Objective: Metabolic syndrome (MetS) is a cluster of risk factors for cardiovascular disease and diabetes. Menopause is associated with an increased risk for MetS. The purpose of this meta-analysis is to better understand the relationship between MetS and menopause. Methods: MEDLINE and EMBASE were searched for all the associated articles on (1) MetS components in postmenopausal women vs. premenopausal women, (2) comparison of MetS incidence between surgical menopause and natural menopause, (3) the effect of hormone therapy (HT) with 17β-estradiol (E2) compared to conjugated equine estrogen (CEE) on MetS components among postmenopausal women. A meta-analysis was applied by Review Manager 5.3 software. Results: All comparable indicators were significantly unfavorably changed in postmenopausal women compared to premenopausal women except for high density lipoprotein cholesterol. Women who underwent surgical menopause suffered a 1.51-fold higher risk for MetS compared to those with natural menopause. HT with E2 provided more benefits for levels of triglyceride and diastolic blood, while CEE showed a better effect on both high and low density lipoprotein cholesterol levels. Conclusions: Menopause nearly adversely affects all components of MetS, and surgical menopause may lead to a higher incidence of MetS compared to natural menopause. HT with various preparations may have different effects on MetS components. These results may clarify the management of menopause-related MetS in clinical practice.

Context Perfluoroalkyl and polyfluoroalkyl substances (PFASs), a group of ubiquitous environmental chemicals with properties of endocrine disruption, are often detectable in humans. Objective The current study investigated the association between exposure to PFAS and primary ovarian insufficiency (POI). Design, Patients, Interventions, and Main Outcome Measures Levels of plasma PFAS were measured in 120 Chinese women with overt POI and 120 healthy control subjects from 2013 to 2016. Associations between PFAS levels and odds of POI, as well as hormonal profiles, were evaluated using multiple logistic regression and multiple linear regression models. Results Levels of perfluorooctanate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorohexanesulfonate (PFHxS) were positively associated with the risks of POI (highest vs. lowest tertile, PFOA: OR, 3.80; 95% CI, 1.92–7.49; PFOS: OR, 2.81; 95% CI, 1.46–5.41; PFHxS: OR, 6.63; 95% CI, 3.22–13.65). In patients with POI, levels of PFOS and PFHxS exposure were positively associated with FSH (PFOS: adjusted β, 0.26; 95% CI, 0.15 to 0.38; PFHxS: adjusted β, 0.16; 95% CI, 0.04 to 0.28) and negatively associated with estradiol (PFOS: adjusted β, −0.30; 95% CI, −0.47 to −0.12; PFHxS: adjusted β, −0.19; 95% CI, −0.37 to −0.02). Exposure to PFOS and PFOA was associated with elevation of prolactin (PFOS: adjusted β, 0.17; 95% CI, 0.06 to 0.29; PFOA: adjusted β, 0.16; 95% CI, 0.01 to 0.30) or with a decrease of free triiodothyronine (PFOS: adjusted β, −0.88; 95% CI, −1.64 to −0.09; PFOA: adjusted β, −0.90; 95% CI, −1.88 to 0.09) and thyroxine (PFOS: adjusted β, −2.99; 95% CI, −4.52 to −1.46; PFOA: adjusted β, −3.42; 95% CI, −5.39 to −1.46). Conclusion High exposure to PFOA, PFOS, and PFHxS is associated with increased risk of POI in humans.

In view of the discrepancies about the GnRH antagonist (GnRH-ant) ovarian stimulation protocols having some potential advantages compared with the GnRH agonist (GnRH-a) protocols in poor ovarian responders IVF/ICSI, a meta-analysis of the published data was performed to compare the efficacy of GnRH-ant versus GnRH-a protocols for ovarian stimulation in IVF poor response patients. We searched for all published articles indexed in MEDLINE (1950–2010), EMBASE (1974–2010) and China National Knowledge Infrastructure (CNKI, 1994–2010). Any randomized controlled study that compared the GnRH-ant with GnRH-a in ovarian stimulation protocols for poor responders undergoing IVF/ICSI was included, and data were extracted independently by two reviewers. The searches yielded 64 articles, from which 14 studies met the inclusion criteria. We performed this meta-analysis involving 566 IVF patients in a GnRH-ant protocol group and 561 patients in a GnRH-a protocol group with Review Manager 4.2 software. Odds ratio (OR) and weighted mean difference (WMD) with 95% confidence intervals (CIs) were used to evaluate dichotomous and continuous data, respectively. Fourteen eligible studies were included in this meta-analysis. GnRH-ant protocols resulted in a statistically significantly lower duration of stimulation compared with GnRH-a protocols (P = 0.04; WMD: −1.88, 95% CI: −3.64, −0.12), but there was no significant difference in the number of oocytes retrieved (P = 0.51; WMD: −0.17, 95% CI −0.69, 0.34) or the number of mature oocytes retrieved (P = 0.99; WMD: −0.01, 95% CI: −1.14, 1.12). Moreover, no significant difference was found in the cycle cancellation rate (CCR, P = 0.67; OR: 1.01, 95% CI: 0.71–1.42) or clinical pregnancy rate (CPR, P = 0.16; OR: 1.23, 95% CI: 0.92, 1.66). Clear advantage was gained in duration of stimulation with GnRH-ant in poor ovarian responders undergoing IVF, although there was no statistical difference in the number of oocytes retrieved, the number of mature oocytes retrieved, the CCR and CPR between GnRH-ant and GnRH-a protocols. These results may be helpful to our clinical practice. However, further controlled randomized prospective studies with larger sample sizes are needed.

Objective: Premature ovarian failure, a reproductive dysfunction characterized by follicle loss leads to premature menopause. Apoptosis of granulosa cells may be responsible for the associated follicle depletion. MicroRNAs are expressed abundantly in granulosa cells and play an important role in follicular atresia. Evidence suggests that signal transducer and activator of transcription 3 (STAT3) is involved in follicle growth and female fertility. Methods: We incubated cultured mouse granulosa cells (mGCs) with increasing doses of cisplatin (CP) for varying periods. Cell proliferation and apoptosis were measured by Cell Counting Kit-8 assay, flow cytometry, and protein expression of cleaved caspase-3. Western blot analysis was used to assess STAT3 and phospho-STAT3 after mGCs were transfected with a microRNA-125a-5p (miR-125a-5p) mimic and a miR-125a-5p inhibitor, respectively. Luciferase reporter assay was conducted to determine the relationship between miR-125a-5p and STAT3. Results: CP reduced mGC viability, progesterone levels, and estradiol levels. miR-125a-5p was up-regulated in CP-treated mGCs, whereas STAT3 was down-regulated. Increased apoptosis and cleaved caspase-3 were observed in mGCs transfected with a miR-125a-5p mimic or STAT3 interference fragment. Protein expression of STAT3 and phospho-STAT3 was up-regulated or down-regulated when transfected with a miR-125a-5p inhibitor or miR-125a-5p mimic, respectively. Luciferase reporter assays indicated that miR-125a-5p targets the 3′ untranslated region of STAT3. Conclusions: Overexpression of miR-125a-5p promotes mGC apoptosis by targeting STAT3. Our findings imply the important role of miR-125a-5p in the pathogenesis of premature ovarian failure.