Intrauterine hyponutrition reduces fetal testosterone production and postnatal sperm count in the C57BL/6N
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PROVIDER: PRJNA773429 | ENA |
REPOSITORIES: ENA
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Project description:There has been growing interest in the relationship between maternal undernutrition and reproductive disorders in male offspring. In the present study, we determined the effects of maternal calorie restriction throughout the critical period for in utero development of the male reproductive system, termed the “masculinization programming window” on the reproductive system of mice. The intratesticular testosterone concentration of the fetuses of calorie-restricted (R) dams was lower than in control fetuses at 17.5 days post coitum. In addition, there was global down-regulation of genes encoding steroidogenic enzymes and a low sperm count in the offspring of R dams (R-offspring) at 6 weeks of age. Microarray analysis of the testes of the offspring identified dysregulation of several genes that might explain the derangement in spermatogenesis in the R-offspring. Thus, the present study provides insights into the impact of maternal undernutrition on the male reproductive system in mice. The deleterious effects probably originate in lower androgen exposure during the “masculinization programming window.”
2021-10-22 | GSE186345 | GEO
Project description:BackgroundAlthough intrauterine hyponutrition is regarded as a risk factor for the development of "testicular dysgenesis syndrome" (TDS) in the human, underlying mechanism(s) remain largely unknown.MethodsTo clarify the underlying mechanism(s), we fed vaginal plug-positive C57BL/6N female mice with regular food ad libitum throughout the pregnant course (control females) (C-females) or with 50% of the mean daily intake of the C-females from 6.5 dpc (calorie-restricted females) (R-females), and compared male reproductive findings between 17.5-dpc-old male mice delivered from C-females (C-fetuses) and those delivered from R-females (R-fetuses) and between 6-week-old male mice born to C-females (C-offspring) and those born to R-females (R-offspring).ResultsCompared with the C-fetuses, the R-fetuses had (1) morphologically normal external genitalia with significantly reduced anogenital distance index, (2) normal numbers of testicular component cells, and (3) significantly low intratesticular testosterone, in association with significantly reduced expressions of steroidogenic genes. Furthermore, compared with the C-offspring, the R-offspring had (1) significantly increased TUNEL-positive cells and normal numbers of other testicular component cells, (2) normal intratesticular testosterone, in association with normal expressions of steroidogenic genes, (3) significantly reduced sperm count, and normal testis weight and sperm motility, and (4) significantly altered expressions of oxidation stress-related, apoptosis-related, and spermatogenesis-related genes.ConclusionsThe results, together with the previous data including the association between testosterone deprivation and oxidative stress-evoked apoptotic activation, imply that reduced fetal testosterone production is the primary underlying factor for the development of TDS in intrauterine hyponutrition, and that TDS is included in the clinical spectrum of Developmental Origins of Health and Disease.
| S-EPMC8901363 | biostudies-literature
Project description:This study aimed at generating a reference data set of C57BL/6N small RNA expression at baseline conditions
2020-01-09 | E-MTAB-7617 | biostudies-arrayexpress
Project description:Characterisation of adult C57BL/6N sperm small RNA
| PRJEB30920 | ENA
Project description:About 10% of couples of reproductive age worldwide suffer from infertility, with male factors accounting for about 50%, and testosterone is essential for male fertility, but the mechanisms behind the poor sperm quality and abnormally low blood testosterone levels in diabetic patients are unclear. In this study, we found that the peptide Apelin (APLN) significantly inhibited testosterone secretion from Leydig cells (LCs), which in turn led to decreased sperm quality. APLN was found to be localized to leydig cells in the testes of several diabetic mice, and its expression was significantly increased. The addition of APLN to mouse leydig cells decreased testosterone content and decreased the expression of genes related to testosterone synthesis, but the addition of ML221, an APLN receptor inhibitor, significantly increased the expression of testosterone synthesis genes. Injecting ML221 into diabetic mice significantly increased testosterone levels in the blood, increased sperm count as well as enhanced sperm motility and ultimately increased live birth rate of mice after in vitro fertilization. Proteomics revealed that ML221 significantly increased the expression of NR2F2 and further activated the transcription of testosterone synthesis genes. This study will further use mouse and cellular models to completely unravel the specific mechanisms by which APLN inhibits testosterone secretion and elucidate the causes of decreased sperm quality in diabetic patients. This study provides a new clinical target for the development of drugs to improve fertility in diabetic patients.
2025-02-24 | GSE289564 | GEO
Project description:About 10% of couples of reproductive age worldwide suffer from infertility, with male factors accounting for about 50%, and testosterone is essential for male fertility, but the mechanisms behind the poor sperm quality and abnormally low blood testosterone levels in diabetic patients are unclear. In this study, we found that the peptide Apelin (APLN) significantly inhibited testosterone secretion from Leydig cells (LCs), which in turn led to decreased sperm quality. APLN was found to be localized to leydig cells in the testes of several diabetic mice, and its expression was significantly increased. The addition of APLN to mouse leydig cells decreased testosterone content and decreased the expression of genes related to testosterone synthesis, but the addition of ML221, an APLN receptor inhibitor, significantly increased the expression of testosterone synthesis genes. Injecting ML221 into diabetic mice significantly increased testosterone levels in the blood, increased sperm count as well as enhanced sperm motility and ultimately increased live birth rate of mice after in vitro fertilization. Proteomics revealed that ML221 significantly increased the expression of NR2F2 and further activated the transcription of testosterone synthesis genes. This study will further use mouse and cellular models to completely unravel the specific mechanisms by which APLN inhibits testosterone secretion and elucidate the causes of decreased sperm quality in diabetic patients. This study provides a new clinical target for the development of drugs to improve fertility in diabetic patients.
2025-02-24 | GSE289563 | GEO
Project description:Analysis of the transcriptome of testes of hypogonadal mice that had been pretreated with testosterone proprionate for 2 weeks then submitted to testosterone withdrawal. Keywords = testis, hypogonadal mice, testosterone Keywords: other
2003-05-28 | GSE438 | GEO
Project description:ER stress could affect many tissues, especially liver, in which non-alcoholic fatty liver disease, liver steatosis, etc. have been reported relative. But there still lack systematic insight into ER stress in liver, which can be obtained by transcriptomics of the tissue. Here, tunicamycin was utilized to induce ER stress in C57BL/6N mice. And microarray was performed to get the transcriptome alteration. Microarray of liver from tunicamycin-injected C57Bl/6N mice
2021-02-23 | GSE167299 | GEO
Project description:Birth cohort studies and experimental investigations in animals link gestational diabetes mellitus (GDM) with impaired cognitive performance in the first filial generation (F1). We found that intrauterine hyperglycemia exposure resulted in behavior abnormality and cognitional functional disorder of both F1- and F2-GDM male mice. Methylome of sperm of F1 adult male mice from control pregnant mice (F1-C) and GDM pregnant mice (F1-GDM) revealed differentially methylated genes enriched in neurodevelopmental process.
2021-08-25 | GSE142502 | GEO
Project description:The objective of this study was to determine the relationship between strict morphology as assessed on the initial semen analysis during fertility workup and pregnancy rates after intrauterine insemination. This is a retrospective study of couples undergoing intrauterine insemination from 2007 to 2012. Couple characteristics and semen analysis parameters were recorded and evaluated. Risk ratios (RR) and 95% confidence intervals (95% CI) were calculated, accounting for within-couple (cluster) correlation among repeated intrauterine insemination cycles. Four hundred thirty-five women (average ± standard deviation age 31.7 ± 4.8) undergoing 1,287 intrauterine insemination cycles were analyzed. Fecundability was not statistically different when low strict morphology (≤1% and 2-4%) was compared to the reference range of morphology > 14% [RR 0.99 (0.41-2.40) and 0.90 (0.48-1.70)]. Results were unchanged when adjusted for female characteristics, medication, and inseminating total motile sperm count [aRR 1.22 (0.51-2.93) and 1.00 (0.53-1.91)]. Evaluating combined effects of morphology with inseminating total motile sperm count, pregnancy rates among cycles with total motile count < 5 million and strict morphology ≤ 4% normal were reduced when compared to cycles with total motile count > 20 million and morphology > 4% normal (RR 0.37, 95% CI 0.17-0.82). These relationships remained when evaluating live birth/ongoing pregnancy per cycle. In intrauterine insemination cycles, initial strict morphology was associated with subsequent fecundability only when inseminating total motile count was below 5 million. For cycles with total motile count above this threshold, no impact of low morphology on success rates with intrauterine insemination was observed.
| S-EPMC11922279 | biostudies-literature