provide details of the visible changes the clinician must note in order to document the normal progression of puberty. Disorders of puberty can be classified by the timing of onset of sexual characteristics into either precocious or delayed puberty. A more useful concept, however, than the abnormalities of timing of puberty is whether the pubertal development is true (consonant) or if there is a pseudo-puberty (absence of consonance). This is of greater significance in relation to the pathophysiology and, therefore, the investigations and therapies which will be required. The use of either well known or new agents that may be used for treatment of pubertal disorders are presented.

Adolescent↗