Gynecological Endocrinology最新文献

Objective: This study explored the association between ω-6 to ω-3 polyunsaturated fatty acids (PUFAs) and metabolic syndrome in women experiencing climacteric syndrome.

Methods: The study involved 186 female participants and utilized surveys, anthropometric measurements (waist circumference, height, BMI, waist-to-height ratio), blood pressure assessments, and blood samples for lipid profile, glucose, insulin, HbA1c analysis. Serum PUFAs levels were analyzed using gas chromatography-mass spectrometry.

Results: The study found significantly higher measurements of waist circumference, waist-to-height ratio, systolic and diastolic blood pressure in postmenopausal women with metabolic syndrome compared to the control group. In addition, the metabolic syndrome group showed significantly higher levels of fasting blood glucose, triglycerides, low-density lipoprotein cholesterol, HbA1c, insulin, triglyceride to high-density lipoprotein ratio, and total cholesterol to high-density lipoprotein ratio. Furthermore, the study also identified significant differences among premenopausal women, postmenopausal women with metabolic syndrome, and postmenopausal women without metabolic syndrome in terms of omega-3 alpha-linolenic acid, omega-3 docosahexaenoic acid, omega-6 arachidonic acid, and omega-6 to omega-3 ratio.

Conclusions: We observed that high ω-6 arachidonic acid and ω-6/ω-3 ratio and low ω-3 ALA and ω-3 DHA were associated with high TG and WHtR. High TG and WHtR levels in postmenopausal women are associated with increased risk of Mets.

Objective: To disclose the relationships between serum LH and reproductive outcomes in Gonadotropin-releasing hormone (GnRH) antagonist protocol pretreated with luteal estradiol.

Methods: 371 patients, pretreated with estradiol, followed the GnRH antagonist protocol. They were divided into four groups based on the quartiles of serum LH levels on the day of gonadotropin (Gn) initiation(LH_GI) and trigger (LH_trigger). Data on various pregnancy outcomes were collected.

Results: As serum LH_GI increased, anti-Müllerian hormone (AMH) level, antral follicle count (AFC), LH_trigger, estradiol (E₂) and P on the trigger day, E₂/oocytes, and oocyte numbers increased and peaked in Q4, while Gn dose decreased. Good-quality embryo and blast formation rates increased and peaked in Q3. LH_GI <3.93 mIU/ml impaired ongoing pregnancy rate and LBR. After adjusting for AMH and AFC, the impacts were not significant. As LH_trigger increased, E₂/oocytes and good-quality embryo rate increased and peaked in T4 and implantation rate increased and peaked in T3. LH_trigger <1.49 mIU/ml independently influenced clinical pregnancy rate (CPR) after adjusting for AMH and AFC. LH_GI was positively related to AMH, AFC, LH_trigger, blast formation rate and negatively related to BMI, age and Gn dose. LH_trigger was positively related to E2/oocytes and good quality embryo rate.

Conclusions: Lower serum LH represents as a potential indicator for embryo quality and reproductive outcomes in GnRH antagonist fixed protocol pretreated with estradiol. Early identification of excessive suppression of LH levels will benefit individuals with normal ovarian reserve more.

Pregnancy is a critical period marked by intricate physiological changes and maintaining maternal and fetal well-being is paramount. Inositols, a group of naturally occurring sugar alcohols, have gained attention for their potential benefits during pregnancy. This abstract provides a comprehensive review of the current literature on using inositols, primarily myo-inositol (MI) and D-chiro-inositol (DCI) in pregnancy. Inositols are crucial in cellular signal transduction and insulin sensitivity, making them integral to various physiological processes. Several studies suggest that inositols may contribute to preventing and managing gestational diabetes mellitus (GDM). MI, in particular, has shown promise in improving insulin sensitivity and mitigating insulin resistance, thereby influencing glucose metabolism. As our understanding of inositol's role in pregnancy deepens, it may emerge as a valuable supplement to enhance maternal and fetal health outcomes.

Aims: This study aims to explore the alterations of dendritic cells (DCs) subpopulations in ectopic endometrial lesions and unveil the underlying mechanisms.

Materials and methods: Patients with endometriosis (n = 81) and women without endometriosis (n = 19) were recruited in this study. Dendritic cells (DCs) in the endometrial samples were counted after immunohistochemistry staining. The proportion of myeloid DCs and plasmacytoid DCs was calculated by flow cytometry. Primary DCs were isolated from tissues, and the cell viability and apoptosis were examined by MTT assay and flow cytometry. Cytokines were detected by the enzyme-linked immunosorbent assay. Differentially expressed genes were filtered by analyzing two datasets that were downloaded from GEO database and detected by RT-qPCR in tissues and isolated DCs. The function of HSD11B1 was examined in an endometrial stromal cell-DCs co-culture system and in vitro cultured DCs.

Results: Reduced myeloid DCs and increased CD11c-CD304-DCs were found in ectopic endometrium compared to control endometrium and eutopic endometrium from endometriosis patients. Myeloid DCs isolated from ectopic endometrium expressed less CD80, CD83, CD86 and had reduced proliferation, increased apoptosis, and reduced cytokine production. The expression of HSD11B1 was significantly increased in both ectopic endometrium and isolated myeloid DCs. Overexpression of HSD11B1 in immature DCs could repress DCs maturation and cytokine production. Endometrial stromal cells overexpressing HSD11B1 secreted increased cortisol, which repressed DCs maturation.

Conclusions: HSD11B1 is upregulated in ectopic endometrial lesions, which may contribute to endometriosis through repressing myeloid DCs maturation.

Objective: To comprehensively assess the dose-response association between dietary glycemic index (GI) and glycemic load (GL) and gestational diabetes mellitus (GDM) risk.

Methods: PubMed, Embase, Cochrane Library, Web of Science, CNKI, WanFang, and VIP databases were searched up to May 29, 2024. Studies with at least three exposure categories were included. Dose-response analysis was also performed when covariates were adjusted in the included studies.

Results: Thirteen studies involving 39,720 pregnant women were included. A linear relationship was found between GI and the risk of GDM (χ² = 4.77, P_{non-linearity} = .0923). However, association was not significant (χ² = 0.06, p = .8000). For every unit increase in GI (range 0-30), GDM risk increased by 0.29%. After adjusting for covariates, the linear relationship persisted (χ² = 4.95, P_{non-linearity} = .084) with no significant association (χ² = 0.08, p = .7775). For GL, a linear relationship was also found (χ² = 4.17, P_{non-linearity} =.1245), but GL was not significantly associated with GDM risk (χ² = 2.63, p = .1049). The risk of GDM increased by 0.63% per unit increase in GL. After covariate adjustment, a significant association was observed (χ² = 6.28, p = .0122).

Conclusion: No significant association between GI and GDM risk was found. After adjusting for covariates, GL shows a significant association with GDM risk. Our findings emphasize the importance of considering dietary GL in managing the risk of GDM. Future research should continue to explore these relationships with standardized diagnostic criteria and robust adjustment for potential confounders.

Objective: Anthropometric measurement provides a simple, noninvasive approach to evaluate obesity in pregnant women. We aimed to develop a predictive model utilizing anthropometric index for gestational diabetes mellitus (GDM), the most common obesity-related complications during pregnancy.

Methods: A prospective cohort of 4709 women was enrolled in Qingdao, China. Logistic regression model was constructed to determine the association of body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT) in the first trimester (<14 weeks' gestation) with GDM. The discrimination ability for GDM was assessed using areas under the receiver operating characteristic (ROC) curve (AUC). Delong tests were performed to compare AUC values between different measures.

Results: The GDM incidence was 19.50%. GDM risk increased with VAT during early pregnancy, and the risk increased by 117% (OR = 2.17, 95% CI: 1.23-2.83) to 326% (OR = 4.26, 95% CI: 2.29-7.91) in pregnant women with the second quartile or above after adjusting for confounders (all p<.05). Combined index using VAT and BMI demonstrated superior predictive power for GDM compared with BMI alone (p<.05), but didn't differ from VAT (p>.05). Overall, VAT was positively correlated with GDM occurrence, outperforming BMI, WHR, WHtR and SAT in the predicative model. A first-trimester VAT cutoff of 27.05 mm might be promising for GDM risk stratification.

Conclusions: First-trimester routine ultrasound screening may facilitate earlier identification and intervention of GDM. Pregnant women with VAT above the optimal threshold (27.05 mm) might benefit from targeted GDM monitoring.

Background: It has been recognized that the gonadotropin-releasing hormone antagonist (GnRH-ant) protocol has a detrimental effect on clinical outcomes compared to the GnRH agonist (GnRH-a) protocol during in vitro fertilization-fresh embryo transfer (IVF-ET) cycles. However, the related mechanisms were unclear.

Methods: A total of 18,561 patients, who underwent fresh IVF-ET cycles in the Center for Assisted Reproduction of Jiangxi Maternal and Child Health Hospital from January 2014 to September 2021, were retrospectively analyzed. The propensity score matching (PSM) technique was used to control for confounding factors between the GnRH-ant and GnRH-a groups. Human endometrial stromal cells (hESCs) were collected for primary culture and treated with relevant receptor antagonists and activators. RT-PCR, Western Blot, immunofluorescence staining, cell migration and adhesion assays, and animal experiments were employed to elucidate the molecular mechanism by which GnRH antagonist affects the migration and adhesion ability of hESCs.

Results: There was no statistical difference between the two groups in terms of baseline characteristics after matching basal status by propensity score matching. The result showed that the endometrial thickness (10.4 ± 2.35 vs. 11.03 ± 2.61 mm, p < .001) on trigger day was significantly lower in the GnRH-ant group. Compared with the GnRH-a protocol, the implantation rate (39.71% vs. 50.36%, p < .001), biochemical pregnancy rate (64.26% vs. 72.7%, p < .001), clinical pregnancy rate (56.39% vs. 65.24%, p < .001), live birth rate (45.25% vs. 56.1%, p < .001) in the GnRH-ant group were significantly decreased. Contrarily, the rate of early miscarriage in the GnRH-ant group (13.95% vs. 9.04%, p < .001) was higher than in the GnRH-a group. Furthermore, after treating with GnRH-ant, hESCs showed a reduced expression of HOXA10 and MMP-9 proteins, and a weakened migration ability. Subsequently, by establishing the co-culture system of hESCs and JAR trophoblast spheroids, we found that GnRH-ant inhibited the adhesion and invasion ability of trophoblast cells. Moreover, we also found a decreased expression and phosphorylation of c-kit receptor in decidualized hESCs after treating with GnRH-ant. Similar results as observed above were also confirmed when inhibiting the activation of c-kit receptor by imatinib.

Conclusions: GnRH-ant could reduce the motility of hESCs by inhibiting the expression and activation of the C-kit receptor, which impaired the process of embryo implantation.