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PubMedDate not supplied

Early puberty in girls: the case of premature adrenarche.

In this article we examine the issue of early puberty in girls. First, a brief overview of normal pubertal development is provided, including the two endocrine components of puberty: gonadarche and adrenarche. Second, we critically discuss the controversy regarding whether puberty truly is occurring earlier in girls. Third, we emphasize one type of early puberty, the case of premature adrenarche (PA). PA is used to illustrate the importance of identifying types of early puberty, evaluating the types to determine causality, determining whether follow-up of early puberty is necessary, and showing the potential ramifications of ignoring this variation in pubertal development. Findings from a pilot study comparing PA and on-time puberty children are used to show the importance of determining whether early puberty is normal in all cases.

Adrenal Glands↗
PubMed1989

The metoclopramide test: a useful tool with the luteinizing hormone-releasing hormone test in distinguishing between constitutional delay of puberty and hypogonadotropic hypogonadism.

To evaluate the effectiveness of intravenous metoclopramide, alone or in combination with luteinizing hormone-releasing hormone (LH-RH), in distinguishing between constitutional delay of puberty and hypogonadotropic hypogonadism, 12 patients with constitutional delay of puberty and 10 patients with hypogonadotropic hypogonadism were studied. All patients received 10 mg/m2 of intravenous metoclopramide and 100 micrograms of intravenous LH-RH on separate days. The mean prolactin (PRL) response following metoclopramide was significantly higher in the constitutional delay of puberty group when compared with the hypogonadotropic hypogonadism patients (P less than 0.01 at 15, 30, 45, and 60 minutes); all patients with constitutional delay of puberty increased their PRL level to greater than or equal to 60 ng/ml, except one who had a peak PRL level of 38 ng/ml. While only 2 of the hypogonadotropic hypogonadism subjects reached a peak PRL concentration of greater than or equal to 60 ng/ml, 4 had peak PRL levels greater than 38 ng/ml. The mean LH and follicle-stimulating hormone (FSH) responses after LH-RH were significantly higher in the constitutional delay of puberty group (P less than 0.01 at 30, 45, and 60 minutes for LH and P less than 0.01 at 45 and 60 minutes for FSH). All constitutional delay of puberty subjects responded to both the metoclopramide and LH-RH tests, while patients with hypogonadotropic hypogonadism responded only to one or to neither of these tests. Therefore, while metoclopramide alone did not allow us to clearly distinguish constitutional delay of puberty from hypogonadotropic hypogonadism, the combined use of both of these stimuli permitted us to detect all subjects with constitutional delay of puberty.

Adolescent↗
PubMed2000

[Precocious puberty in children adopted from foreign countries].

AIMS: Precocious puberty has been more frequently observed in the population of children adopted from abroad. A study was therefore carried out to assess the prevalence of this early onset of puberty. POPULATION AND METHODS: In this study, 13 cases of precocious puberty have been examined in ten adopted girls and three adopted boys, and the clinical characteristics and other contributing factors have been described. In this study group, three of the cases were familial. In addition, a questionnaire was also completed by 99 French families with children adopted from abroad, and analyzed to determine the frequency of early pubertal development. The parameters included were age, weight and height at the time of adoption, date of onset of puberty, for the girls age at first menstruation, and current height and weight. RESULTS: It was determined that the 13 children had a very high growth recovery rate from the time that they arrived in France. For the period from time of adoption to the onset of puberty, mean height increased from -1.3 to +1.5 standard deviation score (SDS) and the mean weight-for-height factor increased from +1.2 to 1.9 SDS. The weight-height recovery rate following adoption seems to be the direct cause of early pubertal development in certain children, notably in those with a particularly rapid growth rate (between 6 years 6 months and 8 years 9 months for the girls, and between 8 and 10 years for the boys). In children adopted at an early age, a 'biological memory' seems to exist regarding the renutrition phenomenon which was instrumental in accelerating the onset of puberty some years after adoption. An analysis of the survey on the adoptive families showed that the frequency of precocious puberty was 44.9% in the group of 49 girls compared to only 8.6% in the group of 35 adopted boys, and that it mainly concerned children from Africa (57%), followed by those from South and Central America (57%), Asia (45%), and Eastern Europe (29%). CONCLUSION: A higher rate of precocious puberty was found in the adopted girls, with a significantly lower rate in the adopted boys. The etiological factors involved seemed to be mainly nutritional, and influenced by leptin and insulin-like growth factor 1 (IGF1) levels. The role of the latter and their interaction with other factors, particularly the ethnic aspect, remains to be determined via the study of a larger series of adopted children.

Adoption↗
PubMed2004

Precocious puberty at an endocrine centre in Jordan.

BACKGROUND: Data from developed countries about precocious puberty are abundant; data from developing countries are limited. Causes are different, and diagnostic and treatment possibilities are very expensive. The present study aimed to display the spectrum of initial presentation and aetiology among children with precocious puberty and to assess any association between th e clinical features and the underlying cause of the condition. PATIENTS AND METHOD: Forty-three girls and seven boys with precocious puberty were diagnosed at the Endocrine Clinic of Jordan University Hospital and at The National Center for Diabetes, Endocrinology and Genetics, Amman, Jordan, between the 1984 and 2003. RESULTS: Mean age for the girls with precocious puberty was 4.1 years +/- 2.5 SD and for the boys was 2.4 years +/- 1.9 SD. Among the girls, 21% presented with breast development only, 9% with pubic hair appearance only and 70% with multiple signs. All the boys presented with pubic hair appearance and enlarged genitalia. Organic causes for precocious puberty were detected in 42% of the girls and in all the boys. Idiopathic precocious puberty was more common among the girls presenting with breast development only (89%) compared with those presenting with multiple presenting signs (50%), and also was more common among girls presenting between 6 and 8 years (82%) than among those presenting < 6 years of age (42%). Congenital adrenal hyperplasia was diagnosed in four boys and four girls, and hypothyroidism in three girls. CONCLUSION: Precocious puberty in the girls was usually of idiopathic origin when it presented with breast development only and at age older than 6 years. Congenital adrenal hyperplasia and hypothyroidism could represent important causes for precocious puberty in our community.

Child, Preschool↗
PubMed2006

Early influences on the tempo of puberty.

Fetal growth retardation appears to be associated with an increased risk of premature adrenarche, early puberty, polycystic ovary syndrome and associated fertility problems. In a rat model of intrauterine growth retardation, based on ligation of the uterine arteries, the onset of puberty was delayed in female pups, with anovulation during the first cycle. The ovaries showed a lower number of follicles. The onset of puberty was also delayed in male pups. Testosterone production was lower in these growth-retarded rats compared with controls. The relationship between birth weight and the onset of puberty and pubertal progression in different cohorts of healthy children has been examined. In girls, no differences were observed in timing and progression of puberty, including age of menarche, between groups of different birth weights. In boys, a relatively delayed onset of puberty was observed in those with low birth weight, with a normally timed progression. In children with low birth weight, particularly boys, higher dehydroepiandrosterone levels were found compared with children with a normal birth weight, indicating an overactive adrenal gland in children with low birth weight. These data indicate that impaired fetal growth may have long-lasting effects on pubertal development. The fact that results of human studies on the relationship between fetal growth and the onset of puberty are often controversial may be explained by the heterogeneity of children born small for gestational age with respect to the intrauterine insult that they experience. From rat studies, it is clear that a serious intrauterine insult associated with growth failure can lead to dysregulation of puberty and gonadal function.

Adolescent↗
PubMed2003

Delayed puberty associated with inflammatory bowel disease.

Delayed puberty frequently complicates the clinical course of young patients with inflammatory bowel disease, more often in Crohn's disease than ulcerative colitis. Undernutrition has been thought to be the main reason for delayed puberty in these patients. However, puberty may be delayed despite a normal nutritional status. Observations in patients with inflammatory bowel disease and in rats with experimental colitis suggest that inflammatory mediators may have a direct adverse influence, independent of undernutrition, on the onset and progression of puberty. Serum androgens are consistently reported to be reduced in patients with delayed puberty and inflammatory bowel disease. This reduction is not necessarily secondary to a reduction in gonadotrophins as serum concentrations of gonadotrophins have been reported to be normal or even increased in some studies. Management of delayed puberty involves calorie supplements to correct undernutrition and treatment of inflammation. Observations in boys with delayed puberty and controlled studies in experimental models of intestinal inflammation suggest that testosterone therapy can accelerate puberty.

Animals↗
PubMed2000

Increased fetal glucocorticoid exposure delays puberty onset in postnatal life.

The fetal environment is now recognized as a key determinant of the adult phenotype, being linked to development of diseases, including hypertension, as well as the timing of puberty. Such links may be related, in part, to the level of fetal exposure to maternal glucocorticoids in utero, which is normally regulated by placental expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11beta-HSD). The present study examined whether manipulation of fetal glucocorticoid exposure, either directly or indirectly via 11beta-HSD inhibition, influences the subsequent timing of puberty. Administration of dexamethasone acetate at low (LDEX, 0.25 microg/ml drinking water) or high doses (HDEX, 1 microg/ml) or carbenoxolone (CBX, 2 x 10 mg/day, sc; an inhibitor of 11beta-HSD) to pregnant rats from day 13 to term (day 23) reduced offspring birthweight (LDEX: 9%; HDEX: 27%; CBX: 8%) and resulted in a subsequent delay in the onset of puberty in females (control: 41.4 +/- 0.5; LDEX: 44.8 +/- 0.7; HDEX: 48.5 +/- 0.4; CBX: 43.6 +/- 0.5 days). Importantly, the effects of CBX were not observed in the absence of maternal adrenals, indicating that they were mediated by increased fetal exposure to endogenous maternal glucocorticoids. In contrast, maternal treatment with metyrapone (MET; an inhibitor of glucocorticoid synthesis; 500 microg/ml drinking water from day 13) increased birthweight by 5% and advanced puberty onset in male offspring (control: 48.8 +/- 1.0; MET: 45.7 +/- 0.8 days). Changes in the timing of puberty onset were not attributable to changes in either bodyweight at puberty or peripubertal plasma leptin concentrations. Peripubertal plasma LH was also unaffected in animals with delayed puberty but was elevated in male offspring of MET-treated mothers. Collectively, these results demonstrate that fetal glucocorticoid exposure is an important determinant of the timing of puberty onset in postnatal life, and that this effect is operable within the normal physiological range of glucocorticoid concentrations.

Aging↗
PubMed2006

A homozygous R262Q mutation in the gonadotropin-releasing hormone receptor presenting as constitutional delay of growth and puberty with subsequent borderline oligospermia.

CONTEXT: The GnRH receptor plays a central role in regulating gonadotropin synthesis and release, and several mutations in the GNRHR gene have been reported in patients with idiopathic or familial forms of isolated hypogonadotropic hypogonadism (IHH). OBJECTIVE: The objective of the study was to investigate whether partial loss-of-function mutations in the GnRH receptor might be responsible for delayed puberty phenotypes. PATIENTS: Patients included sibling pairs with delayed puberty (n = 8) or those in whom one brother had delayed puberty and another had hypogonadotropic hypogonadism (n = 3). METHODS: Methods included mutational analysis of the GNRHR gene. RESULTS: A homozygous R262Q mutation in the GnRH receptor was identified in two brothers from one family. In this kindred, the proband presented at 15 yr of age with delayed puberty. After a short course of testosterone, he seemed to be progressing through puberty appropriately and was discharged from follow-up. His younger brother was also referred with delayed puberty but showed little progress after treatment. Frequent sampling revealed detectable but apulsatile LH and FSH release. His clinical progress was consistent with IHH, and he requires ongoing testosterone replacement. CONCLUSIONS: Homozygous partial loss-of-function mutations in the GnRH receptor, such as R262Q, can present with variable phenotypes including apparent delayed puberty. Ongoing clinical vigilance might be required when patients are discharged from follow-up, especially when there is a family history of delayed puberty or IHH because oligospermia and reduced bone mineralization can occur with time.

Adolescent↗
PubMed1994

Serum insulin-like growth factor-I in 1030 healthy children, adolescents, and adults: relation to age, sex, stage of puberty, testicular size, and body mass index.

Serum levels of insulin-like growth factor-I (IGF-I) increase with age and pubertal development. The large variation in circulating IGF-I levels in adolescence makes it difficult to use the IGF-I value of a single child in the assessment of his growth status. In addition, the interference of IGF-binding proteins in many IGF-I assays contributes to this problem. We measured IGF-I in acid-ethanol-extracted serum from 1030 healthy children, adolescents, and adults, employing a RIA that reduces interference of IGF-binding proteins by using monoiodinated Tyr31-[125I]des-(1-3)IGF-I as radioligand. Mean serum IGF-I concentrations increased slowly in prepubertal children from 80-200 micrograms/L with a further steep increase during puberty to approximately 500 micrograms/L. After puberty, a subsequent continuous fall in circulating IGF-I levels was apparent throughout adulthood to a mean of 100 micrograms/L at the age of 80 yr (P < 0.0001). Girls had maximal IGF-I levels at 14.5 yr of age, whereas boys had peak IGF-I levels 1 yr later. This is almost 2 yr later than average peak height velocity. The large variation in serum IGF-I levels during puberty was diminished when data were separated according to sex and Tanner stage of puberty. Interestingly, we found a significant variation with age within the Tanner stages; there was an increase in serum IGF-I concentrations with age in the early pubertal stages and a decrease in the late stages (P < 0.05). Serum IGF-I increased concomitantly with increasing testicular volume. Multiple regression analysis revealed that serum IGF-I levels predicted height velocity in the following year (r = 0.33; P < 0.0001). Body mass index did not correlate significantly with serum IGF-I in prepubertal children in a multiple regression analysis. In conclusion, there was a significant variation in serum IGF-I levels with age within a given Tanner stage of puberty in addition to the well known increase with increasing age or pubertal stage. Accordingly, the effects of sex, age, and puberty on serum IGF-I cannot be separated into simple additive components when studying 1030 children in a cross-sectional design. Thus, the age-, sex-, and puberty-corrected IGF-I values may, in fact, improve the use of serum IGF-I as a diagnostic tool to distinguish between a child with retarded puberty and a GH-deficient individual.

Adolescent↗
PubMed2001

Intrauterine growth retardation and puberty in girls.

Some, albeit not all studies on the relationship between intrauterine growth retardation (IUGR) and female pubertal development have found an earlier and rapidly progressing puberty as well as concomitant disorders of related functional systems such as polycystic ovary syndrome and short stature. These pubertal changes are part of a growing list of IUGR-related diseases, which includes non-insulin dependent diabetes mellitus and coronary heart disease. A pulsatile release of gonadotropin releasing hormone is thought to be a conditio-sinne-qua-non for the initiation of puberty. In the absence of prospective studies on gonadotropin releasing hormone pulse patterns in IUGR-children other markers of pubertal development such as age at menarche have been deployed. From these studies it is not clear, however, whether the findings of an earlier onset of puberty in IUGR-girls merely reflect a more rapid progression of puberty. Both the role for IUGR and the mechanisms behind the onset of puberty are still elusive. Assuming a connection between IUGR and pubertal development, parallels can be drawn between hypotheses on the longterm consequences of IUGR and hypotheses on the initiation of puberty. For example, the somatometer concept proposes a role for fat mass in the initiation of puberty, which is compatible with the hypothesis on non-skeletal catch-up growth after IUGR. The debate on the origins of puberty and the role of IUGR mainly focuses on nature and nurture. Judgmentally, studies in mono- and dizygotic twins discordant for birth weight may be of particular help.

Adipose Tissue↗
PubMedDate not supplied

Secondary central precocious puberty in a girl with McCune-Albright syndrome responds to treatment with GnRH analogue.

GnRH analogues have been used with variable success for the treatment of precocious puberty in children with McCune-Albright syndrome (MAS). In general, children with a bone age of less than 13.5 yr have been reported not to have benefitted from GnRH therapy. In contrast, we have successfully treated a young girl with MAS and--probably secondary--central precocious puberty using Decapeptyl, a long acting GnRH analogue. The girl with MAS presented at the age of six years with café au lait spots, osseous lesions and precocious puberty. At initial presentation height was 130.7 cm (> 97 percentile), weight 27.5 kg (> 97 percentile), Tanner stage B3, PH3. Bone age was 11 yr. Magnetic resonance imaging of the brain was normal. Endocrine function tests were normal with the exception of biochemical evidence of central precocious puberty: LHRH test: LH 0.9/20.3, FSH 4.3/12.7 (mU/ml), E2 15.6 pg/ml. Therapy was started with 3.75 mg GnRH analogue i.m. every four weeks and was intensified two years after the beginning of therapy to 3.75 mg i.m. every three weeks. Three years after the start of treatment bone age was 12 yr and growth velocity was 2.5 cm/year. Tanner stage was B3, PH3 and LHRH testing revealed biochemical evidence for suppression of gonadotropins: LH < 0.5/1.0, FSH 1.9/2.5 (mU/ml). We hypothesize that a subgroup of patients with MAS might present with a central form of precocious puberty. This may be particularly so in children with a bone age greater than or equal to 11 yr. Central precocious puberty in these children might follow extensive sex steroid exposure due to the peripheral precocious puberty induced by the activating mutation of the Gs protein gene. This central form of precocious puberty responds to therapy with GnRH analogues.

Brain↗
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↗
PubMed1994

MR imaging diagnosis of central precocious puberty: importance of changes in the shape and size of the pituitary gland.

OBJECTIVE: Central precocious puberty occurs as a result of premature pituitary stimulation and increased secretion of gonadotropins. The aims of this study were to analyze MR imaging findings in the pituitary glands of children with central precocious puberty compared with matched control subjects, to define MR imaging-derived variables useful in the diagnosis of central precocious puberty, and to correlate MR imaging-derived variables with the hormonal profile and other imaging and clinical findings. MATERIALS AND METHODS: Twenty-six children with central precocious puberty (two boys and 24 girls) were divided into two subgroups according to MR imaging findings: idiopathic (21 patients) and nonidiopathic (five patients: three hypothalamic hamartomas, one pineal tumor, one empty sella syndrome). The control group consisted of 17 normal age- and sex-matched children (two boys, 15 girls). Analyzed parameters included pituitary height, length, width, midsagittal cross-sectional area, calculated volume, and shape. The shape was assessed by a pituitary grading system and two other shape indexes (length-to-height and length-to-width ratios). Pituitary grade was defined by the concavity of the upper pituitary surface (grade 1 = marked concavity, grade 2 = mild concavity, grade 3 = flat, grade 4 = mild convexity, grade 5 = marked convexity). RESULTS: Pituitary grade showed a highly significant difference among groups (p < .001). Area, height, and length-to-height ratio were significantly different (p < .05), whereas length, width, length-to-width ratio, and volume were not. There was no significant difference in any of the variables compared between idiopathic and nonidiopathic groups. When selected variables (pituitary grade, area, height, length) in the central precocious puberty group were stratified by bone age and findings on pelvic sonograms, patients with advanced bone age had a significantly higher pituitary grade (p < .01) and had a tendency toward a greater pituitary length. Pituitary size and shape correlated with the hormonal profile. CONCLUSION: Change in pituitary grade is the most helpful variable for the diagnosis of central precocious puberty in a prepubertal child. A high pituitary grade (4 or above) is highly predictive of central precocious puberty, with the highest specificity and positive predictive value, but with low sensitivity. The use of combinations of high pituitary grade with two other positive findings (height and area greater than 1 SD from the respective means in the control group) improves the sensitivity, specificity, and predictive value of MR imaging in the diagnosis of central precocious puberty.

Analysis of Variance↗
PubMed1996

Effects of exposure to an estrual female on the attainment of puberty in gilts.

A total of 304 prepubertal gilts were randomly allocated to 4 treatment groups across 10 replications for a 50 d treatment period beginning at 170 d of age. The 4 treatment groups consisted of: 1) Gilts that were continuously exposed to one of a group of older, ovariectomized females that had been treated with 2 mg/ml estradiol benzoate to stimulate estrus (SE); 2) Gilts that were continuously exposed to an older, anestrous, ovariectomized female (OVX); 3) Gilts that were exposed to a mature boar for 15 min/d (BE); 4) Gilts that were isolated from any direct physical contact with other pigs (C). A gilt was considered to have attained puberty when she exhibited a standing reflex when mounted by the boar (BE group only) or to pressure applied manually to the back or had plasma progesterone concentrations > 2 ng/ml for 2 consecutive weeks. Data were analyzed as a randomized complete block design with treatment and replication in the model. A higher percentage of gilts attained puberty in the BE group than in the 3 other groups (52 vs 26, 30 and 32%, BE vs SE, OVX and C, respectively; P = 0.002). Gilts exposed to an estrual female or a mature boar attained puberty sooner after treatment was initiated than gilts in other treatment groups (12.6 and 17.8 vs 26.7 and 24.1 d, SE and BE vs OVX and C, respectively; P = 0.0003). Of the gilts attaining puberty during the experimental period, the highest percentage of gilts exhibited estrus within 10 d of treatment in the SE group (55.0 vs 26.1, 37.8 and 16.7%, BE vs SE, OVX and C, respectively; P = 0.05). Age at puberty was also lower SE or BE than OVX or C groups (176.3 and 181.0 vs 189.4 and 188.1 d, respectively; P = 0.0001). Weight at puberty was unaffected by treatment. These results suggest that exposure to an estrual female was effective in stimulating peripubertal females to express estrus, thus reducing the age at puberty. Boar exposure had a stimulatory effect not only at the initiation of exposure but throughout the experimental period, resulting in a higher percentage of gilts attaining puberty.

Journal Article↗
PubMed2005

Growth hormone-releasing factor (GRF) induced growth hormone advances puberty in female buffaloes.

Exogenous bovine growth hormone-releasing factor (bGRF) at the dose rate of 10 microg/100 kg body weight was administered intravenously (i.v.) to six Murrah buffalo heifers as treatment group, while another six buffalo heifers served as control group which received the vehicle (0.9% NaCl solution) at an interval of 15 days for a period of 9 months to study the effect of bGRF on puberty onset associated with temporal hormonal changes in peri-pubertal buffalo heifers. Blood samples were collected at 3-day interval from all the animals during the experimental period and plasma harvested was assayed for growth hormonal (GH), luteinizing hormone (LH) and progesterone. The day that plasma progesterone was greater than 1.0 ng/ml for three consecutive sampling days was defined as the day of puberty. Exogenous bGRF administration increased (P = 0.02) plasma GH concentration in treatment group over control group during the treatment of bGRF as well as during the peri-pubertal period. Plasma progesterone concentrations increased transiently earlier (P = 0.05) by 58.5 days in bGRF-treated buffaloes than that in the control group. However, plasma LH concentrations were unaffected by the treatment of bGRF (P = 0.48). Both plasma GH and LH in the buffalo heifers increased (P < 0.01) over time preceding puberty and the higher hormonal concentrations were maintained during the onset of puberty, and thereafter, the concentrations of both the hormones declined (P < 0.05) after puberty. GH and LH were positively correlated both before puberty (r = +0.59 and +0.63; P < 0.05 for control and treatment group, respectively) and after puberty (r = +0.42 and +0.46; P < 0.05 for control and treatment group, respectively) indicating the interaction and/or close relationship of GH and LH in the mechanism of puberty in buffalo species.

Animals↗
PubMed2004

Gonadal hormones masculinize and defeminize reproductive behaviors during puberty in the male Syrian hamster.

Three experiments were conducted to test whether testicular hormones secreted during puberty masculinize and defeminize the expression of adult reproductive behavior. Experiment 1 tested the hypothesis that gonadal hormones during puberty masculinize behavioral responses to testosterone (T) in adulthood. Male hamsters were castrated either before puberty (noTduringP) or after puberty (TduringP). All males were implanted with a 2.5-mg T pellet 6 weeks following castration and tested once for masculine reproductive behavior 7 days after the onset of T replacement. TduringP males displayed significantly more mounts, intromissions, and ejaculations than noTduringP males. Experiment 2 tested the hypothesis that gonadal hormones during puberty defeminize behavioral responses to estrogen (EB) and progesterone (P). Eight weeks following castration, noTduringP and TduringP males were primed with EB and P and tested for lordosis behavior with a stud male. Behavioral responses of males were compared to that of ovariectomized (OVX) and hormone primed females. NoTduringP males and OVX females displayed significantly shorter lordosis latencies than TduringP males. Experiment 3 investigated whether prolonged T treatment or sexual experience could reverse the deficits in masculine behavior caused by the absence of T during puberty. Extending the T treatment from 7 to 17 days did not ameliorate the deficits in masculine behavior caused by absence of T during puberty. Similarly, when the level of sexual experience was increased from one to three tests, the deficits in masculine behavior persisted. These studies demonstrate that gonadal hormones during puberty further masculinize and defeminize neural circuits and behavioral responsiveness to steroid hormones in adulthood.

Animals↗
PubMed1999

Embryo production by ovum pick up in unstimulated calves before and after puberty.

The possibility of producing embryos from oocytes repeatedly collected from unstimulated calves was tested, and results obtained before and after puberty were compared in the same animals. Ovum pick-up (OPU) coupled with in vitro embryo production was used on 2 sets of 7 and 9 calves, aged 7 to 10 m.o. at the start of the experiment. The oocytes were collected twice a week during a 2-m.o. period before puberty and a 1-m.o. period after puberty. Oocytes were fertilized and co-cultured with cumulus cells in modified synthetic oviduct fluid (SOF) up to Day 7 post insemination. Some Day 7 blastocysts were vitrified and transferred to recipient heifers. An average of 3.8 to 6.8 follicles was punctured per OPU session; 1.9 to 3.1 oocytes were collected, of which more than 60% were of good quality. The number of punctured follicles and collected oocytes varied between donors. Blastocyst rates of 19 to 27% were obtained for the 2 sets. Three normal calves were born from the transfer of 20 vitrified embryos. While no significant difference was observed for the first set of calves, a significant decrease in the number of punctured follicles was observed after puberty in the second set. A direct correlation was also obtained between the number of follicles punctured before and after puberty in the same animal. In conclusion, oocytes can be collected by repeated OPU in calves 7 to 10 m.o. old without affecting their growth or the onset of puberty. An average of 5 to 11 (range 0 to 16) blastocysts per donor was produced over 2 month. However, important variations were found between donors. The correlation observed for the number of follicles punctured before and after puberty suggests that this parameter is determined before puberty.

Age Factors↗
PubMed1983

Influence of season on sexual development in heifers: age at puberty as related to growth and serum concentrations of gonadotropins, prolactin, thyroxine and progesterone.

An experiment was done to test the hypothesis that seasonal changes in environment during the first and second 6 months of life influence age at puberty in heifers. Twenty-eight Angus X Holstein heifers, born in March (M) or September (S), were reared under natural conditions until 6 months of age. From 6 to 12 months of age, heifers were reared in environmental chambers programmed to simulate seasonal changes in temperature and photoperiod characteristic of spring, summer and early autumn (Sp-F chamber) or autumn, winter and early spring (F-Sp chamber). S were younger (P less than 0.06) at puberty than M, and Sp-F were younger (P less than 0.08) than F-Sp for both M and S. Mean ages at puberty were 295 for S, Sp-F; 319 for S, F-Sp; 321 for M, Sp-F and 346 days for M, F-Sp. Average daily gain (ADG) between 6 and 9 months of age [1.03 kg/day (S) vs. 0.91 kg/day (M)] and mean concentrations of serum luteinizing hormone (LH) between 6 and 7 months of age [3.45 ng/ml (S) vs. 0.47 ng/ml (M)] were greater (P less than 0.01) for S than M, suggesting an association between these traits and date of birth effects on age at puberty. Differences in these traits did not seem to be involved in the chamber effect on age at puberty, since ADG from 6-9 months of age was greater (P less than 0.05) for F-Sp heifers and chamber did not generally affect LH concentrations. Serum concentrations of follicle-stimulating hormone (FSH) were not significantly influenced by month of birth or chamber, but concentrations tended to decrease with age. Serum concentrations of thyroxine (T4) were higher in M than S at 6 months of age (7.8 micrograms/dl vs. 6.3 micrograms/dl) but not at other times, and chamber did not have a significant affect. Prolactin (Prl) concentrations paralleled patterns of temperature and day length and did not appear to be related to age. Although cattle are not seasonal breeders, these results demonstrate that season of birth and season of attainment of puberty influence age at puberty in heifers. Season may have influenced age at puberty by affecting serum concentrations of LH or Prl, or growth rate.

Animals↗