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1
Bormann, Charles L., Gary D. Smith, Vasantha Padmanabhan, and Theresa M. Lee. "Prenatal testosterone and dihydrotestosterone exposure disrupts ovine testicular development." REPRODUCTION 142, no. 1 (July 2011): 167–73. http://dx.doi.org/10.1530/rep-10-0210.
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Androgens play important roles during the first trimester of intrauterine life, coinciding with genital tract differentiation, during virilization and maintenance of secondary male characteristics, and during initiation of spermatogenesis. Little is known about the impact of inappropriate exposure to excess androgens during fetal development on male sexual maturation and reproduction. The objectives of this study were to determine the effects of prenatal 5α-dihydrotestosterone (DHT) and testosterone treatment during ovine sexual differentiation on post-pubertal testicular formation and subsequent potential for fertility as assessed by epididymal sperm characteristics. Rams prenatally treated with testosterone exhibited increased testicular weight relative to age-matched controls and prenatal DHT-treated rams (P<0.05), as well as elevated total and free testosterone concentrations compared with DHT-treated rams (P=0.07 and P<0.05 respectively). The percentage of progressively motile sperm from the epididymis was significantly reduced in prenatal DHT-treated but not testosterone-treated rams compared with control rams (P<0.05). The testosterone-treated rams had a greater number of germ cell layers than DHT-treated rams, but comparable to the controls. Prenatal testosterone-treated rams had significantly larger seminiferous tubule diameter and lumen diameter compared with prenatal DHT-treated (P<0.05). Significantly, more prenatal DHT- and testosterone-treated rams (P<0.05) had occluded tubule lumen than control rams. Findings from this study demonstrate that exposure to excess testosterone/DHT during male fetal sexual differentiation have differential effects on post-pubertal testicular size, seminiferous tubule size and function, sperm motility, and testosterone concentrations.
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Montag, Christian, Benjamin Bleek, Svenja Breuer, Holger Prüss, Kirsten Richardt, Susanne Cook, J. Scott Yaruss, and Martin Reuter. "Prenatal testosterone and stuttering." Early Human Development 91, no. 1 (January 2015): 43–46. http://dx.doi.org/10.1016/j.earlhumdev.2014.11.003.
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Guibert, Floriane, Sophie Lumineau, Kurt Kotrschal, Erich Möstl, Marie-Annick Richard-Yris, and Cécilia Houdelier. "Trans-generational effects of prenatal stress in quail." Proceedings of the Royal Society B: Biological Sciences 280, no. 1753 (February 22, 2013): 20122368. http://dx.doi.org/10.1098/rspb.2012.2368.
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The prenatal environment is a source of phenotypic variability influencing the animal's characteristics. Prenatal stress affects not only the development of offspring, but also that of the following generation. Such effects have been best documented in mammals but can also be observed in birds, suggesting common processes across phylogenetic orders. We found previously that Japanese quail females stressed during laying produced offspring with higher fearfulness, probably related to modulation of testosterone levels in their eggs. Here, we evaluated long-term effects of prenatal stress by analysing reproductive traits of these F 1 offspring and, then, the development of their subsequent (F 2 ) offspring. The sexual behaviour of F 1 prenatally stressed (F1PS) males was impaired. F1PS females' eggs contained less yolk and more albumen, and higher yolk testosterone and progesterone levels than did F 1 prenatal control females. The fearfulness of F 2 prenatally stressed quail was greater than that of F 2 prenatal control quail. These F 2 behavioural differences paralleled those evidenced by their parents, suggesting trans-generational transmission of prenatal stress effects, probably mediated by egg compositions of F1PS females.
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Zhou, Yu, Min Gong, Yingfei Lu, Jianquan Chen, and Rong Ju. "Prenatal androgen excess impairs beta-cell function by decreased sirtuin 3 expression." Journal of Endocrinology 251, no. 1 (October 1, 2021): 69–81. http://dx.doi.org/10.1530/joe-21-0129.
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Prenatal androgen exposure induces metabolic disorders in female offspring. However, the long-term effect of maternal testosterone excess on glucose metabolism, especially on pancreatic beta-cell function, is rarely investigated. Our current study mainly focused on the effects of prenatal testosterone exposure on glucose metabolism and pancreatic beta- cell function in aged female offspring. By using maternal mice and their female offspring as animal models, we found that prenatal androgen treatment induced obesity and glucose intolerance in aged offspring. These influences were accompanied by decreased fasting serum insulin concentration, elevated serum triglyceride, and testosterone concentrations. Glucose stimulated insulin secretion in pancreatic beta cells of aged female offspring was also affected by prenatal testosterone exposure. We further confirmed that increased serum testosterone contributed to downregulation of sirtuin 3 expression, activated oxidative stress, and impaired pancreatic beta-cell function in aged female offspring. Moreover, over-expression of sirtuin 3 in islets isolated from female offspring treated with prenatal testosterone normalized the oxidative stress level, restored cyclic AMP, and ATP generation, which finally improved glucose-stimulated insulin secretion in beta cells. Taken together, these results demonstrated that prenatal testosterone exposure caused a metabolic disturbance in aged female offspring via suppression of sirtuin 3 expression and activation of oxidative stress in pancreatic beta cells.
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Hines, Melissa. "Prenatal testosterone and gender-related behaviour." European Journal of Endocrinology 155, suppl_1 (November 2006): S115—S121. http://dx.doi.org/10.1530/eje.1.02236.
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Testosterone plays an important role in mammalian brain development. In neural regions with appropriate receptors testosterone, or its metabolites, influences patterns of cell death and survival, neural connectivity and neurochemical characterization. Consequently, testosterone exposure during critical periods of early development produces permanent behavioural changes. In humans, affected behaviours include childhood play behaviour, sexual orientation, core gender identity and other characteristics that show sex differences (i.e. differ on average between males and females). These influences have been demonstrated primarily in individuals who experienced marked prenatal hormone abnormalities and associated ambiguities of genital development (e.g. congenital adrenal hyperplasia). However, there is also evidence that testosterone works within the normal range to make some individuals within each sex more sex-typical than others. The size of testosterone-related influences, and perhaps even their existence, varies from one sex-typed characteristic to another. For instance: prenatal exposure to high levels of testosterone has a substantial influence on sex-typical play behaviour, including sex-typed toy preferences, whereas influences on core gender identify and sexual orientation are less dramatic. In addition: there appears to be little or no influence of prenatal testosterone on mental rotations ability, although mental rotations ability shows a marked sex difference. These findings have implications for basic understanding of the role of testosterone in normative gender development, as well as for the clinical management of individuals with disorders of sex development (formerly called intersex syndromes).
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Culbert, K. M., S. A. Burt, C. L. Sisk, J. T. Nigg, and K. L. Klump. "The effects of circulating testosterone and pubertal maturation on risk for disordered eating symptoms in adolescent males." Psychological Medicine 44, no. 11 (January 9, 2014): 2271–86. http://dx.doi.org/10.1017/s0033291713003073.
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BackgroundTestosterone may be a biological factor that protects males against eating disorders. Elevated prenatal testosterone exposure is linked to lower levels of disordered eating symptoms, but effects emerge only after mid-puberty. Whether circulating levels of testosterone account for decreased risk for disordered eating in boys after mid-puberty is currently unknown; however, animal data support this possibility. In rodents, prenatal testosterone's masculinizing effects on sex-differentiated behaviors emerge during puberty when circulating levels of testosterone increase and ‘activate’ the expression of masculinized phenotypes. This study investigated whether higher levels of circulating testosterone predict lower levels of disordered eating symptoms in adolescent boys, and in particular whether effects are associated with advancing pubertal maturation.MethodParticipants were 213 male twins from the Michigan State University Twin Registry. The Minnesota Eating Behavior Survey and Eating Disorder Examination Questionnaire assessed several disordered eating symptoms. The Pubertal Development Scale assessed pubertal status. Afternoon saliva samples were assayed for testosterone using enzyme immunoassays.ResultsConsistent with animal data, higher levels of circulating testosterone predicted lower levels of disordered eating symptoms in adolescent boys and effects emerged with advancing puberty. Results were not accounted for by several important covariates, including age, adiposity, or mood/anxiety symptoms.ConclusionsFindings suggest that elevated circulating testosterone may be protective and underlie decreased risk for eating pathology in males during/after puberty, whereas lower levels of testosterone may increase risk and explain why some, albeit relatively few, males develop eating disorders.
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Recabarren, Mónica P., Pedro P. Rojas-Garcia, Ralf Einspanier, Vasantha Padmanabhan, Teresa Sir-Petermann, and Sergio E. Recabarren. "Pituitary and testis responsiveness of young male sheep exposed to testosterone excess during fetal development." REPRODUCTION 145, no. 6 (June 2013): 567–76. http://dx.doi.org/10.1530/rep-13-0006.
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Prenatal exposure to excess testosterone induces reproductive disturbances in both female and male sheep. In females, it alters the hypothalamus–pituitary–ovarian axis. In males, prenatal testosterone excess reduces sperm count and motility. Focusing on males, this study tested whether pituitary LH responsiveness to GNRH is increased in prenatal testosterone-exposed males and whether testicular function is compromised in the testosterone-exposed males. Control males (n=6) and males born to ewes exposed to twice weekly injections of 30 mg testosterone propionate from days 30 to 90 and of 40 mg testosterone propionate from days 90 to 120 of gestation (n=6) were studied at 20 and 30 weeks of age. Pituitary and testicular responsiveness was tested by administering a GNRH analog (leuprolide acetate). To complement the analyses, the mRNA expression of LH receptor (LHR) and that of steroidogenic enzymes were determined in testicular tissue. Basal LH and testosterone concentrations were higher in the testosterone-exposed-males. While LH response to the GNRH analog was higher in the testosterone-exposed males than in the control males, testosterone responses did not differ between the treatment groups. The testosterone:LH ratio was higher in the control males than in the testosterone-exposed males of 30 weeks of age, suggestive of reduced Leydig cell sensitivity to LH in the testosterone-exposed males. The expression of LHR mRNA was lower in the testosterone-exposed males, but the mRNA expression of steroidogenic enzymes did not differ between the groups. These findings indicate that prenatal testosterone excess has opposing effects at the pituitary and testicular levels, namely increased pituitary sensitivity to GNRH at the level of pituitary and decreased sensitivity of the testes to LH.
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Eme, Robert. "Greater Male Exposure to Prenatal Testosterone." Violence and Gender 2, no. 1 (March 2015): 19–23. http://dx.doi.org/10.1089/vio.2014.0024.
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Truzzi, Anna, Vincenzo Paolo Senese, Peipei Setoh, Cristian Ripoli, and Gianluca Esposito. "In utero testosterone exposure influences physiological responses to dyadic interactions in neurotypical adults." Acta Neuropsychiatrica 28, no. 5 (April 8, 2016): 304–9. http://dx.doi.org/10.1017/neu.2016.15.
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ObjectiveWe investigated how different levels of prenatal exposure to testosterone influence physiological reactions to dyadic interactions, hypothesising that higher levels of prenatal testosterone are linked to greater physiological responses.MethodAutonomic nervous system responses to dyadic interactions focussed on social or physical norms were measured. Physiological assessment of excitability (heart rate, facial temperature) and a behavioural assessment (Likert items judgements) were run on 25 neurotypical participants who had distinct testosterone exposure levels in utero. In utero exposure to testosterone was assessed measuring 2D : 4D (ratio between the lengths of the index and the ring fingers).ResultsHigher testosterone exposure participants showed greater physiological arousal: a greater heart rate decrease, independent from scenario type (p<0.05), and opposite facial temperature changes in response to social (increase) (vs.) physical scenarios (decrease) were found (Left-cheek: p<0.05; Right-cheek: p<0.05).ConclusionThese findings suggest a long-term influence of prenatal environment on adults’ physiological responses during social situations.
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Cardoso, Rodolfo C., Almudena Veiga-Lopez, Jacob Moeller, Evan Beckett, Anthony Pease, Erica Keller, Vanessa Madrigal, Gregorio Chazenbalk, Daniel Dumesic, and Vasantha Padmanabhan. "Developmental Programming: Impact of Gestational Steroid and Metabolic Milieus on Adiposity and Insulin Sensitivity in Prenatal Testosterone-Treated Female Sheep." Endocrinology 157, no. 2 (December 9, 2015): 522–35. http://dx.doi.org/10.1210/en.2015-1565.
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Abstract Prenatally testosterone (T)-treated sheep present metabolic disruptions similar to those seen in women with polycystic ovary syndrome. These females exhibit an increased ratio of small to large adipocytes, which may be the earliest event in the development of adult insulin resistance. Additionally, our longitudinal studies suggest the existence of a period of compensatory adaptation during development. This study tested whether 1) in utero cotreatment of prenatally T-treated sheep with androgen antagonist (flutamide) or insulin sensitizer (rosiglitazone) prevents juvenile insulin resistance and adult changes in adipocyte size; and 2) visceral adiposity and insulin sensitivity are both unaltered during early adulthood, confirming the predicted developmental trajectory in this animal model. Insulin sensitivity was tested during juvenile development and adipose tissue distribution, adipocyte size, and concentrations of adipokines were determined during early adulthood. Prenatal T-treated females manifested juvenile insulin resistance, which was prevented by prenatal rosiglitazone cotreatment. Neither visceral adiposity nor insulin sensitivity differed between groups during early adulthood. Prenatal T-treated sheep presented an increase in the relative proportion of small adipocytes, which was not substantially prevented by either prenatal intervention. A large effect size was observed for increased leptin concentrations in prenatal T-treated sheep compared with controls, which was prevented by prenatal rosiglitazone. In conclusion, gestational alterations in insulin-glucose homeostasis likely play a role in programming insulin resistance, but not adipocyte size distribution, in prenatal T-treated sheep. Furthermore, these results support the notion that a period of compensatory adaptation of the metabolic system to prenatal T exposure occurs between puberty and adulthood.
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Le-Ha, Chi, Lawrence J. Beilin, Sally Burrows, Jeffrey A. Keelan, Martha Hickey, and Trevor A. Mori. "Prenatal Testosterone Associates With Blood Pressure in Young Adults." Hypertension 77, no. 5 (May 2021): 1756–64. http://dx.doi.org/10.1161/hypertensionaha.120.16256.
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Preclinical evidence suggests that adult blood pressure (BP) may be modified by the prenatal endocrine environment. Specifically, in several animal models, higher prenatal testosterone exposure increases the risk of hypertension in later life. We investigated the prospective association between prenatal testosterone levels (as measured in umbilical cord blood) and BP at 20 to 27 years in 434 participants from the Raine Study. As expected, median bioavailable testosterone, the fraction of total testosterone either free or bound to serum albumin, was higher in males than females (0.12 [Q1–Q3, 0.09–0.19] versus 0.07 [Q1–Q3, 0.05–0.1] nmol/L; P <0.001). Mean (SD) systolic BP was 122.9 (±12.3) and 110.9 (±9.5) mm Hg at age 20 years and 122.4 (±11) and 111.2 (±9.1) mm Hg at 27 years in males and females, respectively. Using hierarchical mixed-effects models, higher cord blood bioavailable testosterone concentrations were associated with higher levels of systolic BP ( P =0.007) and diastolic BP ( P =0.002) in young adults at 20 and 27 years, after adjusting for change in BP over time and potential confounders. In these models, one SD increase in bioavailable testosterone equated to a 1 mm Hg increase in systolic BP (regression coefficient, 11.1 [95% CI, 4.1–21.11]) and diastolic BP (regression coefficient, 10.15 [95% CI, 3.67–15.93]). There was no significant difference detected between males and females in the association between bioavailable testosterone and adult BP. These data from a large unselected population indicate that higher fetal testosterone levels in late pregnancy are associated with higher BP in young adulthood.
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Recabarren, Sergio E., Pedro P. Rojas-García, Mónica P. Recabarren, Victor H. Alfaro, Rosita Smith, Vasantha Padmanabhan, and Teresa Sir-Petermann. "Prenatal Testosterone Excess Reduces Sperm Count and Motility." Endocrinology 149, no. 12 (July 31, 2008): 6444–48. http://dx.doi.org/10.1210/en.2008-0785.
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The reproductive system is extremely susceptible to insults from exposure to exogenous steroids during development. Excess prenatal testosterone exposure programs neuroendocrine, ovarian, and metabolic deficits in the female, features seen in women with polycystic ovary disease. The objective of this study was to determine whether prenatal testosterone excess also disrupts the male reproductive system, using sheep as a model system. The extent of reproductive disruption was tested by assessing sperm quantity and quality as well as Leydig cell responsiveness to human chorionic gonadotropin. Males born to mothers treated with 30 mg testosterone propionate twice weekly from d 30 to 90 and with 40 mg testosterone propionate from d 90 to 120 of pregnancy (T-males) showed a significant reduction (P < 0.05) in body weight, scrotal circumference, and sperm count compared with control males. Mean straight line velocity of sperms was also lower in T-males (P < 0.05). Circulating testosterone levels in response to the human chorionic gonadotropin did not differ between groups. These findings demonstrate that exposure to excess testosterone during fetal development has a negative impact on reproductive health of the male offspring, raising concerns relative to unintended human exposure to steroidal mimics in the environment.
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Schwarz Walsted, Anne. "Finger lengths and behavior: Is the 2D:4D index of interest in forensic medicine?" Scandinavian Journal of Forensic Science 19, no. 2 (December 31, 2013): 55–58. http://dx.doi.org/10.2478/sjfs-2013-0009.
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ABSTRACT The relationship between the second and the fourth digit in the human hand, the 2D:4D index, is considered a putative marker of exposure to prenatal testosterone. Much research has been done in the attempt to associate the 2D:4D index and physical characteristics as well as cognitive skills and behavioral patterns. It has been suggested that these characteristics and behavioral patterns may be linked to high levels of testosterone. The basis for considering the 2D:4D index a marker of prenatal exposure to testosterone, and the influence of prenatal and circulating testosterone on behavior are reviewed. Furthermore, it is discussed whether forensic medicine may benefit from identification of a marker of behavioral predispositions. It seems that it is not possible to derive any valid information on predispositions from finger length ratio, however the field of 2D:4D research might benefit from forensic studies.
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Terburg, David, Jiska S. Peper, Barak Morgan, and Jack van Honk. "Sex differences in human aggression: The interaction between early developmental and later activational testosterone." Behavioral and Brain Sciences 32, no. 3-4 (August 2009): 290. http://dx.doi.org/10.1017/s0140525x09990367.
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AbstractThe relation between testosterone levels and aggressive behavior is well established. From an evolutionary viewpoint, testosterone can explain at least part of the sex differences found in aggressive behavior. This explanation, however, is mediated by factors such as prenatal testosterone levels and basal levels of cortisol. Especially regarding sex differences in aggression during adolescence, these mediators have great influence. Based on developmental brain structure research we argue that sex differences in aggression have a pre-pubertal origin and are maintained during adolescence. Evidence of prenatal, adolescent, and adult levels of testosterone in relation to aggression taken together, support Archer's argument for sexual selection as the driver of sex differences in aggression.
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Roberts, Bethan A., and Michelle M. Martel. "Prenatal testosterone and preschool Disruptive Behavior Disorders." Personality and Individual Differences 55, no. 8 (November 2013): 962–66. http://dx.doi.org/10.1016/j.paid.2013.08.002.
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Beking, T., R. H. Geuze, M. van Faassen, I. P. Kema, B. P. C. Kreukels, and T. G. G. Groothuis. "Prenatal and pubertal testosterone affect brain lateralization." Psychoneuroendocrinology 88 (February 2018): 78–91. http://dx.doi.org/10.1016/j.psyneuen.2017.10.027.
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Utevska, S. V. "Experimental autoimmune encephalomyelitis (EAE) course in prenatally stressed rat males, the offspring of mothers with different sensitivity to EAE." Faktori eksperimental'noi evolucii organizmiv 24 (August 30, 2019): 244–48. http://dx.doi.org/10.7124/feeo.v24.1109.
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Aim. The research is aimed at investigating the effect of prenatal stress on the incidence and course of experimental autoimmune encephalomyelitis (EAE) as well as the level of sex hormones in 200-days-old male rats, offspring of females with different sensitivity to EAE induction. Methods. The incidence and severity of EAE including duration of latent period, duration of the period from the first to the maximum manifestation of motor disfunction, mean clinical scores, maximum level of motor disfunction (maximum clinical scores) were analyzed in rats with induced EAE. Serum testosterone, estradiol and progesterone levels were measure during Enzyme-Linked Immunosorbent Assay (ELISA). Results. The estradiol level of prenatally stressed males was significantly lower than in rats from the control group. Sensitive to EAE test male rats had lower testosterone levels than EAE resistant males, and the offspring of EAE sensitive mothers were more resistant to EAE induction than the offspring of EAE resistant mothers. Conclusions. Without significant changes in the course of EAE, the reduction in incidence depends on a combination of factors such as mother's sensitivity to EAE induction and prenatal stress.
Keywords: experimental autoimmune encephalomyelitis (EAE), prenatal stress, sex hormones, sensitivity to EAE induction.
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Jackson, Leslie M., Andrea Mytinger, Eila K. Roberts, Theresa M. Lee, Douglas L. Foster, Vasantha Padmanabhan, and Heiko T. Jansen. "Developmental Programming: Postnatal Steroids Complete Prenatal Steroid Actions to Differentially Organize the GnRH Surge Mechanism and Reproductive Behavior in Female Sheep." Endocrinology 154, no. 4 (April 1, 2013): 1612–23. http://dx.doi.org/10.1210/en.2012-1613.
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Abstract In female sheep, estradiol (E2) stimulates the preovulatory GnRH/LH surge and receptive behavior, whereas progesterone blocks these effects. Prenatal exposure to testosterone disrupts both the positive feedback action of E2 and sexual behavior although the mechanisms remain unknown. The current study tested the hypothesis that both prenatal and postnatal steroids are required to organize the surge and sex differences in reproductive behavior. Our approach was to characterize the LH surge and mating behavior in prenatally untreated (Control) and testosterone-treated (T) female sheep subsequently exposed to one of three postnatal steroid manipulations: endogenous E2, excess E2 from a chronic implant, or no E2 due to neonatal ovariectomy (OVX). All females were then perfused at the time of the expected surge and brains processed for estrogen receptor and Fos immunoreactivity. None of the T females exposed postnatally to E2 exhibited an E2-induced LH surge, but a surge was produced in five of six T/OVX and all Control females. No surges were produced when progesterone was administered concomitantly with E2. All Control females were mounted by males, but significantly fewer T females were mounted by a male, including the T/OVX females that exhibited LH surges. The percentage of estrogen receptor neurons containing Fos was significantly influenced in a brain region-, developmental stage-, and steroid-specific fashion by testosterone and E2 treatments. These findings support the hypothesis that the feedback controls of the GnRH surge are sensitive to programming by prenatal and postnatal steroids in a precocial species.
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Bütikofer, Aline, David N. Figlio, Krzysztof Karbownik, Christopher W. Kuzawa, and Kjell G. Salvanes. "Evidence that prenatal testosterone transfer from male twins reduces the fertility and socioeconomic success of their female co-twins." Proceedings of the National Academy of Sciences 116, no. 14 (March 18, 2019): 6749–53. http://dx.doi.org/10.1073/pnas.1812786116.
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During sensitive periods in utero, gonadal steroids help organize biological sex differences in humans and other mammals. In litter-bearing species, chromosomal females passively exposed to prenatal testosterone from male littermates exhibit altered physical and behavioral traits as adults. The consequences of such effects are less well understood in humans, but recent near-doubling of twinning rates in many countries since 1980, secondary to advanced maternal age and increased reliance on in vitro fertilization, means that an increasing subset of females in many populations may be exposed to prenatal testosterone from their male co-twin. Here we use data on all births in Norway (n= 728,842, including 13,800 twins) between 1967 and 1978 to show that females exposed in utero to a male co-twin have a decreased probability of graduating from high school (15.2%), completing college (3.9%), and being married (11.7%), and have lower fertility (5.8%) and life-cycle earnings (8.6%). These relationships remain unchanged among the subsets of 583 and 239 females whose male co-twin died during the first postnatal year and first 28 days of life, respectively, supporting the interpretation that they are due primarily to prenatal exposure rather than to postnatal socialization effects of being raised with a male sibling. Our findings provide empirical evidence, using objectively measured nation-level data, that human females exposed prenatally to a male co-twin experience long-term changes in marriage, fertility, and human capital. These findings support the hypothesis of in utero testosterone transfer between twins, which is likely affecting a small but growing subset of females worldwide.
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Sathyanarayana, Sheela, Emily Barrett, Samantha Butts, Christina Wang, and Shanna Helen Swan. "Phthalate exposure and reproductive hormone concentrations in pregnancy." REPRODUCTION 147, no. 4 (April 2014): 401–9. http://dx.doi.org/10.1530/rep-13-0415.
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Some phthalate chemicals can affect hormone physiology in utero, resulting in adverse reproductive health outcomes in animal models. It is unknown whether these exposures are related to circulating maternal hormone concentrations during pregnancy. We used multivariate linear regression to estimate associations between phthalate metabolite concentrations and concurrent serum-free and total testosterone and estradiol (E2) levels in 180 pregnant women in the Study for Future Families. We also examined associations between prenatal serum hormone concentrations and anogenital outcome in infants. All analyses were adjusted for appropriate confounding variables. Total testosterone, free testosterone, and E2 concentrations ranged from 8 to 406 ng/dl, 0.03 to 1.2 ng/dl, and 529 to 40 600 pg/ml respectively. We observed an inverse association between log-sum di-2-ethylhexyl phthalate (DEHP) metabolite concentrations and lower log-total testosterone concentrations (−0.15, 95% CI −0.26, −0.04) and log-free testosterone (−0.15, 95% CI −0.27, −0.03). This relationship persisted regardless of fetal sex. Similarly, we observed an inverse association between log monobutyl phthalate (MBP) concentrations and log-total and -free testosterone concentrations in women carrying male fetuses. Monoethyl phthalate (MEP) concentrations were positively associated with log-total and -free testosterone concentrations in women carrying male fetuses (0.09, 95% CI 0.003, 0.17 and 0.10, 95% CI 0.01, 0.19 respectively). Prenatal hormone concentrations were not significantly associated with infant anogenital outcomes. Our preliminary data suggest that DEHP metabolite, MBP, and MEP exposures during pregnancy are associated with prenatal sex steroid hormone concentrations, but sex steroid hormone concentrations were not associated with infant reproductive outcomes.
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Cardoso, Rodolfo C., and Vasantha Padmanabhan. "Developmental Programming of PCOS Traits: Insights from the Sheep." Medical Sciences 7, no. 7 (July 11, 2019): 79. http://dx.doi.org/10.3390/medsci7070079.
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Polycystic ovary syndrome (PCOS) is a complex disorder that results from a combination of multiple factors, including genetic, epigenetic, and environmental influences. Evidence from clinical and preclinical studies indicates that elevated intrauterine androgen levels increase the susceptibility of the female offspring to develop the PCOS phenotype. Additionally, early postnatal endocrine and metabolic imbalances may act as a “second-hit”, which, through activational effects, might unmask or amplify the modifications programmed prenatally, thus culminating in the development of adult disease. Animal models provide unparalleled resources to investigate the effects of prenatal exposure to androgen excess and to elucidate the etiology and progression of disease conditions associated with this occurrence, such as PCOS. In sheep, prenatal treatment with testosterone disrupts the developmental trajectory of the fetus, culminating in adult neuroendocrine, ovarian, and metabolic perturbations that closely resemble those seen in women with PCOS. Our longitudinal studies clearly demonstrate that prenatal exposure to testosterone excess affects both the reproductive and the metabolic systems, leading to a self-perpetuating cycle with defects in one system having an impact on the other. These observations in the sheep suggest that intervention strategies targeting multiple organ systems may be required to prevent the progression of developmentally programmed disorders.
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De Neys, Wim, Astrid Hopfensitz, and Jean-François Bonnefon. "Low second-to-fourth digit ratio predicts indiscriminate social suspicion, not improved trustworthiness detection." Biology Letters 9, no. 2 (April 23, 2013): 20130037. http://dx.doi.org/10.1098/rsbl.2013.0037.
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Testosterone administration appears to make individuals less trusting, and this effect has been interpreted as an adaptive adjustment of social suspicion, that improved the accuracy of trusting decisions. Here, we consider another possibility, namely that testosterone increases the subjective cost of being duped, decreasing the propensity to trust without improving the accuracy of trusting decisions. In line with this hypothesis, we show that second-to-fourth digit ratio (2D : 4D, a proxy for effects of testosterone in the foetus) correlates with the propensity to trust, but not with the accuracy of trusting decisions. Trust game players ( n = 144) trusted less when they had lower 2D : 4D (high prenatal testosterone), but their ability to detect the strategy of other players was constant (and better than chance) across all levels of digit ratio. Our results suggest that early prenatal organizing effects of testosterone in the foetus might impair rather than boost economic outcomes, by promoting indiscriminate social suspicion.
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Abi Salloum, Bachir, Carol Herkimer, James S. Lee, Almudena Veiga-Lopez, and Vasantha Padmanabhan. "Developmental Programming: Prenatal and Postnatal Contribution of Androgens and Insulin in the Reprogramming of Estradiol Positive Feedback Disruptions in Prenatal Testosterone-Treated Sheep." Endocrinology 153, no. 6 (March 27, 2012): 2813–22. http://dx.doi.org/10.1210/en.2011-2074.
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Prenatal testosterone (T) excess compromises the estradiol (E2) positive feedback. This study tested the hypothesis that antagonizing androgen action or improving insulin sensitivity prenatally would prevent positive feedback disruptions from developing, whereas postnatal intervention with androgen antagonist or insulin sensitizer would ameliorate the severity of disruptions in prenatal T-treated females. The E2 positive feedback response was tested at 16 wk of age in the following groups of animals: 1) control, 2) prenatal T, 3) prenatal T plus the androgen antagonist, flutamide, 4) prenatal T plus insulin sensitizer, rosiglitazone, 5) prenatal T and postnatal androgen antagonist, and 6) prenatal T and postnatal insulin sensitizer (n = 7–21 animals/group). Prenatal T treatment involved the administration of T propionate (100 mg, im) twice weekly from d 30 to 90 of gestation. Prenatal interventions involved daily sc administration of androgen antagonist (15 mg/kg) or oral administration of insulin sensitizer (8 mg) for the same duration. Postnatal treatments began at 8 wk of age and involved daily oral administration of androgen antagonist (15 mg/kg) or insulin sensitizer (0.11 mg/kg). None of the prenatal/postnatal interventions increased number of animals responding or prevented the time delay in LH surge response to the E2 positive feedback challenge. In contrast, the postnatal treatment with androgen antagonist or insulin sensitizer increased total LH released in response to E2 positive feedback challenge, compared with the T animals. Overall, these interventional studies indicate that timing and magnitude of the LH surge are programmed by different neuroendocrine mechanisms with postnatal androgens and insulin determining the size and prenatal estrogen likely the timing of the LH surge.
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King, Andrew J., N. Bari Olivier, P. S. Mohankumar, James S. Lee, Vasantha Padmanabhan, and Gregory D. Fink. "Hypertension caused by prenatal testosterone excess in female sheep." American Journal of Physiology-Endocrinology and Metabolism 292, no. 6 (June 2007): E1837—E1841. http://dx.doi.org/10.1152/ajpendo.00668.2006.
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Polycystic ovary syndrome (PCOS), a leading cause of infertility, affects ∼10% of women of reproductive age. The etiology and pathophysiology of PCOS are poorly understood. PCOS is multifaceted and includes reproductive abnormalities and components of the metabolic syndrome such as insulin resistance, obesity, dyslipidemia, and hypertension. Exposure to excess testosterone (T) during the prenatal period may predispose individuals to PCOS phenotype. The goal of this study was to determine whether hypertension and dyslipidemia occur in a well-characterized model of PCOS produced by prenatal treatment of sheep with T. Radiotelemetry was used to measure blood pressure over a 24-h period in conscious, undisturbed animals. To normalize circulating estradiol levels across treatment, control ( n = 4) and prenatal T-treated (100 mg T propionate im twice weekly from days 30 to 90 of fetal life, n = 4) 2-yr-old females were ovariectomized, instrumented with a radiotelemetry transmitter, and clamped with early follicular phase levels of estrogen using an implant. Six days later, a 24-h recording period commenced. Prenatal T-treated sheep were hypertensive compared with control sheep, and heart rate tended to be higher. T-treated sheep had hyperglycemia, insulin resistance, hypernatremia, and hyperchloremia, and both total and LDL cholesterol tended to be higher. Plasma aldosterone and epinephrine were significantly lower in T-treated sheep, whereas norepinephrine was unchanged. This first-ever use of radiotelemetric blood pressure recordings in sheep demonstrates that mild hypertension, a risk factor reported in some women with PCOS, is also a feature of the sheep model of PCOS produced by prenatal T treatment.
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Piffer, Renata C., Patrícia C. Garcia, Daniela C. C. Gerardin, Wilma G. Kempinas, and Oduvaldo C. M. Pereira. "Semen parameters, fertility and testosterone levels in male rats exposed prenatally to betamethasone." Reproduction, Fertility and Development 21, no. 5 (2009): 634. http://dx.doi.org/10.1071/rd08203.
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The present study investigated the long-term effects of prenatal betamethasone exposure on sperm quality and count, fertility and plasma testosterone levels in adult male rats. Pregnant rats received 0.1 mg kg–1 betamethasone on Days 12, 13, 18 and 19 of pregnancy. This treatment impaired sperm quality, sperm production, fertility and plasma testosterone levels in adult male offspring compared to the control group. Thus, the results of the present study indicate that the long-term effects of prenatal betamethasone exposure may be deleterious to offspring. The consequent decrease in testosterone production during adulthood, in association with damaged semen parameters, may explain for the observed decrease in the capacity of adult male offspring to themselves generate viable descendants.
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Veiga-Lopez, Almudena, James S. Lee, and Vasantha Padmanabhan. "Developmental Programming: Insulin Sensitizer Treatment Improves Reproductive Function in Prenatal Testosterone-Treated Female Sheep." Endocrinology 151, no. 8 (June 16, 2010): 4007–17. http://dx.doi.org/10.1210/en.2010-0124.
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Prenatal testosterone (T) excess causes reproductive and metabolic disruptions including insulin resistance, attributes of women with polycystic ovary syndrome. This study tested the hypothesis that insulin resistance contributes toward severity of reproductive disruptions in prenatally T-treated females. Pregnant sheep were injected im with 100 mg of T-propionate semiweekly from d 30–90 of gestation. Immediately after the first breeding season, a subset of controls and prenatal T-treated (TR) sheep were administered an insulin sensitizer (rosiglitazone; 8 mg/d) orally for 8 months. Untreated control and prenatal T-treated females (T group) were studied in parallel. Biochemical analyses revealed rosiglitazone to be safe for use in sheep. Glucose tolerance tests performed before and after the insulin sensitizer treatment found that insulin sensitizer decreased cumulative insulin, cumulative insulin/glucose ratio, and insulin area under the curve by about 50% and increased the insulin sensitivity index by about 70% in the TR compared with the T group. Twenty percent of TR females showed a reduced number of cycles in the second relative to first breeding season as opposed to 80% of T group females showing such deterioration. Insulin sensitizer treatment also decreased the number of aberrant cycles (≥18 d) during the second breeding season in the TR group relative to the first as opposed to the T group females showing an increase in the second breeding season relative to the first. These findings provide evidence that insulin sensitizer treatment prevents further deterioration of the reproductive axis in prenatal T-treated sheep, a finding of translational relevance to women with polycystic ovary syndrome.
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Padmanabhan, V., P. Smith, and A. Veiga-Lopez. "Developmental programming: impact of prenatal testosterone treatment and postnatal obesity on ovarian follicular dynamics." Journal of Developmental Origins of Health and Disease 3, no. 4 (March 7, 2012): 276–86. http://dx.doi.org/10.1017/s2040174412000128.
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Prenatal testosterone (T) excess leads to reproductive dysfunctions in sheep with obesity exaggerating such defects. Developmental studies found ovarian reserve is similar in control and prenatal T sheep at fetal day 140, with prenatal T females showing increased follicular recruitment and persistence at 10 months of age (postpubertal). This study tested whether prenatal T sheep show accelerated depletion prepubertally and whether depletion of ovarian reserve would explain loss of cyclicity in prenatal T females and its amplification by postnatal obesity. Stereological examinations were performed at 5 (prepubertal, control and prenatal T) and 21 months of age (control, prenatal T and prenatal T obese, following estrus synchronization). Obesity was induced by overfeeding from weaning. At 5 months, prenatal T females had 46% less primordial follicles than controls (P < 0.01), supportive of increased follicular depletion. Depletion rate was slower and a higher percentage of growing follicles was present in 21-month compared with 5-month-old prenatal T females (P < 0.01). Postnatal obesity did not exaggerate the impact of prenatal T on follicular recruitment indicating that compounding effects of obesity on loss of cyclicity females is not due to depletion of ovarian reserve. Assessment of follicular dynamics across several time points during the reproductive lifespan (this and earlier study combined) provides evidence supportive of a shift in follicular dynamics in prenatal T females from one of accelerated follicular depletion initiated before puberty to stockpiling of growing follicles after puberty, a time point critical in the development of the polycystic ovary syndrome phenotype.
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Tschirren, Barbara, Ann-Kathrin Ziegler, Joel L. Pick, Monika Okuliarová, Michal Zeman, and Mathieu Giraudeau. "Matrilineal inheritance of a key mediator of prenatal maternal effects." Proceedings of the Royal Society B: Biological Sciences 283, no. 1838 (September 14, 2016): 20161676. http://dx.doi.org/10.1098/rspb.2016.1676.
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Sex-linkage is predicted to evolve in response to sex-specific or sexually antagonistic selection. In line with this prediction, most sex-linked genes are associated with reproduction in the respective sex. In addition to traits directly involved in fertility and fecundity, mediators of maternal effects may be predisposed to evolve sex-linkage, because they indirectly affect female fitness through their effect on offspring phenotype. Here, we test for sex-linked inheritance of a key mediator of prenatal maternal effects in oviparous species, the transfer of maternally derived testosterone to the eggs. Consistent with maternal inheritance, we found that in Japanese quail ( Coturnix japonica ) granddaughters resemble their maternal (but not their paternal) grandmother in yolk testosterone deposition. This pattern of resemblance was not due to non-genetic priming effects of testosterone exposure during prenatal development, as an experimental manipulation of yolk testosterone levels did not affect the females' testosterone transfer to their own eggs later in life. Instead, W chromosome and/or mitochondrial variation may underlie the observed matrilineal inheritance pattern. Ultimately, the inheritance of mediators of maternal effects along the maternal line will allow for a fast and direct response to female-specific selection, thereby affecting the dynamics of evolutionary processes mediated by maternal effects.
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Fink, Bernhard, John T. Manning, and Nick Neave. "The second to fourth digit ratio, sociosexuality, and offspring sex ratio." Behavioral and Brain Sciences 28, no. 2 (April 2005): 283–84. http://dx.doi.org/10.1017/s0140525x05300057.
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Previous research has suggested that offspring sex ratio may be influenced by the actions of prenatal sex steroids, principally androgens. The relative length of the second (index finger) to the fourth digit (ring finger) has been reported to be a proxy to prenatal testosterone levels. This trait is sexually dimorphic, such that males display a significantly lower 2D:4D ratio (indicating higher testosterone exposure), and this dimorphism appears robust across different populations. We suggest that digit ratio (2D:4D) may form a useful marker to help explain variation in sex ratio and sociosexuality.
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Bábíčková, Janka, Veronika Borbélyová, L'ubomíra Tóthová, Katarína Kubišová, Pavol Janega, Július Hodosy, and Peter Celec. "The Renal Effects of Prenatal Testosterone in Rats." Journal of Urology 193, no. 5 (May 2015): 1700–1708. http://dx.doi.org/10.1016/j.juro.2014.12.093.
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Patel, Anisha, and Scott A. Rivkees. "Prenatal Virilization Associated with Paternal Testosterone Gel Therapy." International Journal of Pediatric Endocrinology 2010 (2010): 1–4. http://dx.doi.org/10.1155/2010/867471.
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Ratcliffe, Shirley G., Graham Read, Huiqi Pan, Claudine Fear, Richard Lindenbaum, and Jennifer Crossley. "Prenatal Testosterone Levels in XXY and XYY Males." Hormone Research 42, no. 3 (1994): 106–9. http://dx.doi.org/10.1159/000184157.
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Patel, Anisha, and ScottA Rivkees. "Prenatal Virilization Associated with Paternal Testosterone Gel Therapy." International Journal of Pediatric Endocrinology 2010, no. 1 (2010): 867471. http://dx.doi.org/10.1186/1687-9856-2010-867471.
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Baker, Jessica H., Paul Lichtenstein, and Kenneth S. Kendler. "Intrauterine testosterone exposure and risk for disordered eating." British Journal of Psychiatry 194, no. 4 (April 2009): 375–76. http://dx.doi.org/10.1192/bjp.bp.108.054692.
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SummaryPrevious research has suggested that prenatal testosterone exposure masculinises disordered eating by comparing opposite- and same-gender twins. The objective of the current study is to replicate this finding using a sample of 439 identical and 213 fraternal females, 461 identical and 344 fraternal males, and 361 males and 371 females from opposite-gender twin pairs. Disordered eating was compared across twin types using the Eating Disorder Inventory–2. Inconsistent with previous findings, a main effect of co-twin gender was not found. Our results raise questions about the validity of prior evidence of the impact of prenatal testosterone exposure on patterns of disordered eating.
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Ellis, Lee, Russell Eisenman, and Anthony Hoskin. "MATERNAL ACTIVITY DURING PREGNANCY AND SEXUALLY DIMORPHIC TRAITS IN OFFSPRING." Journal of Biosocial Science 50, no. 1 (April 3, 2017): 114–23. http://dx.doi.org/10.1017/s0021932017000074.
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SummaryStudies have found positive correlations between prenatal exposure to testosterone and masculinization of offspring traits, particularly among females. The present study sought to determine if physical or sexual activity by the mother during pregnancy was related to masculinized/defeminized offspring traits in adulthood. Data were obtained from a large sample of North American college students (offspring) and their mothers. Information about maternal activity levels during pregnancy were reported retrospectively by each mother. The offspring provided self-ratings of various sexually dimorphic traits. Several significant correlations were found. By and large, as maternal physical activity increased, feminine mannerisms decreased and masculine mannerisms increased in the offspring, particularly for females. Maternal physical activity was also associated with increased upper- and lower-body strength and especially with adult height among offspring. Sexual activity by the mother was only associated with upper-body strength and adult height, particularly of the female offspring. Several sexually dimorphic physical traits in offspring are associated with maternal activity levels during pregnancy. Prenatal testosterone is almost certainly involved. The associations could either reflect genetic influences (given that prenatal testosterone is highly heritable) or an effect of maternal testosterone being transferred to the developing fetus. More research is needed to assess the relative merit of these two possibilities.
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Coren, Stanley. "Prenatal testosterone exposure, left-handedness, and high school delinquency." Behavioral and Brain Sciences 21, no. 3 (June 1998): 369–70. http://dx.doi.org/10.1017/s0140525x98321226.
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Prenatal exposure to high levels of testosterone may lead to increased probability of left-handedness. Extrapolating from arguments by Mazur & Booth leads to a prediction of increased incidence of antisocial behavior among left-handers. Six hundred ninety-four males were tested for seven indicators of delinquency in high school. Left-handers were more likely to display such behaviors, providing indirect evidence for the hypothesized behavioral effects of testosterone.
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Osadchuk, Ludmila V., Bjarne O. Braastad, Ilpo Huhtaniemi, and Morten Bakken. "Alterations of the pituitary - gonadal axis in the neonatal blue fox (Alopex lagopus) exposed to prenatal handling stress." Reproduction, Fertility and Development 12, no. 4 (2000): 119. http://dx.doi.org/10.1071/rd99082.
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Handling is a stressor for blue foxes. The influence of preterm handling (1 min daily) of vixens was investigated in 68, 10-day-old cubs, 34 male and 34 female. Body, gonadal and pituitary weight, ano-genital distance, gonadal testosterone and oestradiol content and in vitro production, and pituitary LH content were measured in all cubs. The gonads were frozen or incubated in vitro with, or without, added hCG (2.5 IU per sample). The gonadal incubates and homogenates were analysed for testosterone and oestradiol by radioimmunoassay and the pituitary homogenates for LH by immunofluorometric assay. The results indicate that neonatal fox gonads actively produce steroids and that there are significant sex differences in basal steroid production and response of the gonads to hCG, and in pituitary LH content. Maternal stress resulted in a significant reduction of morphometric and hormonal measures of the reproductive system in neonatal blue foxes, with more drastic effects in female cubs. Gonadal weights were lower in cubs of both sexes from stressed vixens (65.7 4.3 v. 50.6 1.8 mg for the ovaries and 23.2 1.0 v. 17.7 1.0 mg for the testes, control v. stressed animals, P<0.01). The ano-genital distance in female offspring of stressed vixens was reduced (1.1 0.04 v. 0.9 0.03 cm, P<0.01). Basal ovarian oestradiol and testosterone production were decreased in cubs from prenatally stressed animals in comparison with controls (43.5 3.5 v. 32.6 3.7 pg ovary–1 h–1 and 0.40 0.16 v. 0.12 0.03 ng ovary–1 h–1, P<0.05). Prenatal stress did not affect either pituitary weights or LH content in either sex. There were no significant differences in ano-genital distance, testicular content of testosterone, or in vitro testosterone production between control and treated male cubs. In conclusion, these findings suggest that prenatal handling stress impaired the neonatal reproductive development of the female offspring, but had no marked effects on males. Sex-specific effects of prenatal handling stress on the reproductive development in foxes may be linked with the gender differences in responses of the hypothalamus–pituitary–adreno-cortical axis to stress conditions in this species.
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Martel, Michelle M., and Bethan A. Roberts. "Prenatal testosterone increases sensitivity to prenatal stressors in males with disruptive behavior disorders." Neurotoxicology and Teratology 44 (July 2014): 11–17. http://dx.doi.org/10.1016/j.ntt.2014.05.001.
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KLUMP, KELLY L., KYLE L. GOBROGGE, PATRICK S. PERKINS, DAVID THORNE, CHERYL L. SISK, and S. MARC BREEDLOVE. "Preliminary evidence that gonadal hormones organize and activate disordered eating." Psychological Medicine 36, no. 4 (December 12, 2005): 539–46. http://dx.doi.org/10.1017/s0033291705006653.
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Objective. Eating disorders are more common in females than in males. Gender differences may be due to organizational (i.e. prenatal) and activational (i.e. post-natal) gonadal hormone effects that influence sex differences in behavior. This preliminary set of studies examined these effects by investigating relationships between eating disorder symptoms, prenatal testosterone exposure, and adult levels of estrogen in women.Method. We examined organizational associations by investigating relationships between disordered eating and finger-length ratios, which are known to be somatic markers of prenatal testosterone exposure. Participants included 113 adult female twins drawn from the community. Disordered eating was assessed with the total score from the Minnesota Eating Behavior Survey (MEBS). Finger lengths were hand scored using a ruler and photocopies of both hands. We also investigated activational influences by examining associations between circulating levels of estradiol and disordered eating symptoms. Two independent samples of adult females (n's=24 and 25) drawn from the community were used for this study. Disordered eating was again assessed with the MEBS total score, while saliva samples were used for assessing estradiol.Results. Positive associations were found between disordered eating and both finger-length ratios and circulating estradiol levels.Conclusions. Findings suggest that lower levels of prenatal testosterone exposure and higher adult levels of estradiol are associated with increased eating disorder symptoms. We hypothesize that the relatively low level of testosterone before birth in females permits their brains to respond to estrogens at puberty, when the hormones activate the genes contributing to disordered eating in vulnerable girls.
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Whitehouse, Andrew J. O., Syed Zulqarnain Gilani, Faisal Shafait, Ajmal Mian, Diana Weiting Tan, Murray T. Maybery, Jeffrey A. Keelan, et al. "Prenatal testosterone exposure is related to sexually dimorphic facial morphology in adulthood." Proceedings of the Royal Society B: Biological Sciences 282, no. 1816 (October 7, 2015): 20151351. http://dx.doi.org/10.1098/rspb.2015.1351.
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Prenatal testosterone may have a powerful masculinizing effect on postnatal physical characteristics. However, no study has directly tested this hypothesis. Here, we report a 20-year follow-up study that measured testosterone concentrations from the umbilical cord blood of 97 male and 86 female newborns, and procured three-dimensional facial images on these participants in adulthood (range: 21–24 years). Twenty-three Euclidean and geodesic distances were measured from the facial images and an algorithm identified a set of six distances that most effectively distinguished adult males from females. From these distances, a ‘gender score’ was calculated for each face, indicating the degree of masculinity or femininity. Higher cord testosterone levels were associated with masculinized facial features when males and females were analysed together ( n = 183; r = −0.59), as well as when males ( n = 86; r = −0.55) and females ( n = 97; r = −0.48) were examined separately ( p -values < 0.001). The relationships remained significant and substantial after adjusting for potentially confounding variables. Adult circulating testosterone concentrations were available for males but showed no statistically significant relationship with gendered facial morphology ( n = 85, r = 0.01, p = 0.93). This study provides the first direct evidence of a link between prenatal testosterone exposure and human facial structure.
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Perakis, A., and F. Stylianopoulou. "Effects of a prenatal androgen peak on rat brain sexual differentiation." Journal of Endocrinology 108, no. 2 (February 1986): 281–85. http://dx.doi.org/10.1677/joe.0.1080281.
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ABSTRACT Exposure of the developing female brain to a 5α-dihydrotestosterone surge on day 18 of gestation resulted in defeminization and slight masculinization of the brain. In contrast, abolition of the androgenic effects of the testosterone peak naturally occurring in male fetuses on day 18 of gestation by exposure of the developing male brain to cyproterone acetate, at that time, resulted in demasculinization while feminization was not affected. On the basis of these results, we suggest that both the prenatal testosterone peak and the high testosterone levels occurring in males neonatally are necessary for aromatization sufficient to effect complete male rat brain sexual differentiation. J. Endocr. (1986) 108, 281–285
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Peper, Jiska S., Rachel M. Brouwer, G. Caroline M. van Baal, Hugo G. Schnack, Marieke van Leeuwen, Dorret I. Boomsma, René S. Kahn, and Hilleke E. Hulshoff Pol. "Does having a twin brother make for a bigger brain?" European Journal of Endocrinology 160, no. 5 (May 2009): 739–46. http://dx.doi.org/10.1530/eje-08-0915.
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ObjectiveBrain volume of boys is larger than that of girls by ∼10%. Prenatal exposure to testosterone has been suggested in the masculinization of the brain. For example, in litter-bearing mammals intrauterine position increases prenatal testosterone exposure through adjacent male fetuses, resulting in masculinization of brain morphology.DesignThe influence of intrauterine presence of a male co-twin on masculinization of human brain volume was studied in 9-year old twins.MethodsMagnetic resonance imaging brain scans, current testosterone, and estradiol levels were acquired from four groups of dizygotic (DZ) twins: boys from same-sex twin-pairs (SSM), boys from opposite-sex twin-pairs (OSM), girls from opposite-sex twin-pairs (OSF), and girls from same-sex twin-pairs (SSF; n=119 individuals). Data on total brain, cerebellum, gray and white matter volumes were examined.ResultsIrrespective of their own sex, children with a male co-twin as compared to children with a female co-twin had larger total brain (+2.5%) and cerebellum (+5.5%) volumes. SSM, purportedly exposed to the highest prenatal testosterone levels, were found to have the largest volumes, followed by OSM, OSF and SSF children. Birth weight partly explained the effect on brain volumes. Current testosterone and estradiol levels did not account for the volumetric brain differences. However, the effects observed in children did not replicate in adult twins.ConclusionsOur study indicates that sharing the uterus with a DZ twin brother increases total brain volume in 9-year olds. The effect may be transient and limited to a critical period in childhood.
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Vergauwen, Jonas, Ton G. G. Groothuis, Marcel Eens, and Wendt Müller. "Testosterone influences song behaviour and social dominance – But independent of prenatal yolk testosterone exposure." General and Comparative Endocrinology 195 (January 2014): 80–87. http://dx.doi.org/10.1016/j.ygcen.2013.10.014.
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Nada, Shadia E., Robert C. Thompson, and Vasantha Padmanabhan. "Developmental Programming: Differential Effects of Prenatal Testosterone Excess on Insulin Target Tissues." Endocrine Reviews 31, no. 5 (October 1, 2010): 775. http://dx.doi.org/10.1210/edrv.31.5.9982.
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Polycystic ovarian syndrome (PCOS) is the leading cause of infertility in reproductive-aged women with the majority manifesting insulin resistance. To delineate the causes of insulin resistance in women with PCOS, we determined changes in the mRNA expression of insulin receptor (IR) isoforms and members of its signaling pathway in tissues of adult control (n = 7) and prenatal testosterone (T)-treated (n = 6) sheep (100 mg/kg twice a week from d 30-90 of gestation), the reproductive/metabolic characteristics of which are similar to women with PCOS. Findings revealed that prenatal T excess reduced (P < 0.05) expression of IR-B isoform (only isoform detected), insulin receptor substrate-2 (IRS-2), protein kinase B (AKt), peroxisome proliferator-activated receptor-γ (PPARγ), hormone-sensitive lipase (HSL), and mammalian target of rapamycin (mTOR) but increased expression of rapamycin-insensitive companion of mTOR (rictor), and eukaryotic initiation factor 4E (eIF4E) in the liver. Prenatal T excess increased (P < 0.05) the IR-A to IR-B isoform ratio and expression of IRS-1, glycogen synthase kinase-3α and -β (GSK-3α and -β), and rictor while reducing ERK1 in muscle. In the adipose tissue, prenatal T excess increased the expression of IRS-2, phosphatidylinositol 3-kinase (PI3K), PPARγ, and mTOR mRNAs. These findings provide evidence that prenatal T excess modulates in a tissue-specific manner the expression levels of several genes involved in mediating insulin action. These changes are consistent with the hypothesis that prenatal T excess disrupts the insulin sensitivity of peripheral tissues, with liver and muscle being insulin resistant and adipose tissue insulin sensitive.
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Nada, Shadia E., Robert C. Thompson, and Vasantha Padmanabhan. "Developmental Programming: Differential Effects of Prenatal Testosterone Excess on Insulin Target Tissues." Endocrinology 151, no. 11 (September 15, 2010): 5165–73. http://dx.doi.org/10.1210/en.2010-0666.
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Polycystic ovarian syndrome (PCOS) is the leading cause of infertility in reproductive-aged women with the majority manifesting insulin resistance. To delineate the causes of insulin resistance in women with PCOS, we determined changes in the mRNA expression of insulin receptor (IR) isoforms and members of its signaling pathway in tissues of adult control (n = 7) and prenatal testosterone (T)-treated (n = 6) sheep (100 mg/kg twice a week from d 30–90 of gestation), the reproductive/metabolic characteristics of which are similar to women with PCOS. Findings revealed that prenatal T excess reduced (P < 0.05) expression of IR-B isoform (only isoform detected), insulin receptor substrate-2 (IRS-2), protein kinase B (AKt), peroxisome proliferator-activated receptor-γ (PPARγ), hormone-sensitive lipase (HSL), and mammalian target of rapamycin (mTOR) but increased expression of rapamycin-insensitive companion of mTOR (rictor), and eukaryotic initiation factor 4E (eIF4E) in the liver. Prenatal T excess increased (P < 0.05) the IR-A to IR-B isoform ratio and expression of IRS-1, glycogen synthase kinase-3α and -β (GSK-3α and -β), and rictor while reducing ERK1 in muscle. In the adipose tissue, prenatal T excess increased the expression of IRS-2, phosphatidylinositol 3-kinase (PI3K), PPARγ, and mTOR mRNAs. These findings provide evidence that prenatal T excess modulates in a tissue-specific manner the expression levels of several genes involved in mediating insulin action. These changes are consistent with the hypothesis that prenatal T excess disrupts the insulin sensitivity of peripheral tissues, with liver and muscle being insulin resistant and adipose tissue insulin sensitive.
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Osadchuk, L. V., B. O. Braastad, A. L. Hovland, and M. Bakken. "Reproductive and pituitary-adrenal axis parameters in normal and prenatally stressed prepubertal blue foxes (Alopex lagopus)." Animal Science 76, no. 3 (June 2003): 413–20. http://dx.doi.org/10.1017/s135772980005863x.
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AbstractMan-animal relationships are involved in the process of fox domestication. Handling being an important part of man-animal contacts, causes stress responses in farm-bred blue foxes. The purpose of this study was to determine how prenatal stress induced by handling pregnant vixens influences certain morphometric and hormonal parameters of adrenocortical and gonadal function in the prepubertal offspring. Blue fox females were subjected to daily handling sessions, each of 1 min, in the last trimester of pregnancy (term = 52 days). Plasma concentrations of ACTH, cortisol, progesterone, oestradiol and testosterone, as well as the in vitro adrenal and gonadal production of steroids were measured by radio-immunoassay in control (C, no. = 56) and prenatally stressed (PS, no. = 56) blue fox cubs of both sexes at the age of 6 to 7 months. Prenatal stress decreased plasma concentration of cortisol (C: 31·0 (s.e. 4·3) v. PS: 22·7(s.e. 1·6) ng/ml, P < 0·05) as well as progesterone (C: 1·00(s.e. 0·10) v. PS: 0·65(s.e. 0·05) ng/ml, P < 0·05) in female cubs. Prenatal stress did not cause any changes in adrenal or gonadal weights, plasma concentrations of testosterone or oestradiol, or in vitro adrenal or gonadal steroid production, in either sex. It is concluded that persistent handling of pregnant blue foxes did not affect the prepubertal development of the reproductive system but resulted in disregulation in the hypothalamic-pituitary-adrenal axis in the female offspring.
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Dinsdale, Natalie, Pablo Nepomnaschy, and Bernard Crespi. "The evolutionary biology of endometriosis." Evolution, Medicine, and Public Health 9, no. 1 (January 1, 2021): 174–91. http://dx.doi.org/10.1093/emph/eoab008.
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Abstract We provide the first analysis and synthesis of the evolutionary and mechanistic bases for risk of endometriosis in humans, structured around Niko Tinbergen's four questions about phenotypes: phylogenetic history, development, mechanism and adaptive significance. Endometriosis, which is characterized by the proliferation of endometrial tissue outside of the uterus, has its phylogenetic roots in the evolution of three causally linked traits: (1) highly invasive placentation, (2) spontaneous rather than implantation-driven endometrial decidualization and (3) frequent extensive estrogen-driven endometrial proliferation and inflammation, followed by heavy menstrual bleeding. Endometriosis is potentiated by these traits and appears to be driven, proximately, by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic–pituitary–ovarian (HPO) axis, and at low levels, it can result in an altered trajectory of reproductive and physiological phenotypes that in extreme cases can mediate the symptoms of endometriosis. Polycystic ovary syndrome, by contrast, is known from previous work to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes opposite to those found in endometriosis. The hypothesis that endometriosis risk is driven by low prenatal testosterone, and involves extreme expression of some reproductive phenotypes, is supported by a suite of evidence from genetics, development, endocrinology, morphology and life history. The hypothesis also provides insights into why these two diametric, fitness-reducing disorders are maintained at such high frequencies in human populations. Finally, the hypotheses described and evaluated here lead to numerous testable predictions and have direct implications for the treatment and study of endometriosis. Lay summary: Endometriosis is caused by endometrial tissue outside of the uterus. We explain why and how humans are vulnerable to this disease, and new perspectives on understanding and treating it. Endometriosis shows evidence of being caused in part by relatively low testosterone during fetal development, that ‘programs’ female reproductive development. By contrast, polycystic ovary syndrome is associated with relatively high testosterone in prenatal development. These two disorders can thus be seen as ‘opposite’ to one another in their major causes and correlates. Important new insights regarding diagnosis, study and treatment of endometriosis follow from these considerations.
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Puttabyatappa, Muraly, Rodolfo C. Cardoso, Carol Herkimer, Almudena Veiga-Lopez, and Vasantha Padmanabhan. "Developmental programming: postnatal estradiol modulation of prenatally organized reproductive neuroendocrine function in sheep." Reproduction 152, no. 2 (August 2016): 139–50. http://dx.doi.org/10.1530/rep-16-0065.
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Gestational testosterone (TS) excess, acting via both the androgenic and estrogenic pathways, advances puberty and disrupts the neuroendocrine estradiol (E2) feedback and periovulatory hormonal dynamics in female sheep. These prenatally programmed defects may be subject to postnatal modifications by continued organizational and/or activational effects of steroids. This study investigated (1) the organizational contribution of prenatal estrogen excess and (2) the impact of postnatal exposure to E2in modulating the effects of prenatal androgen excess (TS and dihydrotestosterone (DHT)) on puberty, neuroendocrine feedback mechanisms, and periovulatory hormonal dynamics in sheep. Pregnant Suffolk sheep were treated with TS, DHT, E2, or E2plus DHT (ED) from days 30 to 90 of gestation. A subset of the control (C), TS, and DHT female offspring received a constant-release E2implant postnatally. Findings revealed that (1) prenatal E2-treatment failed to reproduce the neuroendocrine disruptions predicted to be programmed by the estrogenic pathway and (2) prenatal E2D-treatment did not adequately replicate the reproductive neuroendocrine defects induced by prenatal TS excess. More importantly, continuous postnatal E2-treatment, while delaying the onset of puberty and reducing the inhibitory effects of E2on tonic luteinizing hormone (LH) release, failed to amplify the E2-positive feedback and periovulatory defects induced by prenatal TS-treatment. Our results indicate that disruptions in E2-positive feedback mechanisms and periovulatory gonadotropin secretion induced by prenatal TS-treatment are programmed predominantly during the prenatal life with postnatal exposure to E2excess not contributing further to these disruptions.
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Hsu, Hseng-Kuang, Rei-Cheng Yang, Huei-Chuan Shih, Ya-Lun Hsieh, U.-Yang Chen, and Chin Hsu. "Prenatal Exposure of Testosterone Prevents SDN-POA Neurons of Postnatal Male Rats From Apoptosis Through NMDA Receptor." Journal of Neurophysiology 86, no. 5 (November 1, 2001): 2374–80. http://dx.doi.org/10.1152/jn.2001.86.5.2374.
Full textAbstract:
The role of N-methyl-d-aspartate (NMDA) receptor in mediating the effect of testosterone exposure prenatally on neuronal apoptosis in the sexual dimorphic nucleus of the preoptic area (SDN-POA) of rats was studied. The endogenous testosterone was diminished by prenatal stress (PNS) or simulated by testosterone exposure (TE) to understand the effect of testosterone on NR1 (a functional subunit protein of NMDA receptor) expression and neuronal apoptosis. To further study whether the testosterone, after being converted into estradiol, modulates NR1 expression, 4-androstein-4-ol-3,17-dione (ATD; an aromatase inhibitor) was used to block the conversion of estradiol from testosterone. The expressions of the NR1 mRNA and NR1 subunit protein were quantified by RT-PCR and western blotting analysis, respectively. In addition, a noncompetitive antagonist of NMDA receptor, MK-801, was used to find out whether blockage of NMDA receptor affects the naturally occurring apoptosis in SDN-POA. The results showed the following. 1) Expression of perinatal NR1 subunit protein in the central part of the medial preoptic area of male rats was significantly higher than that of females, especially on postnatal days 1 and 3. 2) The testosterone level of male fetuses on embryonic day 18 was significantly higher than that of females, while the testosterone level of TE females or PNS males was similar to that of intact males or intact females, respectively. 3) The apoptotic incidence of intact male rats was significantly less than that of females, and the apoptosis was stimulated by PNS in male or inhibited by TE in female. 4) The expression of NR1 subunit protein could be inhibited by PNS or ATD-treatment in male, while stimulated by TE in female. 5) NR1 mRNA showed no significant difference among intact male, PNS male, ATD-treated male, TE female and intact female rats. 6) The low apoptotic incidence of male rats was significantly increased when NMDA receptor was blocked by MK-801. These results suggest that testosterone, after being converted to estradiol, may prevent the SDN-POA neurons of male rats from apoptosis through enhancing the expression of NR1 at the posttranscriptional level.
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Meijer, Willemijn M., Anna E. van’t Veer, Marinus H. van IJzendoorn, and Marian J. Bakermans-Kranenburg. "Prenatal testosterone, oxytocin and cortisol levels in relation to prenatal and postnatal paternal involvement." Psychoneuroendocrinology 83 (September 2017): 24. http://dx.doi.org/10.1016/j.psyneuen.2017.07.304.
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