prenatal testosterone
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2022 ◽  
Vol 136 ◽  
pp. 105623
Author(s):  
Niamh Dooley ◽  
Amber Ruigrok ◽  
Rosemary Holt ◽  
Carrie Allison ◽  
Alexandros Tsompanidis ◽  
...  

2021 ◽  
Vol 8 (3) ◽  
pp. 013-018
Author(s):  
Timipa Richard Ogoun ◽  
Pere-ere Sarah Tobia ◽  
Rita Osain

Humans, primates, birds and reptiles have demonstrated sexually dimorphism in the length of their 2nd and 4th digits otherwise known as 2D:4D, with males on the average having lower values than females. This difference has been associated with the differential exposure of prenatal testosterone relative to estrogen during intrauterine life. This present study assesses the 2d:4d ratio amongst students of the federal Polytechnic Ekowe, Bayelsa state of Nigeria. A total of 299 students (males n=150 and females n=149) participated in the study. The length of 2nd and 4th digits were measured with digital Vernier caliper from the basal crease to the tip of the finger, and 2nd digit length (2D) was divided by 4th digit (4D) to obtain 2D:4D ratio. The results of this study showed no significant difference between 2D right and left and 4D right and left for same sex (0.98±0.04 and 0.98±0.04 for males and 0.96±0.05 and 0.96±0.05 for female). Sexual dimorphism exits between sexes which is an indication that prenatal hormones have played a fundamental role on humans, during developmental stages.


2021 ◽  
Author(s):  
Melanie Monica de Wit ◽  
Sander Begeer ◽  
Michel Guillaume Nivard ◽  
Elsje van Bergen

Background: Having twin and non-twin siblings might influence autistic traits both prenatally and postnatally. The twin testosterone transfer hypothesis suggests that girls with a twin brother are exposed to higher levels of prenatal testosterone than girls with a twin sister. Prenatally, increased testosterone exposure could masculinize neural development and increase autistic traits. Postnatally, siblings may provide example behaviour, which could reduce autistic traits. Methods: We studied pre- and postnatal influences of twin and non-twin siblings on (mother and teacher-reported) autistic traits in 7,714 dizygotic twins. We examined the effect of gender of the proband child and of the siblings. We fitted regression models (for boys and girls separately) with as predictors sex of co-twin and having older and/or younger siblings. Results: Prenatally, girls’ (mother-reported) autistic traits were slightly lower for those with a twin brother than those with a twin sister, β = -.08, p = .001. This difference was not replicated in teacher-reported autistic traits, β = .01, p = .734. Boys’ (mother and teacher-reported) autistic traits were not related to the sex of their cotwin, p’s > .05. Postnatally, girls’ teacher-reported autistic traits were slightly higher if they had an older brother, β = .07, p = .013. Other than this small effect, girls’ autistic traits were not related to having siblings. Likewise, boys’ autistic traits were not related to having siblings. Conclusions: We do not find increased autistic traits in girls with a twin brother compared to a twin sister. This finding contributes to the body of literature that rejects the twin testosterone transfer hypothesis. In all, we find little evidence for pre- and postnatal sibling influences. Besides, our findings suggest that parent reports on autistic traits in twins might be slightly biased. Our findings align with ASD’s high heritability and absence of shared-environmental influences.


Endocrinology ◽  
2021 ◽  
Author(s):  
Nadia Saadat ◽  
Muraly Puttabyatappa ◽  
Venkateswaran R Elangovan ◽  
John Dou ◽  
Joseph N Ciarelli ◽  
...  

Abstract Prenatal testosterone (T)-treated female sheep manifest peripheral insulin resistance, ectopic lipid accumulation and insulin signaling disruption in liver and muscle. This study investigated transcriptional changes and transcriptome signature of prenatal T excess-induced hepatic and muscle-specific metabolic disruptions. Genome-wide coding and non-coding (nc) RNA expression in liver and muscle from 21-month-old prenatal T-treated (T propionate 100mg intramuscular twice weekly from days 30 to 90 of gestation; Term: 147 days) and control females were compared. Prenatal T (1) induced differential expression of mRNAs in liver (15 down, 17 up) and muscle (66 down, 176 up) (FDR<0.05, absolute log2 fold change>0.5); (2) downregulated mitochondrial pathway genes in liver and muscle; (3) downregulated hepatic lipid catabolism and PPAR signaling gene pathways; (4) modulated ncRNA metabolic processes gene pathway in muscle and (5) downregulated 5 uncharacterized long ncRNA (lncRNA) in the muscle but no ncRNA changes in the liver. Correlation analysis showed downregulation of lncRNAs LOC114112974 and LOC105607806 was associated with decreased TPK1, and LOC114113790 with increased ZNF470 expression. Orthogonal Projections to Latent Structures Discriminant Analysis identified mRNAs HADHA and SLC25A45, and miRNAs MIR154A, MIR25 and MIR487B in liver and ARIH1 and ITCH and miRNAs MIR369, MIR10A and MIR10B in muscle as potential biomarkers of prenatal T-excess. These findings suggest downregulation of mitochondria, lipid catabolism, and PPAR signaling genes in liver and dysregulation of mitochondrial and ncRNA gene pathways in muscle are contributors of lipotoxic and insulin resistant hepatic and muscle phenotype. Gestational T excess programming of metabolic dysfunctions involve tissue-specific ncRNA modulated transcriptional changes.


Author(s):  
Bernard Crespi

ABSTRACT Evidence linking endometriosis to low prenatal testosterone, and evidence that risk of polycystic ovary syndrome (PCOS) is associated with high prenatal testosterone, has motivated the hypothesis that endometriosis and PCOS exhibit inverse comorbidity. The inverse comorbidity hypothesis predicts that populations exhibiting higher prevalence of one disorder should show lower prevalence of the other. To test this prediction, data were compiled from the literature on the prevalence of endometriosis and PCOS, levels of serum testosterone in women during pregnancy, and digit ratios as indicators of prenatal testosterone, in relation to variation in inferred or observed population ancestries. Published studies indicate that rates of endometriosis are highest in women from Asian populations, intermediate in women from European populations, and lowest in women from African populations (i.e., with inferred or observed African ancestry); by contrast, rates of PCOS show evidence of being lowest in Asian women, intermediate in Europeans, and highest in individuals from African populations. Women from African populations also show higher serum testosterone during pregnancy (which may increase PCOS risk, and decrease endometriosis risk, in daughters), and higher prenatal testosterone (as indicated by digit ratios), than European women. These results are subject to caveats involving ascertainment biases, socioeconomic, cultural and historical effects on diagnoses, data quality, uncertainties regarding the genetic and environmental bases of population differences, and population variation in the causes and symptoms of PCOS and endometriosis. Despite such reservations, the findings provide convergent, preliminary support for the inverse comorbidity model, and they should motivate further tests of its predictions.


2021 ◽  
pp. 1-10
Author(s):  
J. T. Manning ◽  
B. Fink ◽  
L. Mason ◽  
R. Trivers

Abstract Digit ratio – a putative measure of prenatal sex steroids – may be related to body mass index (BMI). However, reports of correlations between 2D:4D and BMI have yielded mixed results with some studies showing no relationship while others have reported positive associations in men or women only. This study considers associations between self-reported 2D:4D and BMI in a large online survey (i.e. the BBC Internet Study). At the individual level, there was a weak positive association between 2D:4D and BMI in both sexes with greater effect sizes in women. Body mass index was positively related to age and negatively related to parental income; however, the relationship between 2D:4D and BMI was independent of both variables. At the national level, mean 2D:4D per country showed positive associations with mean national BMI but those correlations were restricted to females. It is concluded that BMI is positively related to low prenatal testosterone and high prenatal oestrogen. Parental income inequality may influence both prenatal sex steroids (through a ‘Trivers–Willard’ effect) and BMI such that increases in inequality result in reductions in prenatal testosterone and increases in BMI at the individual and national level.


2021 ◽  
Author(s):  
Yu Zhou ◽  
Min Gong ◽  
Yingfei Lu ◽  
Jianquan Chen ◽  
Rong Ju

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 down regulation 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 adenosine monophosphate and adenosine triphosphate generation, which finally improved glucose stimulated insulin secretion in beta cells. Taken together, these results demonstrated that prenatal testosterone exposure caused metabolic disturbance in aged female offspring via suppression of Sirtuin 3 expression and activation of oxidative stress in pancreatic beta cells.


2021 ◽  
Vol 8 (2) ◽  
pp. 130-134
Author(s):  
K Muthu Prathibha ◽  
Kathrina Joseph ◽  
Dharunya Pachaiyappan ◽  
Soma Sri Harsha

The 2D:4D ratio is a sexually dimorphic trait, negatively related to prenatal testosterone which in turn influences the areas in brain, critical for learning and memory. The objective of the present study was to compare the 2D:4D ratios between sexes, right / left hands and correlate with mean scores of learning and memory. The cross-sectional study was conducted in 116 participants (80 males and 36 females) of 18 -19 years of age. Lengths of index and ring fingers were measured using vernier calipers to calculate 2D:4D ratios. Free & Placement recall and Working visual memory (Visual N Back test) were assessed. Verbal learning ability was assessed using Rey’s Auditory Verbal Learning Test (AVLT). Mean 2D:4D ratios of right hand (0.96±0.051) were significantly lower than left hand (0.98±0.1; p = 0.036). Females had higher ratios than males in both hands. In Free recall (FR) and Placement Recall (PR) tests, average hits and errors scores of females and males were comparable. In Visual N Back test, there were statistically significant correlations between 2D:4D ratios and mean hits & errors scores (M >F). The mean hits score in AVLT was lower in males (13.9±1.4) when compared to females (14.2±1.0). The findings of the present study can help us to associate a simple measure like 2D:4D ratio to learning abilities of an individual. Also, 2D:4D ratio, a non invasive measure can be used to evaluate one’s cognitive abilities with regard to memory and learning.


Hypertension ◽  
2021 ◽  
Vol 77 (5) ◽  
pp. 1756-1764
Author(s):  
Chi Le-Ha ◽  
Lawrence J. Beilin ◽  
Sally Burrows ◽  
Jeffrey A. Keelan ◽  
Martha Hickey ◽  
...  

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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