Age Of Puberty Onset Research Articles

Puberty Onset and Preservation of Fertility in Male Patients with Sickle Cell Disease Treated with Hydroxyurea: Data from the European Sickle Cell Disease Cohort - Hydroxyurea Extension (ESCORT-HU Extension) Study

Introduction Reproductive health is a major concern in male patients with sickle cell disease (SCD). SCD is associated with pubertal delay (Soliman 2021), however, limited large-scale studies exist on the age of puberty onset in male SCD patients. Additionally, men without hydroxyurea (HU) therapy often experience decreased fertility, with less than 10% having normal semen analysis results according to WHO guidelines (Berthaut 2008). HU treatment may further reduce fertility in many patients (Berthaut 2017). To address these concerns, various fertility preservation strategies have been developed for male SCD patients on HU, including sperm cryopreservation for pubescent boys and adults before starting HU, and temporary HU discontinuation when therapy is initiated in infancy for sperm banking, at best with monthly transfusion during the period without HU. Methods The ongoing European Sickle Cell Disease Cohort - Hydroxyurea Extension (ESCORT-HU Extension) study is a multicentric, prospective, non-interventional study aiming to better document the safety profile of HU. It focuses on poorly understood or documented risks, including puberty and fertility. Around 2000 HU-treated patients are expected to participate over a 5-year duration. The study includes both patients who were previously enrolled in the initial ESCORT-HU study and new patients who meet specific inclusion criteria. Results As of June 28, 2023, a total of 1860 patients were included in the study in France (92% of patients), Germany, Greece and Italy. Median age of patients at inclusion was 24 [IQR: 14-40] years with 44.4% being males, and 87% having the HbSS genotype. At enrollment, 455 (56.5%) males were in the pubescent stage, and 72 males transitioned into the pubescent stage since then. Median duration of HU exposure at the time of analysis was 8.5 [IQR: 6.4-11.6] years. Onset of puberty The mean age at Tanner V stage did not significantly differ between males who reached puberty before starting HU and those who reached puberty after (15.0 [IQR: 14.0-16.0] years vs. 15.2 [IQR: 14.0-16.0] years, respectively). Semen cryopreservation Among the 527 pubescent males, 293 started HU at or after 17 years old with 117/240 (49%) who had a cryopreservation. 234 started HU before the age of 17 years, 23/207 (11%) had a cryopreservation. Unknown data were reported for 80 patients. Median age at cryopreservation was 26.0 [IQR: 21.0-33.0] years. Semen analysis A total of 104 semen analysis were reported in the database with 66 performed before HU treatment initiation and 24 after, with 9 of them without any HU interruption prior the sampling. In 14 cases, the documentation on HU stopping was not available. Among the 66 patients tested before HU treatment initiation, results were not available in 34. They were normal in 25 (78%), abnormal in 7 (22%) (4 qualitative anomalies, 2 azoospermia, 1 both quantitative and qualitative anomalies). For the 24 patients who performed semen analysis after HU initiation, 11 temporarily discontinued the treatment for the procedure, with 3 having normal results, 7 having abnormal results, results not available in 1. One of the patients with oligospermia used successfully its previously cryopreserved semen for his partner's pregnancy. Nine patients did not stop HU before the procedure, with 7 having abnormal results, 1 normal, and result not available in 1. Information on HU interruption during the cryopreservation was not available for 4 patients (Table 1). Four patients have semen analysis results before and after HU treatment (Table 2). Conclusion: This study shows no impact of HU on the age of puberty in males. Data on fertility need to be completed but we show that semen cryopreservation has been well adopted in Europe, since approximately 50% of patients over the age of 17 at HU initiation included in France have undergone this procedure, which is free in France. We confirm a significant proportion of semen abnormalities but not in all cases. The impact of HU on fertility is complex, and cryopreservation appears to be beneficial in mitigating potential adverse effects, with at least one baby in our cohort born after use of cryopreserved semen.

Persistent high exposure to exogenous phthalates and endogenous sex hormones associated with early pubertal onset among children: A 3.5-year longitudinal cohort study in China

BackgroundEarly onset of puberty could have significant impacts on childhood health, but the extent to which it was affected by phthalate esters (PAEs) and sex hormone disruption was not understood. The aim of this study is to investigate the associations between exposure to PAEs and sex hormone disruption and early onset of puberty in children. MethodsA longitudinal cohort study was conducted in China from May 2017 to Oct 2020, involving 740 children during consecutive visits. The onset of puberty was evaluated using Tanner definition, and early puberty was defined as an onset age less than the first 25 %, with cut-offs of 10.33 and 8.97 years for boys and girls, respectively. Serum testosterone (TT), estradiol (E2) and urinary PAE metabolites were measured during three visits. Generalized linear models were used to explore the associations between PAE and sex hormones with the age of puberty onset, while log-binomial regressions were applied to assess the associations of persistent exposure to PAEs and sex hormones with early pubertal onset. ResultsApproximately 86.0 % of boys and 90.2 % of girls completed puberty onset from pre-puberty, and more than 95 % of participants had PAE concentrations higher than the limit of detection. Boys showed higher exposure to PAE pollutants and higher TT levels. Persistent exposure to PAEs was positively associated with early pubertal onset in girls (ARR = 1.97, 95 %CI = 1.12, 3.46). Moreover, persistent exposure to PAEs and E2 had synergistic associations with early pubertal onset in both boys (ARR = 4.77, 95 %CI = 1.06, 21.54) and girls (ARR = 7.07, 95 %CI = 1.51, 33.10). However, PAEs and TT had antagonistic associations only in boys (ARR = 0.44, 95 %CI = 0.07, 2.58). ConclusionLong-term exposure to PAEs might increase the risk of early pubertal onset, and it appears to work in synergy with E2, while in antagonism with TT in boys’ early pubertal onset. Reducing PAEs exposure might promote pubertal health.

ASSOCIATION OF NUTRITIONAL STATUS WITH MENARCHE : A SYSTEMATIC REVIEW

Menarche is the process that takes place when the hypothalamic-pituitary-ovarian (HPO) axis matures. This maturation is dependent on adequate hypothalamic and pituitary function, normal female reproductive anatomy, normal nutrition, and the absence of other long-term disorders. When a woman's reproductive health and overall wellbeing are normal, it is a sign that they are not abnormal. However, the substantial decline in the age at menarche that occurred between the early 19th century and the middle of the 20th century was associated with a significant improvement in nutrition and living conditions brought about by the process of modern civilization. Although genetic factors are responsible for approximately 50–80% of the variation in puberty onset age and milestones, environmental factors also play a role. This article demonstrates that individuals with a poor dietary level reach menarche at a later age. Girls have a greater chance of gaining weight if the foods they consume are high in fat and the nutrients that originate from animal products. It is possible for it to enhance levels of the hormone estrogen, which then supports elevated levels of cholesterol. This cycle continues until the desired effect is achieved.

Intervention Effect of Probiotics on the Early Onset of Puberty Induced by Daidzein in Female Mice.

The relationship between soy isoflavones (SI)-induced gut dysbiosis and puberty onset has not been explored, and the protective effect of probiotic is still controversial. This study investigates the action of daidzein (the main components of SI) and probiotic on the age of puberty onset in female mice. Changes in the gut microbiota and production of short chain fatty acids (SCFAs) metabolism are highlighted to analyze a possible causative relationship to puberty onset in female c57/bl mice. The results demonstrate that daidzein promotes earlier onset of puberty, and can significantly alter the composition of the fecal bacterial community. Furthermore, daidzein alters the gut microbiota such that levels of butyrate, isovalerate, and hexanoate are reduced. Moreover, a probiotic treatment normalizes the timing of puberty onset, likely due to alteration in the gut microbiota to enhance SCFAs production. These findings provide evidence that 95% daidzein has the potential to advance the timing of puberty onset in female mice, and the gut microbiome can be a therapeutic target to regulate the timing of puberty onset.

Effects of Tartrazine on Some Sexual Maturation Parameters in Immature Female Wistar Rats.

Over the past century, the average age for onset of puberty has declined. Several additives present in our food are thought to contribute significantly to this early puberty which is recognized to also affect people’s health in later life. On this basis, the impact of 40-days unique oral administration of the food dye tartrazine (7.5, 27, and 47 mg/kg BW doses) was evaluated on some sexual maturation parameters on immature female Wistar rats. Vaginal opening was evaluated during the treatment period. At the end of the treatments, animals were sacrificed (estrus phase) and the relative weight of reproductive organs, pituitary gonadotrophin and sexual steroids level, cholesterol level in ovaries and folliculogenesis were evaluated. Compared to the control group, animals receiving tartrazine (47 mg/kg BW) showed significantly high percentage of early vaginal opening from day 45 of age, and an increase in the number of totals, primaries, secondaries, and antral follicles; a significant increase in serum estrogen, LH and in uterine epithelial thickness. Our findings suggest that tartrazine considerably disturbs the normal courses of puberty. These results could validate at least in part the global observations on increasingly precocious puberty in girls feeding increasingly with industrially processed foods.

Exposure to non-persistent pesticides and puberty timing: a systematic review of the epidemiological evidence

Numerous modern non-persistent pesticides have demonstrated estrogenic/anti-androgenic activity and have been classified as endocrine-disrupting chemicals (EDCs). Processes involved in puberty development are vulnerable to EDCs, such as compounds that interfere with the metabolism or activity of sex steroids. To conduct a systematic review of epidemiological studies on the relationship between early-life exposure to non-persistent pesticides and puberty timing and/or sexual maturation in girls and boys. A systematic search was carried out using MEDLINE and SCOPUS databases, including original articles published up to November 2020. Thirteen studies were selected after excluding non-original and non-human studies. Exposure to different types of pesticides has been associated with altered puberty timing in girls and/or boys in eight studies. In utero exposure to atrazine has been related to earlier age of menarche in girls; exposure to organophosphate (OP) pesticides has been related to delayed sexual development in boys and girls; childhood pyrethroid exposure has been associated with pubertal delay in girls and pubertal advancement in boys; and prenatal/childhood exposure to multiple pesticides has been linked to earlier puberty onset in girls and pubertal delay in boys. Most of the reviewed studies describe a relationship between pesticide exposure and changes in the age of puberty onset or sex hormone levels, although the quality of the evidence is generally low. Further well-designed longitudinal studies are warranted on specific classes of pesticides and on possible interactions between different types of compounds.

Reproductive disorders in female rats after prenatal exposure to sodium arsenite

Arsenic is a metalloid widely found in the environment in organic and inorganic forms. Exposure to inorganic arsenic forms via drinking water has been associated with an increased incidence of negative health effects, including reproductive disorders and dysfunction of the endocrine system. However, the impact of arsenic exposure on female reproductive development is still unclear. Therefore, in the present study, we evaluated the effects of prenatal exposure to arsenic on the initial sexual development and puberty onset, and in the morphology of the female reproductive organs, estrous cycle regularity and fertility parameters during adulthood. To do that, pregnant female Wistar rats were exposed to 10mg/L sodium arsenite via drinking water from gestational day (GD) 1 until GD 21 and the female offspring was evaluated in different postnatal days. Our results showed that prenatal arsenic exposure induced a decrease of litter weight and morphological masculinization in females at postnatal day 1. Moreover, these females had a delay in the age of puberty onset and alteration in estrous cycle number and length. During adulthood, females from the sodium arsenite group showed an increase in endometrium, myometrium and perimetrium areas, and an imbalance in uterine antioxidant enzyme activity. These animals also presented an increase in post-implantation loss and reabsorption number, leading to reduced viable fetus number. In conclusion, prenatal arsenic exposure in rats was able to promote female masculinization, alter sexual development and impair reproductive performance.

Vinclozolin induced epigenetic transgenerational inheritance of pathologies and sperm epimutation biomarkers for specific diseases.

Exposure to vinclozolin has been shown to induce the epigenetic transgenerational inheritance of increased susceptibility to disease, and to induce transgenerational changes to the epigenome. In the current study, gestating F0 generation rats were exposed to vinclozolin, and the subsequent F1, F2 and transgenerational F3 generations were evaluated for diseases and pathologies. F1 and F2 generation rats exhibited few abnormalities. However, F3 generation rats showed transgenerational increases in testis, prostate, and kidney disease, changes in the age of puberty onset in males, and an increased obesity rate in females. Overall there was an increase in the rate of animals with disease, and in the incidence of animals with multiple diseases. The objective of the current study was to analyze the sperm epigenome of F3 generation rats with specific abnormalities and compare them to rats without those abnormalities, in an effort to find epigenetic biomarkers of transgenerational disease. Unique signatures of differential DNA methylation regions (DMRs) in sperm were found that associated with testis disease, prostate disease and kidney disease. Confounding factors identified were the presence of multiple diseases in the analysis and the limited number of animals without disease. These results further our understanding of the mechanisms governing epigenetic transgenerational inheritance, and may lead in the future to the use of epigenetic biomarkers that will help predict an individual’s susceptibility for specific diseases.

Disorders of Growth and Stature.

1. Laurie R. Braun, MD*,† 2. Rose Marino, MD* 1. *Pediatric Endocrine Unit and 2. †Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA * Abbreviations: ACTH: : adrenocorticotropic hormone CDC: : Centers for Disease Control and Prevention CDGP: : constitutional delay of growth and puberty CNS: : central nervous system FSS: : familial short stature GH: : growth hormone GnRH: : gonadotropin-releasing hormone IGF-BP3: : IGF-1 binding protein 3 IGF-1: : insulin-like growth factor 1 ISS: : idiopathic short stature NPR2 : : natriuretic peptide receptor B rhGH: : recombinant human GH SGA: : small for gestational age SHOX : : short stature homeobox TSH: : thyroid-stimulating hormone T4: : thyroxine It is often challenging to identify children with abnormal growth patterns and distinguish normal growth variants from pathologic variants. After completing this article, readers should be able to: 1. Perform growth measurements and interpret growth charts to be able to identify children with short or tall stature. 2. Differentiate among the common origins of short and tall stature and plan an appropriate diagnostic evaluation for a slowly or rapidly growing child. 3. Describe when treatment is indicated for children with short and tall stature. Growth parameters are routinely measured in general pediatrics, with the goal of identifying children with abnormalities in growth and stature. Short stature is defined as a height less than 2 standard deviations (SDs) below the mean of the “normal” population, while tall stature is defined as a height greater than 2 SDs above the mean of the normal population. Both single growth measurements and the pattern of growth over time (growth velocity) are useful in identifying children with abnormal stature. The growth velocity changes over time, with relatively rapid growth in infancy and early childhood, followed by slower growth (approximately 5 cm per year) in later childhood and then rapid growth again during puberty. There is a range of pubertal peak growth velocities of around 7 to 12 cm per year and 6 to 10.5 cm per year in boys and girls, respectively, representing approximately the 3rd to 97th percentiles. The timing of peak growth velocity varies with the age of puberty onset and frequently reflects familial pubertal and growth patterns. Overall, it is thought that …

Plasma anti-Müllerian hormone profile in heifers from birth through puberty and relationship with puberty onset.

The current study aimed to define the plasma profile of anti-Müllerian hormone (AMH) and follicle stimulating hormone (FSH) in heifers during postnatal life until achieving puberty, as defined by plasma progesterone (P4) profile, to demonstrate a relationship between AMH and age of puberty onset. Blood samples collected from 11 Japanese Black female calves within 1 week after birth (W0) and then biweekly until the sixth week after puberty (WP 6) were assayed for AMH, FSH, and P4. The heifers were classified into two groups based on age of puberty onset: ≤42 weeks (early puberty group; EP, n =4) and ≥44 weeks (late puberty group; LP, n =7). Minimal plasma AMH concentration occurring at W 0 gradually increased to its peak level by W 10 (fourfold higher than W 0; P<0.01) before gradually declining to a steady plateau 6 weeks before puberty (WP -6). The AMH peak was preceded by a significant rise in plasma FSH at W 4, W 6, and W 8 compared with W0. Plasma AMH at W 16 positively correlated with WP 4 and WP 6 (r =0.69 and 0.71, respectively; P<0.05). Overall plasma AMH and FSH was significantly higher and lower in EP compared with LP, respectively. In conclusion, heifers exhibit a characteristic plasma AMH profile during postnatal life, such that plasma AMH at an early prepubertal age could be a biomarker for precocious puberty and postpubertal AMH levels.

Altered puberty timing in recent decades: Implications for adolescence-onset conduct disorder

IntroductionIn industrialised countries, the age of puberty onset has substantially diminished over the last 150 years. Several factors, like improved nutrition and health care have contributed to this, but there are concerns about other factors, like obesity, levels of divorce and chemicals. There is an association between early puberty and externalizing disorders in both girls and boys.AimTo describe trends in advanced puberty timing and adolescence-onset conduct disorder (CD), analyse if an association exists between both and evaluate which measures can be taken to prevent youth from antisocial activities during adolescence.MethodA systematic literature review using Medline, Embase and Psycinfo Databases.ResultsFamily break-up and increased stress are risk factors for adolescence-onset conduct disorder. Obesity is associated with low SES families, so prevention campaigns giving advice on healthy nutrition may be beneficial. On the general level, there is no clear positive correlation between adolescence-onset CD and early puberty over the last decades as numbers of CD are decreasing.ConclusionPotential mental health gains can be obtained to focus on children with multiple risk factors for early puberty. More research is needed to assess, which interventions (diet, advice on body changes, social expectations, etc.) are most useful.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Reproductive disorders in female rats after prenatal exposure to betamethasone.

Betamethasone is the drug of choice for antenatal treatment, promoting fetal lung maturation and decreasing mortality. Previous studies in rats reported male programming and alteration in sperm parameters and sexual behavior following intrauterine betamethasone exposure. The impact on the female reproductive development is not known. In this study, rat female offspring was assessed for sexual development, morphophysiology of the reproductive tract and fertility after maternal exposure to 0.1 mg kg-1 of betamethasone or vehicle on gestational days 12, 13, 18 and 19. The treatment promoted reduction of litter weight on postnatal day 1, morphological masculinization in females, delay in the age of puberty onset, reduction in estrus number, increase in estrous cycle length and increase in luteinizing hormone serum levels and uterus weight. The females from the betamethasone group showed an increase of myometrial uterine area and decrease in endometrial uterine area. These animals also performed less lordosis during the sexual behavior test and showed impaired reproductive performance. The uterus showed higher contraction in the treated group as shown by a pharmacological assay. In conclusion, prenatal betamethasone exposure in rats promoted female masculinization, altered sexual development and reproductive parameters. Copyright © 2017 John Wiley & Sons, Ltd.

Effects of Dietary Glucose on Serum Estrogen Levels and Onset of Puberty in Gilts.

Metabolic signals and the state of energy reserves have been shown to play a crucial role in the regulation of reproductive function. This study was carried out to investigate the effects of dietary glucose levels on puberty onset in gilts. Weight-matched, landrace gilts (n = 36) 162±3 days old, weighing about 71.05±4.53 kg, were randomly assigned to 3 dietary treatment groups of 12 gilts each. The trial lasted until the onset of puberty. Gilts in each group were supplied with diets containing different levels of glucose as follows: i) starch group (SG) was free of glucose, contained 64% corn derived starch; ii) low-dose group (LDG) contained 19.2% glucose and 44.8% corn derived starch; iii) high-dose group (HDG) contained 30% glucose and 30% corn derived starch. Results indicated: i) The growth performance of gilts were not affected by the addition of glucose, but the age of puberty onset was advanced significantly (p<0.05); ii) Compared with the SG, the concentration of insulin significantly increased before puberty in HDG (p<0.05); iii) There was no difference in serum progesterone (P) levels amongst the different feed groups, however, levels of estradiol (E2), luteinizing hormone, and follicle-stimulating hormone were significantly higher at puberty onset in HDG (p<0.05). Overall, our findings indicate that glucose supplementation significantly advances puberty onset, which can have practical purposes for commercial breeding.

Insulin Does Not Target CamkIIα Neurones to Critically Regulate the Neuroendocrine Reproductive Axis in Mice.

Insulin signalling in the brain plays an important role in the central regulation of energy homeostasis and fertility, such that mice exhibiting widespread deletion of insulin receptors (InsR) throughout the brain and peripheral nervous system display diet sensitive obesity and hypothalamic hypogonadism. However, the specific cell types mediating the central effects of insulin on fertility remain largely unidentified. To date, the targeted deletion of InsR from individual neuronal populations implicated in the metabolic control of fertility has failed to recapitulate the hypogonadic and subfertile phenotype observed in brain-specific InsR knockout mice. Because insulin and leptin share similar roles as centrally-acting metabolic regulators of fertility, we used the Cre-loxP system to generate mice with a selective inactivation of the Insr gene from the same widespread neuronal population previously shown to mediate the central effects of leptin on fertility by crossing Insr-flox mice with calcium/calmodulin-dependent protein kinase type IIα (CamkIIα)-Cre mice. Multiple reproductive and metabolic parameters were then compared between male and female Insr-flox/Cre-positive (CamK-IRKO) and Insr-flox/Cre-negative control mice. Consistent with brain-specific InsR knockout mice, CamK-IRKO mice exhibited a mild but significant obesogenic phenotype. Unexpectedly, CamK-IRKO mice exhibited normal reproductive maturation and function compared to controls. No differences in the age of puberty onset, oestrous cyclicity or fecundity were observed between CamK-IRKO and control mice. We conclude that the central effects of insulin on the neuroendocrine reproductive axis are not critically mediated via the same neuronal populations targeted by leptin.

English

Incidence of endocrine disruptors on gonadal development is the cause of many anomalies in the male reproductive system (MRS). Ginkgo biloba is an endocrine disruptor with affinity for β estrogen receptors, which exert an important role in the development of MRS. This study evaluated the effects of G. biloba on the reproductive system of F1 males born to mothers exposed to G. biloba during fetogenesis. Pregnant Wistar rats received, by gavage, 25, 50 or 100 mg/kg/day of G. biloba from the 16th to 20th day of pregnancy. The testicular descent, morphology of the glans penis, sperm concentration, organ weights, testosterone serum concentration, and the structural organization of testicular and epididymal tissues remained unchanged. However, there was an increase in the number of abnormal sperm in all G. biloba-treated groups. These results indicate that G. biloba does not promote maternal toxicity and does not interfere with the fetal and postnatal development and age of puberty onset, but induces the increase of sperm abnormalities. Key words: Ginkgo biloba, sperm abnormality, fetogenesis, estrogen receptor, rat.

Ultrasensitive estrogen levels at 7 years of age predict earlier thelarche: evidence from girls of the growth and obesity Chilean cohort.

Prepubertal estradiol equivalents have been inconsistently linked to age at thelarche; elucidating this relationship becomes relevant given the worldwide decline in the age of puberty onset. Thus, our aim is to assess whether prepubertal girls with higher serum levels of estradiol equivalents at age 7 have a greater risk of presenting early thelarche (ET). Nested case-control study within the Growth and Obesity Cohort Study of 1196 low-middle income children (∼50% girls) from Santiago, Chile. Girls were defined as cases (ET; n=61) if breast bud appeared prior to 8 years of age; controls (n=91) had thelarche >8 years. At 6.7 years, weight, height and waist circumference were measured and a fasting blood sample was obtained for measuring estrogen equivalent (ultrasensitive recombinant cell bioassay), DHEAS, leptin, insulin and IGF1. Beginning at 7 years old, Tanner staging was assessed prospectively twice a year and the appearance of breast bud was assessed by palpation. Mean serum estradiol-equivalent at 6.7 years was 3.9±3.6 pg/ml for cases and 3.6±2.3 pg/ml for controls. Girls with ET had a higher risk of presenting elevated estradiol-equivalent (≥5 pg/ml) at 7 years (OR=2.05, 95% CI: 0.96-4.36) than controls that was borderline significant. However, after adjusting by BMI, insulin and IGF1 at age 7, the association between estradiol-equivalent and ET was significant (OR=2.29 (95% CI: 1.05-5.01)). Chilean girls from low to middle socioeconomic status with ET exhibited double the risk of having high levels of estradiol-equivalent at 7 years than girls with a later age of thelarche. Whole-body adiposity and increased adrenal activity did not explain the observed prepubertal estrogen increase.

Pubertal age based on testicular and epididymal histology in Göttingen minipigs

Göttingen minipigs are used worldwide as nonrodent animal models for toxicologic and pharmaceutical research. Having knowledge of the age for onset of puberty is an important consideration when designing such biomedical experiments. The present study reports an earlier age for puberty on the basis of changes in testicular spermatogenic development in the Göttingen minipig. Testes and epididymides of 24 Göttingen minipigs ranging 5 to 8 weeks of age were obtained for histologic observation after hematoxylin–eosin staining. Microscopic examination was performed to determine the prevalence of cell types (e.g., spermatogonia, primary and secondary spermatocytes, round spermatids, elongated spermatids, luminal sperm) in seminiferous tubules and for the presence of sperm in the cauda epididymis. Puberty was defined as having a majority cell type presence of elongated spermatids in the seminiferous tubules in conjunction with the presence of spermatozoa in the cauda epididymis. Puberty was identified in two males at 6 weeks of age, two males at 7 weeks of age, and in all 6 males at 8 weeks of age. In conclusion, the age of puberty in male Göttingen minipigs occurs by 8 weeks of age, an earlier age than previously reported.

Insulin action on GABA neurons is a critical regulator of energy balance but not fertility in mice.

Insulin signaling in the brain plays an important role in the central regulation of energy homeostasis and fertility, such that mice exhibiting brain-specific deletion of insulin receptors (InsRs) display a diet-sensitive obesogenic phenotype and hypothalamic hypogonadism. However, the specific neurons mediating insulin's central effects on fertility remain largely unidentified. The neurotransmitters γ-aminobutyric acid (GABA) and glutamate are important modulators of fertility and energy homeostasis and are widely distributed in the hypothalamus. We therefore investigated whether insulin signaling via GABAergic or glutamatergic neurons plays an important role in the metabolic regulation of fertility. We used the Cre-loxP system to generate mice with a selective inactivation of the Insr gene from GABAergic (Vgat(+)) or glutamatergic (Vglut2(+)) cells by crossing Insr-flox mice with Vgat-Cre or Vglut2-Cre mice, respectively. Multiple reproductive and metabolic parameters were then compared between male and female Insr-flox/Vgat-Cre(+) (VgatIRKO), Insr-flox/Vglut2-Cre(+) (VglutIRKO), and Insr-flox/Cre-negative control (CON) mice. Female VgatIRKO mice exhibited a significant increase in adult body weight, abdominal fat mass, and fasting plasma insulin and leptin concentrations, but normal fasting glucose concentration and glucose tolerance compared with CON mice. Surprisingly, VgatIRKO and VglutIRKO mice exhibited normal reproductive maturation and function compared with CONs. No differences in the age of puberty onset, estrous cyclicity, or fertility were observed between VgatIRKO, VglutIRKO, and CON mice. However, male VgatIRKO mice exhibited significantly augmented LH concentration and a trend toward reduced seminal vesicle weight compared with CON mice, which may be indicative of primary hypogonadism. Our results therefore demonstrate that insulin signaling via GABAergic and glutamatergic cells is not required for fertility in mice, but show that GABAergic neurons encompass circuitry through which insulin acts to modulate energy homeostasis.

Delayed reproductive development in pubertal male rats exposed to the hypolipemiant agent rosuvastatin since prepuberty

Dyslipidemias are frequently found in children due to obesity, bad eating habits and the lack of physical exercises. Rosuvastatin acts as an HMG-CoA reductase inhibitor, decreasing total cholesterol and triglycerides. This study aimed to investigate initial sexual development and morphological aspect of the testis and epididymis in juvenile rats exposed to rosuvastatin since pre-puberty. Three groups were formed with newly weaned rats: control, whose rats received saline solution 0.9%, rosuvastatin at doses of 3 or 10mg/kg daily by gavage, since post-natal day 21 until puberty onset. In the rosuvastatin-treated groups, the results demonstrated a trend toward a decrease in testosterone concentration, but below the significance level, as well as delays in both the age of puberty onset and in epididymal development. There were also testicular alterations that might be related to delayed puberty and decrease of serum testosterone. In conclusion, rosuvastatin administration to juvenile rats not only delayed puberty onset and epididymal development, but also impaired testicular and epididymal morphology.

Anorexia and bulimia risk as function of anxiety and puberty in Baja California-Mexico college students

Identifying the risk of eating disorders as well as associated variables in nonclinical samples is fundamental to prevention. The main objective of this study was to compare bulimia and anorexia risk depending on anxiety degree and the age of puberty onset in university students. A non experimental transversal explanatory study was carried out using a non probabilistic sample of 420 students from a public university at Ensenada, B.C. Age of participants ranged between 18 and 30 years old (59% female, 41% male) in Ensenada, B.C. Timing of puberty was measured using The Food and Health Questionaire (Gómez Peresmitré), especifically the menarquia /spermarquiaself-report, as well as the a Risk Factors Associated with Eating Disorders Scale (EFRATA) ; The Beck Anxiety Inventory (BAI) was also administered to all students. Among the main findings is that risk of bulimia increases with high anxiety degree and untypical puberty onset. Anorexia risk increases only with high degrees of anxiety. Results are in accordance to previous literature and are discussed within that frame.