Testosterone (T) and vitamin D (VD) interact in androgen deficient men, however, this interaction and subsequent semen quality and bone mineral density (BMD) status is not clear in infertile men. Our objective was to investigate T, VD, semen quality, BMD and their relationships in Chinese infertile men. We conducted a cross-sectional study of 559 men aged 20-40 years, including 195 fertile men, 9 infertile men with known risk factors for osteoporosis (WR) and 355 infertile men without known risk factors for osteoporosis (WOR). WOR infertile men constituted 314 oligo-, astheno-, teratospermic or normospermic infertile men (OATN men) and 41 non-obstructive azoospermic men (NOA men). Differences of parameters were assessed, and the relationships were adjusted by multiple linear regression. WOR infertile men had significantly lower T, lumbar spine and total hip BMD than fertile men (all p < 0.05). Bioavailable T (Bio-T) and 25-hydroxyvitamin D [25(OH)D] were independent determinants of BMD in WOR infertile men (all p < 0.01) but not in fertile men. After stratifying Bio-T, WOR infertile men had lower BMD than fertile men (all p < 0.05) in low Bio-T subgroups (Bio-T ≤ 11.6 nmol/L), but not high Bio-T subgroups (Bio-T > 11.6 nmol/L). 25(OH)D was an independent determinant of sperm motility and morphology in WOR OATN men (all p < 0.05), with only borderline significance in fertile men(motility: p = 0.047; morphology: p = 0.056). T determined sperm concentration (square root) and morphology in WOR OATN men (all p < 0.001). No correlations between T and 25(OH)D were found in all groups. We suggest that infertile men have lower T and BMD than fertile men. 25(OH)D and T were associated with low BMD and poor semen quality in infertile men.

Background Vitamin D plays critical role in the female reproductive system. It seems that vitamin D is associated with clinical pregnancy outcomes of assisted reproductive technologies (ART), but its role remains elusive. This study is aimed to establish whether vitamin D is associated with clinical outcomes of in vitro fertilization (IVF). Methods The cross-sectional study was carried out from January 1st 2017 to December 31st 2017. A total of 848 patients who had indications for IVF were enrolled. The patients were classified by serum 25 (OH) D quartiles. The outcome parameters of IVF were compared in each group, including normal fertilization rate, high quality embryo rate, clinical pregnancy rate, implantation rate and live birth rate. Results The median 25 (OH) D concentration was 15.25 ng/ml. Serum 25 (OH) D levels in women varied with the seasons. We found that serum 25 (OH) D levels were higher in autumn than other seasons, and the lowest level occurred in spring. Follicular fluid (FF) vitamin D levels were positively correlated with serum vitamin D levels ( r = 0.85, P < 0.001). The levels of FF vitamin D were significantly higher than the levels of serum vitamin D ( P < 0.001). Normal fertilization rates were significantly different among four groups ( P = 0.007). The group of women with the highest serum 25 (OH) D levels had the highest normal fertilization rate. However, the clinical pregnancy rate, implantation rate and live birth rates were not significantly different among the four groups when the age, BMI, AMH, seasons of blood drawing, COH protocol, high quality embryo rate and number of embryos transferred were adjusted. In addition, we found that serum 25 (OH) D levels were significantly higher in patients received IVF than patients received R-ICSI ( P = 0.013). Conclusions Among Chinese women, lower serum vitamin D levels are associated with a lower fertilization rate in IVF. However, vitamin D level was not associated with the clinical pregnancy and live birth rate following IVF. Electronic supplementary material The online version of this article (10.1186/s12958-019-0500-0) contains supplementary material, which is available to authorized users.

Advanced maternal-age is a major factor adversely affecting oocyte quality, consequently worsening pregnancy outcomes. Thus, developing strategies to reduce the developmental defects associated with advanced maternal-age would benefit older mothers. Multiple growth factors involved in female fertility have been extensively studied; however, the age-related impacts of various growth factors remain poorly studied. In the present study, we identified that levels of insulin-like growth factor 2 (IGF2) are significantly reduced in the serum and oocytes of aged mice. We found that adding IGF2 in culture medium promotes oocyte maturation and significantly increases the proportion of blastocysts: from 41% in the untreated control group to 64% (50 nM IGF2) in aged mice ( p < 0.05). Additionally, IGF2 supplementation of the culture medium reduced reactive oxygen species production and the incidence of spindle/chromosome defects. IGF2 increases mitochondrial functional activity in oocytes from aged mice: we detected increased ATP levels, elevated fluorescence intensity of mitochondria, higher mitochondrial membrane potentials, and increased overall protein synthesis, as well as increased autophagy activity and decreased apoptosis. Collectively, our findings demonstrate that IGF2 supplementation in culture media improves oocyte developmental competence and reduces meiotic structure defects in oocytes from aged mice.

Background Maternal obesity is a global issue that has devastating effects across the reproductive spectrum such as meiotic defects in oocytes, consequently worsening pregnancy outcomes. Different studies have shown that such types of meiotic defects originated from the oocytes of obese mothers. Thus, there is an urgent need to develop strategies to reduce the incidence of obesity-related oocyte defects that adversely affect pregnancy outcomes. Multiple growth factors have been identified as directly associated with female reproduction; however, the impact of various growth factors on female fertility in response to obesity remains poorly understood. Methods The immature GV-stage oocytes from HFD female mice were collected and cultured in vitro in two different groups (HFD oocytes with and without 50 nM IGF2), however; the oocytes from ND mice were used as a positive control. HFD oocytes treated with or without IGF2 were further used to observe the meiotic structure using different analysis including, the spindle and chromosomal analysis, reactive oxygen species levels, mitochondrial functional activities, and early apoptotic index using immunofluorescence. Additionally, the embryonic developmental competency and embryos quality of IGF2-treated zygotes were also determined. Results In our findings, we observed significantly reduced contents of insulin-like growth factor 2 (IGF2) in the serum and oocytes of obese mice. Our data indicated supplementation of IGF2 in a culture medium improves the blastocyst formation: from 46% in the HFD group to 61% in the HFD + IGF2-treatment group (50 nM IGF2). Moreover, adding IGF2 to the culture medium reduces the reactive oxygen species index and alleviates the frequency of spindle/chromosome defects. We found increased mitochondrial functional activity in oocytes from obese mice after treating the oocytes with IGF2: observed elevated level of adenosine triphosphate, increased mitochondrial distribution, higher mitochondrial membrane potentials, and reduced mitochondrial ultrastructure defects. Furthermore, IGF2 administration also increases the overall protein synthesis and decreases the apoptotic index in oocytes from obese mice. Conclusions Collectively, our findings are strongly in favor of adding IGF2 in culture medium to overcome obesity-related meiotic structural-developmental defects by helping ameliorate the known sub-optimal culturing conditions that are currently standard with assisted reproduction technologies.

Meiotic recombinases RAD51 and DMC1 mediate strand exchange in the repair of DNA double-strand breaks (DSBs) by homologous recombination. This is a landmark event of meiosis that ensures genetic diversity in sexually reproducing organisms. However, the regulatory mechanism of DMC1/RAD51-ssDNA nucleoprotein filaments during homologous recombination in mammals has remained largely elusive. Here, we show that SPIDR (scaffold protein involved in DNA repair) regulates the assembly or stability of RAD51/DMC1 on ssDNA. Knockout of Spidr in male mice causes complete meiotic arrest, accompanied by defects in synapsis and crossover formation, which leads to male infertility. In females, loss of Spidr leads to subfertility; some Spidr−/− oocytes are able to complete meiosis. Notably, fertility is rescued partially by ablation of the DNA damage checkpoint kinase CHK2 in Spidr−/− females but not in males. Thus, our study identifies SPIDR as an essential meiotic recombination factor in homologous recombination in mammals.

As oocyte meiotic maturation, they undergo two successive meiotic M phases, notably lacking an intervening interphase phase. During these M phases, oocytes remain transcriptionally quiescent, and we now know that 'translational repressed mRNAs' are stored in a structure called the mitochondria associated ribonucleoprotein domain (MARDO). LSM14B is one of the abundant proteins of MARDO, and is predicted to bind mRNA, but its function(s) remain elusive. Here, we demonstrate that LSM14B functions to promote MARDO assembly in mouse oocytes. We also found that LSM14B knockout female mice are infertile, and show that the knockout oocytes fail to enter meiosis II, instead entering an aberrant interphase-like stage. Finally, we show that the failure of oocyte maturation results from decreased expression of Cyclin B1. Our study has revealed that the RNA-binding protein LSM14B modulates MARDO assembly and is essential for oocyte meiotic maturation.

SummaryCurrently, obesity has achieved epidemic levels in reproductive‐aged women with a myriad of consequences. Obesity is susceptible to several reproductive complications that eventually affect fertility rates. These complications originate from the deteriorated quality of oocytes from mothers with obesity, which increases the probability of chromosomal aneuploidy, elevated reactive oxygen species production, compromised embryonic developmental competency, and eventually reduced fertility. Maternal obesity is linked to pregnancy complications such as implantation error, abortion, miscarriage, and early pregnancy loss. This review highlights the adverse effects of maternal obesity on female fertility, with a focus on the mechanistic link between maternal obesity and oocyte quality and discusses possible measures to reduce its associated risks.