Gynecological Endocrinology最新文献

Objective: To assess the effects of a 12-week combined treatment with myo-inositol (2 g) and Banaba extract (48 mg) standardized to 1% corosolic acid (MBN) on insulin resistance (HOMA-IR) and hepatic insulin extraction index (HIEI) in overweight and obese postmenopausal women.

Methods: We conducted a retrospective observational study including 31 postmenopausal women (mean age 51 ± 1.2 years) attending the Gynecological Endocrinology Center of Modena, Italy. All patients received daily supplementation with MBN for 12 weeks. Hormonal and metabolic parameters-including fasting glucose, insulin, C-peptide, and HOMA-IR-were assessed before and after treatment. In addition, an oral glucose tolerance test (OGTT) was performed at both time points, with glucose, insulin, and C-peptide curves measured and corresponding area under the curve (AUC) values at 240 minutes calculated. HIEI was calculated as the insulin/C-peptide ratio. Data were analyzed globally and then stratified by family history of diabetes.

Results: After treatment, fasting insulin, HOMA-IR, and HIEI were significantly reduced. The OGTT showed a 23.5% decrease in glucose AUC, with greater reductions in insulin AUC (-42%) compared to C-peptide AUC (-16.8%), suggesting enhanced hepatic insulin clearance. Patients with a family history of diabetes showed reductions in insulin and C-peptide, while those without showed only a decrease in insulin and HIE, with no changes in C-peptide.

Conclusions: Combined MBN supplementation improved insulin sensitivity and hepatic insulin clearance in overweight and obese postmenopausal women, with particularly pronounced effects in those with a family history of diabetes. These findings underscore the potential of targeted integrative strategies to mitigate insulin resistance in this population.

Polycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder in reproductive-aged women, often associated with obesity and dyslipidemia. Semaglutide, a GLP-1 receptor agonist (GLP-1 RA), improves glycemic control and weight, but its effects on PCOS remain unclear. This meta-analysis evaluates semaglutide's impact on BMI and blood lipids in PCOS patients. We searched PubMed, Embase, Cochrane Library, ClinicalTrials.gov, WHO ICTRP, and gray literature sources for RCTs (2010-2025) comparing semaglutide vs. placebo/conventional treatment in PCOS patients. The outcomes included BMI, total cholesterol (TC), triglycerides (TG), LDL-C, and HDL-C. The data were analyzed using RevMan 5.4, with mean differences (MD) and 95% CIs were calculated. Heterogeneity was assessed via I². Eight RCTs (526 patients) were included. Semaglutide significantly reduced BMI (MD: -2.20 kg/m², 95% CI: -2.42 to -1.97, P < 0.001), TC (MD: -0.42 mmol/L, 95% CI: -0.46 to -0.39, P < 0.0001), TG (MD: -0.35 mmol/L, 95% CI: -0.38 to -0.32, P < 0.0001), and LDL-C (MD: -0.31 mmol/L, 95% CI: -0.35 to -0.27, P < 0.0001), but not HDL-C (P = 0.8524). Subgroup analysis showed greater efficacy at doses ≥ 1.0 mg/week and in patients with a baseline BMI > 28 kg/m². Overall evidence quality was moderate to low based on GRADE assessment. Semaglutide significantly improves BMI and lipid profiles in PCOS, particularly at higher doses, and in obese patients. Further long-term studies are needed to confirm safety and reproductive outcomes.

Purpose: To investigate the association between vitamin D receptor (VDR) gene polymorphisms and sub-clinical hypothyroidism (SCH) risk in polycystic ovary syndrome (PCOS) patients.

Methods: Forty-four PCOS patients and 24 controls were enrolled. VDR gene sequences, lipid profiles, and thyroid function were analyzed, with stratification by SCH status for group comparisons.

Results: PCOS patients showed significant differences in fasting glucose, triglycerides, and BMI vs. controls. SCH patients exhibited distinct Apa I genotypes (P < 0.05), with the AC genotype rate (76.47%) significantly higher in PCOS + SCH vs. other groups. Unadjusted/adjusted ORs for SCH patients with the AC genotype were 4.2 (95% CI 1.40-13.10), 5.01 (95% CI 1.53-16.38), and 6.25 (95% CI 1.69-23.09). No other polymorphisms were significant.

Conclusion: This study revealed that the VDR Apa I genotype (AC as a distinct risk factor) was associated with SCH in PCOS patients, suggesting new genetic insights.

Objective: Is there an association between blastocyst expansion grade and early serum β-hCG levels in pregnancies after single euploid embryo transfer?

Methods: This retrospective cohort study included 8394 SEETs performed at a single center. Blastocysts were categorized as CHBs (n = 1677) or PHBs (n = 4612) based on their expansion grade. Serum β-hCG levels were measured on days 9 and 11 post-transfer. A multivariate logistic regression model adjusted for confounders, including maternal age, ovarian reserve, embryo morphology, year of treatment, and day of biopsy.

On day 9 post-transfer, the median β-hCG level was significantly lower in CHBs (118 mIU/mL, IQR = 129.2) compared to PHBs (133 mIU/mL, IQR = 129.8; p < 0.0001). The difference persisted on day 11 post-transfer (CHBs: 290.2 mIU/mL, IQR = 357 vs. PHBs: 327.3 mIU/mL, IQR 358.6; p = 0.018). In multivariate regression, CHB status remained significantly associated with lower β-hCG on day 9 post-transfer (aOR = 0.998, 95% CI: 0.997-0.999), but not on day 11 post-transfer (aOR = 0.999, 95% CI: 0.999-1.0002).

Conclusions: Completely hatched blastocysts (CHBs) with an expansion grade 6 were associated with lower early serum β-hCG levels compared to partially hatched blastocysts (PHBs) with expansion grades 4 and 5. Incorporating expansion grade into prediction models could enhance decision support tools for IVF patients.

Purpose: Pre-eclampsia (PE) is a pregnancy-related disorder for which reliable predictive methods remain limited.

Methods: Data were collected between June 2018 and December 2022. Statistical analyses including Chi-square tests, multivariate logistic regression, and LASSO regression were applied to identify risk factors.

Results: A total of 602 pregnant women were included, with 176 diagnosed with PE and 426 without PE. Significant differences between the PE and control groups were observed for high-risk pregnancy history (HRPH), mean arterial pressure (MAP), preeclampsia monitoring system (MP), uterine artery pulsatility index (UtA-PI), placental growth factor (PLGF), thyroid-stimulating hormone (TSH), and 25-hydroxyvitamin D (25-OH). Multivariate logistic regression showed that low 25-OH (OR = 10.24, p < 0.001), elevated TSH (OR = 5.13, p < 0.001), HRPH (OR = 2.21, p = 0.03), high-risk MP (OR = 1.83, p = 0.03), UtA-PI > 2.25 (OR = 2.95, p < 0.001), and low PLGF (OR = 2.67, p < 0.001) were significantly associated with PE, while high MAP  showed a non-significant trend (OR = 3.06, p = 0.06). ROC analysis indicated that 25-OH had the highest diagnostic efficiency (AUC = 0.719), MAP the lowest (AUC = 0.601), and the combination of 25-OH, TSH, MP, and PLGF achieved the best performance (AUC = 0.843).

Conclusion: The combination of HRPH, MAP, PLGF, TSH, and 25-OH demonstrated strong predictive power for PE, providing valuable guidance for the prevention and management of PE in clinical practice.

Objective: To assess the potential therapeutic effects of glucose-dependent insulinotropic peptide (GIP) on hyperandrogenism.

Methods: Polycystic ovary syndrome (PCOS) mouse models induced by dehydroepiandrosterone (DHEA) were established to evaluate the impact of GIP on androgen synthesis in vivo. Additionally, NCI-H295R cells were utilized for in vitro studies to investigate the effects of GIP on androgen synthesis using various techniques, including CCK8, flow cytometry, RT‒qPCR, WB, ELISA, and RNA sequencing (RNA-seq).

Results: Administration of GIP significantly reduced testosterone secretion in a DHEA-induced PCOS mouse model. Consistent with these findings, GIP treatment decreased testosterone release and downregulated the expression of GIP receptor (GIPR), steroidogenic acute regulatory protein (STAR), cytochrome P450 family 11 subfamily A member 1 (CYP11A1), and cytochrome P450 family 17 subfamily A member 1 (CYP17A1) in NCI-H295R cells. Notably, RNA-seq revealed that PSENEN was the most significantly downregulated gene upon GIP stimulation. Knockdown of PSENEN in NCI-H295R cells further decreased testosterone levels in the culture medium, confirming the inhibitory effect of GIP on androgen synthesis.

Conclusions: Our study demonstrated that the administration of GIP reduces androgen synthesis in PCOS mouse models and at the cellular level, suggesting its potential as a novel therapeutic target for managing PCOS.