Polycystic Ovary Research Articles

Chronotypes in middle-aged women with polycystic ovary syndrome: A population-based study.

Circadian rhythm disruption has been associated with the risk of polycystic ovary syndrome (PCOS), as the evening chronotype (EC) shares several traits with PCOS, including metabolic disorders, cardiovascular diseases, and psychiatric disorders. It has been suggested that the biological clock could be targeted with new, preventive, and therapeutic strategies for PCOS in women with biorhythm disorders. We evaluated inner circadian rhythmicity in middle-aged women with PCOS in a population-based setting, focusing on whether women with PCOS and an EC have a specific subtype in relation to their clinical characteristics. The data derived from the Northern Finland Birth Cohort, a population-based longitudinal birth cohort of 12 058 individuals born in 1966. We compared the circadian phenotype between 314 women with PCOS (according to the Rotterdam criteria) and 1248 women without PCOS at age 46 years using the validated Finnish shortened 6-item Morningness-Eveningness Questionnaire (sMEQ) and the single-item self-assessed morningness-eveningness question. PCOS was not associated with the EC by the sMEQ (p = 0.495) or self-assessment (p = 0.303). The self-assessed morningness-eveningness values differed from the sMEQ chronotype distribution (p < 0.001), nevertheless, the most frequent chronotype was the intermediate chronotype (IC) determined by both chronotyping methods (sMEQ PCOS 47.7% vs. 45.2% non-PCOS; self-assessment PCOS 66.5% vs. 68.4% non-PCOS). The hyperandrogenic PCOS phenotypes A-C did not differ from the non-hyperandrogenic phenotype D as for the chronotype (p = 0.271). The EC was associated in both groups with depressive and anxiety symptoms (PCOS p = 0.012, non-PCOS p < 0.001) and the use of sleep medication (PCOS p = 0.017, non-PCOS p < 0.001). The EC was not over-represented in middle-aged women with PCOS or in the hyperandrogenic PCOS phenotypes A-C in our study. This does not support the need for chronotyping in the comprehensive assessment of women with PCOS. However, as chronotypes tend to change with aging, cross-sectional studies in different age groups are warranted to draw conclusions on the role of chronotypes in PCOS and the associated metabolic risks.

Clinical-exome sequencing unveils the genetic landscape of polycystic ovarian syndrome (PCOS) focusing on lean and obese phenotypes: implications for cost-effective diagnosis and personalized treatment.

Polycystic ovarian syndrome (PCOS) is one of the most common endocrinopathies among reproductive women worldwide, contributing greatly on the incidence of female infertility and gynecological cancers. It is a complex health condition combining of multiple symptoms like androgen excess, uncontrolled weight gain, alopecia, hirsutism, etc. Conventionally PCOS was associated with obesity while it is often found among lean women nowadays, making the disease more critical to diagnose as well treatment. The disorder has an impact on several signal transduction pathways, including steroidogenesis, steroid hormone activity, gonadotrophin regulation, insulin secretion, energy balance, and chronic inflammation. Understanding the aetiology and pathophysiology of PCOS is difficult due to its multiple causes, which include environmental factors, intricate genetic predisposition, and epigenetic modifications. Despite research supporting the role of familial aggregations in PCOS outcomes, the inheritance pattern remains unknown. Henceforth, to reduce the burden of PCOS, it is inevitably important to diagnose at early ages as well as intervene through personalized medicine. With this brief background, it was imperative to elucidate the genetic architecture of PCOS considering BMI as an controlling factor. This study aims to investigate the genetic basis behind obesity-mediated PCOS, focusing on both obese and lean individuals. It uses a comprehensive bioinformatics methodology to depict pathways and functionality enrichment, allowing for cost-effective risk prediction and management. In the present research, the representative study participants (N = 2) were chosen from a cross-sectional epidemiological survey, based on their anthropometric parameters and confirmation of PCOS. Upon voluntary participation and written consent, biological fluids (whole blood and buccal swab) were taken from where DNA was extracted. The clinical-exome sequencing was performed by the Next-generation Illumina platform using the Twist Human Comprehensive Exome Kit. A comprehensive bioinformatics methodology was employed to identify the most important, unique, and common genes. A total of 26,550 variants were identified in clinically important exomes from two samples, with 5170 common and 2232 and 2322 unique among PCOS lean and obese phenotypes, respectively. Only 262 and 94 variants were PCOS-specific in lean and obese PCOS. Three filters were applied to shortlist the most potent variants, with 4 unique variants in lean PCOS, 2 unique variants in obese PCOS, and 5 common variants in both. The study found that leptin signalling impairment and insulin resistance, as well as mutations in CYP1A1, CYP19A1, ESR1, AR, AMH, AdipoR1, NAMPT, NPY, PTEN, EGFR, and Akt, all play significant roles in PCOS in the studied group. Young women in West Bengal, India, are more likely to have co-occurring PCOS, which includes estrogen resistance, leptin receptor insufficiency, folate deficiency, T2DM, and acanthosis nigricans, with obesity being a common phenotypic expression.

Identification and validation of core genes associated with polycystic ovary syndrome and metabolic syndrome.

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder affecting women of reproductive age, affecting reproductive health, and increasing the incidence of diabetes mellitus and hypertension. Metabolic syndrome (MetS) is the most common metabolic disorder. Although clinical studies have shown a close association between PCOS and MetS, the molecular mechanisms are unknown. In this study, datasets of PCOS and MetS were obtained from the Gene Expression Omnibus database; differential expression analysis and weighted gene coexpression network analysis (WGCNA) were performed; and gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses also performed of differentially expressed genes (DEGs). The PCOS- and MetS-coexpressed DEGs were subsequently intersected with the coexpressed genes in the WGCNA module to obtain the core genes. By constructing receiver operating characteristic curves, we verified the predictive effects of the core genes. We also validated the expression of the core genes in the datasets. Finally, we verified the expression of the core genes by quantitative polymerase chain reaction in human follicular fluid granulosa cells. In addition, we used Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts to analyze the immune infiltration of immune cells in PCOS and MetS. Finally, we obtained 52 coexpressed DEGs of PCOS and MetS and 3 coexpressed genes in the WGCNA module. By taking the intersection of coexpressed DEGs and coexpressed genes of the WGCNA module, we get ELOVL fatty acid elongase 7 (ELOVL7) as the core gene. Receiver operating characteristic curve analysis showed that ELOVL7 is a reliable biological marker for PCOS and MetS. The expression level of ELOVL7 in human follicular fluid granulosa cells from PCOS patients was significantly higher than that of controls, as verified by quantitative polymerase chain reaction. This study provides the first evidence of the role of ELOVL7 in developing PCOS and MetS. This gene may serve as a potential diagnostic marker and therapeutic target for both conditions.

Exploring the causal pathway from gut microbiota to polycystic ovary syndrome: A network Mendelian randomization study.

Polycystic ovary syndrome (PCOS) is a complicated endocrine and metabolic syndrome with unclear pathogenesis. The gut microbiota sheds light on the etiology and pathophysiology of PCOS. We used Mendelian randomization (MR) studies to systematically evaluate the pathological mechanism gut microbiota causally associated with PCOS risk. A network MR analysis was performed to estimate the causal effects of gut microbiota and risk factors on PCOS, as well as the mediation effect of risk factors linking gut microbiota to PCOS. The investigation of side effects for the important gut microbiota was subsequently broadened to include phenotypes by performing Phenowide-MR analysis for a range of diseases. Genus Sellimonas id.14369 were causally associated with reduced PCOS risk (odds ratio [OR] = 0.69, 95% confidence interval [CI]: 0.58-0.84, P = 1.22 × 10-4) after multiple testing correction. And Sellimonas retained consistent causal effect estimates after a series of sensitivity analyses. In addition, we observed an indirect effect of Sellimonas on PCOS through body mass index (BMI) using network MR (b = -0.05, 95% CI: -0.09 to -0.01), with a mediated proportion of 12.82% of the total effect. Further, Phenowide-MR analyses showed that the protective effects of Sellimonas on type 2 diabetes and depression (for type 2 diabetes: OR = 0.95, 95% CI: 0.90-0.99, P = .0366; for depression: OR = 0.99, 95% CI: 0.98-1.00, P = .0210). We summarized that the causal path between gut microbiota and type 2 diabetes are also jointly mediated by BMI. Sellimonas may be a protective factor of PCOS, which can affect the occurrence of PCOS through BMI, supporting future studies on the importance of addressing obesity and metabolic issues in preventing and managing PCOS.

Serum pentraxin-3 expression varies according to polycystic ovary syndrome phenotypes.

Pentraxin-3 (PTX-3) is a multibiological protein involved in cumulus cell expansion, fertilization, and implantation. This study was designed to analyze how circulating PTX-3 levels change in women with polycystic ovary syndrome (PCOS). A total of 50 Turkish participants, 35 of whom had PCOS and 15 of whom were fertile, were included in the study. Patients in the PCOS group were divided into 4 different phenotypes according to the NIH criteria (phenotypes A-D). The number of patients in phenotype A was the highest 13 (37.1%). In the calculations made without phenotyping, the serum ptx3 levels of the PCOS group were found to be significantly lower compared to the fertile control group (3.32 ± 0.73 ng/mL vs 4.97 ± 1.29 ng/mL; P < .001). The ptx3 value of phenotypes A and B was significantly lower than phenotype D (P = .008 and P = .009, respectively). When the phenotypes were compared with the fertile control group, the PTX-3 levels of phenotypes A and B were significantly lower than the fertile group. Although the ptx3 levels of phenotypes C and D were lower than the fertile group, the difference did not reach statistical significance. This is the first study to investigate serum ptx3 levels by phenotype in PCOS. While serum PTX-3 levels decreased in phenotypes A and B, ptx3 levels in phenotypes C and D were similar in fertile patients.

In vitro maturation of oocytes: what is already known?

Assisted reproductive technologies (ARTs) involve the laboratory manipulation of gametes and embryos to help couples with fertility problems become pregnant. One of these procedures controlled ovarian stimulation uses pharmacological agents to induce ovarian and follicular maturation in vivo. Despite the effectiveness in achieving pregnancy and live births, some patients may have complications due to over-response to gonadotropins and develop ovarian hyperstimulation syndrome (OHSS). In vitro maturation of oocytes (IVM) has emerged as a technique to reduce the risk of OHSS, particularly in women with polycystic ovary syndrome (PCOS), and for fertility preservation in women undergoing oncological treatment. Although there are some limitations, primarily due to oocyte quality, recent advances have improved pregnancy success rates and neonatal and infant outcomes. Different terms have been coined to describe variations of IVM, and the technique has evolved with the introduction of hormones to optimize results. This review we provide a comprehensive overview of IVM and its reproductive outcomes during ARTs.

Relation of mitochondrial DNA copy number and variants with the clinical characteristics of polycystic ovary syndrome

Mounting evidences suggests mitochondrial dysfunction as a novel contributor in the pathogenesis of PCOS. Herein, we analyzed mtDNA copy number, a biomarker of mitochondrial function in women with PCOS and non-PCOS participants and study its correlation with their clinical characteristics. In this study, we further analyzed association of 383 mtDNA variants, as reported previously by us, with characteristic traits of PCOS and perform structural analysis of mutated protein. Our results indicate relative mitochondrial DNA (mtDNA) copy number to be significantly reduced in women with PCOS compared to non-PCOS group and significantly inversely related to waist to hip ratio (WHR), triglycerides and positively related to high density lipoprotein-cholesterol (HDL-C). After adjustment of the age in the PCOS group, significantly negative correlation of mtDNA copy number with WHR was observed. Unsupervised hierarchical clustering analysis revealed rare, low heteroplasmic mtDNA variants such as 12556G, 1488T, 9200G, 9670G, 3308G, 14480G, 15914T and 5426G to be strongly associated with PCOS related traits. Among these variants, variant 12256G in ND5 gene affected both the flexibility and overall stability of the protein structure. This study is first to reveal significant correlation of mtDNA copy number with WHR in women with PCOS indicating link between mitochondrial dysfunction with central obesity in PCOS. we also first time showed association of rare mtDNA variants with characteristics traits of PCOS highlighting the clinical significance of rare mtDNA variants, which may cumulatively act as early predictors of risk of PCOS and its related comorbidities which may help in the management of PCOS.

Elucidating the Role of Autophagy-related Genes in Polycystic Ovary Syndrome: Implications for Diagnostic Models and Immune Response Regulation.

Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder that negatively affects female reproductive capacity. Although the association between autophagy and PCOS is known, there are few detailed studies on the association between autophagy-related genes and PCOS. Publicly available gene expression datasets (GSE102293, GSE138518, GSE34526, GSE114419, GSE137684, GSE155489) were used in a comprehensive analysis to identify a role for autophagy in PCOS. Batch effects were mitigated using the sva package, followed by WGCNA (weighted gene correlation network analysis) and ss- GSEA (single sample gene set enrichment analysis) to identify autophagy-related genes. Recursive feature elimination (RFE) and LASSO COX methods were used to identify important hub genes, and their correlation with immune cell activity was assessed using ssGSEA and Pearson correlation analysis. High autophagy scores were observed in PCOS samples, and the dark green gene module with the highest autophagy correlation was identified. The differential analysis identified a total of 169 up-regulated genes versus 2 down-regulated genes in the PCOS samples, which were intersected by taking the intersection with the deep green module genes and resulted in 121 key genes. Subsequently, 6 hub genes (MMP25, CSF3R, SLPI, MMP9, CLEC4E, and SIGLEC10) were further identified based on RFE and LASSO algorithms. Diagnostic efficacy based on ROC curves showed six autophagy- associated hub genes with AUC values as high as 0.959 and 0.896 in the training and validation sets, respectively. Finally, we observed that these hub genes are strongly associated with immune function, especially chronic inflammation and aberrant immune activation pathways. In this study, we identified autophagy genes closely related to PCOS and constructed a gene model with high diagnostic accuracy. These findings not only provided potential new biomarkers for the diagnosis of PCOS but also revealed the key role of autophagy in the pathogenesis of PCOS.

Beneficial Effects of Curcumin in Polycystic Ovary Syndrome: A Review of Recent Literature and Underlying Mechanisms.

Polycystic Ovary Syndrome (PCOS) is a common endocrinological disorder that affects women of reproductive age and can lead to infertility. The prevalence of PCOS ranges from 5-21% depending on the diagnostic criteria and study population. Clinical manifestations include irregular or absent menstrual periods, obesity, and signs of hyperandrogenism. PCOS can also lead to long-term consequences such as metabolic syndrome, increased risk of cardiovascular diseases, endometrial cancer, diabetes mellitus, and hypertension. Metformin and oral contraceptive pills are the most commonly used drugs for PCOS management, but their efficiency is limited and they have some considerable side effects. Researchers are looking into alternative therapeutic options such as phytochemicals. Curcumin (CUR) is a polyphenolic compound found in the rhizome of Curcuma longa and has shown promising effects for females with PCOS. CUR exerts its anti-PCOS effects through different mechanisms such as reducing oxidative stress and inflammation, balancing hormone levels, and controlling the blood sugar and lipid profile. It can also reduce insulin resistance, regulate menstruation, and improve ovarian morphology and function. Despite its beneficial effects, CUR faces several challenges and limitations in clinical use, such as low bioavailability, instability, and rapid elimination. Therefore, researchers are investigating the potential of CUR nanoformulations and new drug delivery systems to overcome these barriers. With growing evidence regarding the potential role of CUR in PCOS treatment, we decided to provide an updated summary of the recent literature from clinical and preclinical studies on this topic.

Nicotinamide Mononucleotide Improves Endometrial Homeostasis in a Rat Model of Polycystic Ovary Syndrome by Decreasing Insulin Resistance and Regulating the Glylytic Pathway.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that can lead to insulin resistance (IR) and dysregulation of glucose metabolism, resulting in an imbalance in the endometrial environment, which is unfavorable for embryo implantation of PCOS. This study aims to investigate whether nicotinamide mononucleotide (NMN) improves the stability of the endometrium in a rat model of PCOS and identifies whether it is related to reduce IR and increase glycolysis levels and its potential signaling pathway. Female Sprague-Dawley (SD) rats are fed letrozole and a high-fat diet (HFD) to form the PCOS model, then the model rats are treated with or without NMN. It randomly divided into control, PCOS, and PCOS-NMN groups according to the feeding and treating method. Compared with the PCOS group, the regular estrous cycles are restored, the serum androgen (p<0.01) and fasting insulin levels (p<0.05) are reduced, and endometrial morphology (p<0.05) is improved in NMN-PCOS group. Furthermore, NMN inhibits endometrial cell apoptosis, improves endometrial decidualization transition, reduces IR, restores the expression of glycolysis rate-limiting enzymes, and activates the PI3K/AKT pathway in the uterus. These results suggest that NMN enhances endometrial tissue homeostasis by decreasing uterine IR and regulating the glycolysis through the PI3K/AKT pathway.

Ongoing Clinical Trials for Polycystic Ovarian Syndrome (PCOS) Afflicted Infertility in Women: A Narrative Review.

Polycystic Ovary Syndrome (PCOS) is a highly prevalent endocrine disorder that affects women of reproductive age. PCOS is further correlated with infertility, menstrual dysfunction, and hyperandrogenism. Despite the advanced understanding of reproductive biology, the exact causes of PCOS remain ambiguous. Nevertheless, several factors are believed to contribute to the development of PCOS, including insulin resistance, hyperinsulinemia, obesity, and genetic predispositions. The diagnosis of PCOS is complicated by its phenotypic heterogeneity, which manifests differently in different individuals. Presently, the therapeutic management of PCOS-afflicted infertility depends upon proper pharmaceutical-based therapies aimed at treating underlying symptoms, such as the use of clomiphene citrate, metformin, ovulation-inducing agents, anti-androgens, exogenous gonadotropin administration, laparoscopic ovarian drilling, and in vitro fertilization. The present review focuses on narrating present therapeutic interventions along with lifestyle modifications in PCOS. Furthermore, it focuses on the ongoing clinical trials of various chemotherapeutics to counter PCOS-induced infertility among women.

The Value of Androgen Measures for Diagnosing Polycystic Ovary Syndrome (PCOS) in an Unselected Population.

Polycystic Ovary Syndrome (PCOS) is diagnosed by a combination of three features: hyperandrogenism (biochemical and/or clinical), ovulatory dysfunction, and polycystic ovarian morphology, usually detected by ultrasonography. Our study aimed to determine the need for androgen measurements by using hirsutism to establish hyperandrogenism for diagnosing PCOS in a medically unbiased population. We utilized a pre-existing cohort of unselected (medically unbiased) females aged 18-45years. All underwent a history and physical, including a modified Ferriman-Gallwey (mFG) hirsutism score. Subjects were categorized clinically as eumenorrheic non-hirsute (CONTROLS), menstrual dysfunction only (OLIGO-ONLY), hirsutism only (HIRSUTE-ONLY), or menstrual dysfunction and hirsutism (OLIGO + HIRSUTE). All subjects underwent measurements of androgens using high-quality assays. CONTROLS established the upper normal limit for androgen levels. We defined PCOS using the NIH 1990 criteria. Of 462 individuals with complete evaluations, 311 (67.3%) were CONTROLS, 71 (15.4%) were OLIGO-ONLY, 64 (13.9%) were HIRSUTE-ONLY, and 16 (3.5%) were OLIGO + HIRSUTE. Neither HIRSUTE-ONLY nor OLIGO-HIRSUTE women required androgen measures to demonstrate hyperandrogenism. Among OLIGO-ONLY, 19 (26.8%) demonstrated hyperandrogenemia without hirsutism, with White women significantly more likely than Black women to demonstrate this. In our study of medically unbiased reproductive-aged women using the NIH 1990 criteria for PCOS, only 15.4% of women evaluated (those with menstrual dysfunction only) required androgen measurements. In these women only one-quarter demonstrated hyperandrogenemia. These data provide a strategy to minimize the need for androgen assays, including firstly categorizing subjects by clinical presentation and then assessing circulating androgens in the subgroup with menstrual dysfunction only.

SESN2 Ameliorates Dihydrotestosterone-induced Human Ovarian Granulosa Cell Damage by Activating AMPK/ULK1-mediated Mitophagy.

Sestrin 2 (SESN2) has been reported to participate in the regulation of granulosa cell function in ovarian tissues. However, the role of SESN2 in polycystic ovarian syndrome (PCOS) is still incompletely understood. Here, we investigated the functional role and mechanism of SESN2 in dihydrotestosterone (DHT)-induced granulosa cells. In this study, DHT was utilized to induce PCOS cell model and the AMP-activated protein kinase (AMPK) inhibitor Compound C (CC) was utilized to inhibit the AMPK pathway. qRT-PCR was performed to detect the expression of SESN2 in HGLS cells. Cell apoptosis was evaluated by flow cytometry. Oxidative stress was detected by DCFH-DA staining, superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) kits. The expression of SESN2, cell apoptosis, oxidative stress, mitophagy and AMPK/ULK1 signaling-related proteins were measured by western blot. The results showed that SESN2 was downregulated in DHT-induced granulosa cells. Overexpression of SESN2 inhibited the DHT-induced apoptosis and oxidative stress of HGLS cells. DHT induction aggravated HGLS cell apoptosis and oxidative stress. SESN2 overexpression inhibited the DHT-induced apoptosis and oxidative stress of HGLS cells. In addition, overexpression of SESN2 activated the AMPK/ULK1 signaling pathway and promoted mitophagy. Treatment of CC reversed the regulatory effect of SESN2 on mitophagy. CC also reversed the influences of SESN2 overexpression on apoptosis and oxidative stress in DHT-induced HGLS cells. Overall, SESN2 suppressed DHT-induced apoptosis and oxidative stress in PCOS through AMPK/ULK1-mediated mitophagy.

Metabolic Syndrome, Hepatic Steatosis and Testosterone: A Matter of Sex

Hepatic steatosis is considered the hepatic manifestation of metabolic disorders. Its global prevalence is a growing public health concern, estimated to affect over 30% of the population. Steatosis is strictly linked to metabolic dysfunction, leading to the revised terminology of MASLD (metabolic dysfunction-associated steatotic liver disease). The disease often progresses in conjunction with metabolic syndrome components, significantly increasing cardiovascular and overall mortality risks. The interplay between sex hormones and metabolic dysfunction is crucial, with male hypogonadism and female hyperandrogenism exacerbating the risk and severity of hepatic steatosis. In men, testosterone deficiency is associated with increased visceral adiposity and insulin resistance, creating a vicious cycle of metabolic deterioration. Conversely, in women, hyperandrogenism, particularly in conditions like polycystic ovary syndrome, may lead to severe metabolic disturbances, including hepatic steatosis. Estrogen deficiency also contributes to central adiposity and metabolic syndrome. The aim of this paper is to discuss this complex sex-dimorphic relationship.

Exploring Dermatoglyphics as a Potential Indicator of Female Infertility: A Review of Current Evidence and Future Directions

Female infertility remains a complex and multifaceted issue, impacting millions globally and necessitating a nuanced understanding of its various underlying factors. Dermatoglyphics, the study of unique skin ridge patterns on fingers, palms, toes, and soles, has garnered attention for its potential in revealing embryonic development insights and genetic markers. This paper investigates the hypothetical associations between dermatoglyphics patterns and female infertility. The literature review in this study synthesizes existing research exploring the potential correlations between dermatoglyphics and factors influencing female infertility. Studies suggest that certain dermatoglyphics patterns might be linked to genetic disorders affecting fertility, such as Turner syndrome and polycystic ovary syndrome (PCOS). The field lacks comprehensive studies that directly establish a causal relationship between dermatoglyphics patterns and female infertility. While intriguing correlations have been proposed, more rigorous research, employing larger sample sizes and advanced methodologies, is essential to substantiate these connections. Additionally, this study highlights the necessity of a comprehensive strategy for identifying and treating female infertility. Even though dermatologics may provide new information, it should only be considered one aspect of a thorough diagnostic process that also includes genetic testing, imaging studies, physical exams, medical histories, and hormonal assays.

Correlation and predictive value of systemic immune-inflammation index for dyslipidemia in patients with polycystic ovary syndrome

BackgroundPolycystic ovary syndrome(PCOS) is one of the main factors leading to infertility in women of reproductive age, which is often accompanied by metabolic changes such as obesity and chronic low-grade inflammation. Chronic inflammation may play an important role in the occurrence and development of metabolic diseases. Therefore, it is of great significance to explore the relationship between abnormal lipid metabolism and inflammation in PCOS patients. This study aims to analyze the correlation between systemic immune-inflammatory(SII) markers and dyslipidemia in patients with PCOS and their value in early diagnosis.MethodsA total of 617 PCOS patients aged 20–35 years (according to the Rotterdam diagnostic criteria) who visited the Reproductive Center of the First Hospital of Lanzhou University from January 2020 to December 2022 were included. According to the presence or absence of dyslipidemia, the patients were divided into normal lipid metabolism group and abnormal lipid metabolism group. The clinical data of the patients were collected and analyzed by SPSS software.ResultsThere were 454 patients with normal lipid metabolism and 163 patients with abnormal lipid metabolism. The SII level of the abnormal lipid metabolism group was higher than that of the normal group. As the SII quartile increased, TC, TG and LDL increased, while HDL decreased accordingly. The SII level was positively correlated with TC, TG and LDL, and negatively correlated with HDL (all P < 0.05). Among them, SII had the best predictive efficiency for dyslipidemia of polycyctic ovary syndrome at 489.375 (AUC: 0.718, 95%CI: 0.672–0.764), and SII was still associated with the increased occurrence of PCOS dyslipidemia after excluding confounding factors (P < 0.05). ConclusionThe high level of SII has a correlation with the occurrence of dyslipidemia in PCOS patients, and it has a value in the early diagnosis of PCOS.

Loureirin B Reduces Insulin Resistance and Chronic Inflammation in a Rat Model of Polycystic Ovary Syndrome by Upregulating GPR120 and Activating the LKB1/AMPK Signaling Pathway.

Polycystic ovary yndrome (PCOS) is a common metabolic disorder in women, which is usually associated with insulin resistance (IR) and chronic inflammation. Loureirin B (LrB) can effectively improve insulin resistance and alleviate chronic inflammation, and in order to investigate the therapeutic effect of LrB on polycystic ovary syndrome with insulin resistance (PCOS-IR), we conducted animal experiments. A PCOS-IR rat model was established by feeding a high-fat diet combined with letrozole (1 mg/kg·d for 21 days). The rats were treated with the GPR120 agonists TUG-891 and LrB for 4 weeks. Biochemical parameters (fasting blood glucose, total cholesterol, triglycerides, high- and low-density lipoprotein), hormone levels (serum insulin, E2, T, LH, and FSH), and inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-18) were analyzed. Histopathological analyses of ovaries were performed using hematoxylin/eosin (H&E) staining. Real-time PCR and western blotting were used to assess GPR120, NLRP3, and caspase-1 expression in ovaries, and immunohistochemistry was used to evaluate LKB1 and AMPK protein expression. LrB reduced body weight, Lee's index, ovarian index, ovarian area, and volume in PCOS-IR rats. It lowered fasting blood glucose, serum insulin, and HOMA-IR. LrB decreased total serum cholesterol, triglyceride, and LDL levels and increased HDL levels. It reduced serum T, LH, and LH/FSH and raised serum E2 and FSH levels. LrB downregulated the mRNA and protein expression levels of NLRP3 and Caspase-1, increased the protein and mRNA expression levels of GPR120 in rat ovaries, and increased LKB1 and AMPK protein expression in ovaries, ameliorating ovarian histopathological changes in PCOS-IR rats. Taken together, LrB upregulated GPR120, LKB1, and AMPK protein expression, downregulated NLRP3 and Caspase-1 protein expression, reduced insulin resistance and chronic inflammation, and ameliorated histopathological changes in ovarian tissues in PCOS rats, suggesting its potential as a treatment for PCOS.

The effect of health education on quality of life (QOL) among polycystic ovary syndrome (PCOS) females at Karachi, Pakistan

Objective: To evaluate the effect of nurses-led health education intervention on quality of life among polycystic ovary syndrome females. Method: The quasi-experimental study was conducted from May to August 2022 at the Obstetrics and Gynaecology outpatient department of Dow University Hospital, Karachi, and comprised married females aged 18-45 years, who were diagnosed with polycystic ovary syndrome based on the Rotterdam criteria. Nurses-led health education intervention session was conducted for all the patients. Data was collected using the self-administered polycystic ovaries syndrome quality of life scale. Data was analysed using SPSS 26. Results: Of the 50 females, 26(52%) were aged 26-35 years. There was a significance difference between baseline and post-intervention scores across all domains of quality of life (p&lt;0.05). Also, baseline body mass index of the participants was 30.4±4.711 which went down post-intervention to 29.4±4.800 (p&lt;0.001). Conclusion: Nurses-led health education intervention improved the quality of life and body mass index of polycystic ovary syndrome patients. Key Words: Health education, Quality of life, Polycystic ovary syndrome.

N-acetylcysteine supplementation improves endocrine-metabolism profiles and ovulation induction efficacy in polycystic ovary syndrome

BackgroundPolycystic ovary syndrome (PCOS) affects 6–20% of women worldwide, with insulin resistance and hyperinsulinemia occurring in 50-70% of patients. Hyperinsulinemia exacerbates oxidative stress, contributing to PCOS pathogenesis. N-acetylcysteine (NAC) is an antioxidant and insulin sensitizer that shows promise as a therapeutic for PCOS. Our current study aimed to investigate the effects of NAC supplementation on endocrine-metabolic parameters in PCOS mice and its effect on ovulation induction (OI) efficacy in women with PCOS.MethodsFemale C57BL/6 mice were orally administered letrozole (LE) to induce PCOS and then randomly divided into groups receiving daily oral administration of 160 mg/kg NAC (PCOS + NAC group), 200 mg/kg metformin (PCOS + Met group), or 0.5% carboxymethyl cellulose (drug solvent) (pure PCOS group) for 12 days. Healthy female mice served as pure controls. Estrous cycles were monitored during the intervention. Metabolic and hormone levels, ovarian phenotypes, antioxidant activity in ovarian tissues, and oxidative stress levels in oocytes were assessed post-intervention. Furthermore, a pragmatic, randomized, controlled clinical study was conducted with 230 PCOS women, randomly assigned to the NAC group (1.8 g/day oral NAC, n = 115) or the control group (n = 115). Patients in both groups underwent ≤ 3 cycles of OI with sequential LE and urinary follicle-stimulating hormone (uFSH). Cycle characteristics and pregnancy outcomes were compared between groups.ResultsSimilar to metformin, NAC supplementation significantly improved the estrous cycles and ovarian phenotypes of PCOS mice; reduced the LH concentration, LH/FSH ratio, and T level; and increased glucose clearance and insulin sensitivity. Notably, NAC significantly reduced oocyte ROS levels and increased the mitochondrial membrane potential in PCOS mice. Additionally, NAC significantly enhanced enzymatic and nonenzymatic antioxidant activities in PCOS mouse ovaries, whereas metformin had no such effect. In the clinical trial, compared to women in the control group, women receiving NAC had significantly lower average uFSH dosage and duration (p < 0.005) and significantly greater clinical pregnancy rates per OI cycle and cumulative clinical pregnancy rates per patient (p < 0.005).ConclusionNAC supplementation improved endocrine-metabolic parameters in PCOS mice and significantly enhanced OI efficacy with sequential LE and uFSH in women with PCOS. Therefore, NAC could be a valuable adjuvant in OI for women with PCOS.

Integrated Transcriptome Analysis of lncRNA, miRNA, and mRNA Reveals key Regulatory Modules for Polycystic Ovary Syndrome

Integrated Transcriptome Analysis of lncRNA, miRNA, and mRNA Reveals key Regulatory Modules for Polycystic Ovary Syndrome