To evaluate the effects of a combination of carnitines, L-arginine, L-cysteine and myo-inositol on metabolic and reproductive parameters in PCOS overweight/obese patients.

This was a retrospective study analyzing information of a group of PCOS (n = 25) overweight/obesity patients, not requiring hormonal treatment, selected from the database of the ambulatory clinic of the Gynecological Endocrinology Center at the University of Modena and Reggio Emilia, Modena, Italy. The hormonal profile, routine exams and insulin and C-peptide response to oral glucose tolerance test (OGTT) were evaluated before and after 12 weeks of a daily oral complementary treatment with L-carnitine (500 mg), acetyl-L-carnitine (250 mg), L-arginine (500 mg), L-cysteine (100 mg) and myo-inositol (1 gr). The hepatic insulin extraction index was also calculated.

The mix of complementary substances significantly improved metabolic parameters, homeostatic model assessment for insulin resistance index values and gonadotropin plasma levels. Glucose, C-peptide and insulin response to OGTT was significantly reduced as well as the hepatic insulin extraction index.

The administration of a combination of carnitines, L-arginine, L-cysteine and myoinositol improved gonadotropin plasma levels and insulin sensitivity in overweight/obese PCOS patients and restored hepatic clearance of insulin as demonstrated by the decreased hepatic insulin extraction index.

Polycystic ovarian syndrome (PCOS) is a common gynecological disorder with multifactorial pathogenic risk factors. Combination therapy with metformin and thiazolidinedione derivatives is frequently used, but its synergistic effects have not been thoroughly evaluated. This study aims to compare the therapeutic efficacy of low-dose spironolactone (LDS) at 0.25 mg/kg for 28 days, metformin at 500 mg/kg for 28 days, and a combination of LDS and metformin, against a letrozole (1 mg/kg/day) and 0.5 % carboxymethylcellulose (CMC)-induced PCOS rat model. The study involved five groups of laboratory animals: Group I (Healthy control), Group IIa (Disease control), Group IIb (Metformin), Group IIc (LDS), and Group IId (Metformin + LDS). Therapeutic efficacy was evaluated based on phenotypic, hormonal, and genotypic determinants. Letrozole successfully induced PCOS in the animals, evidenced by elevated levels of Sex Hormone Binding Globulin (SHBG), Follicle Stimulating Hormone (FSH), and progesterone, as well as the presence of multiple ovarian cysts. Hierarchical Cluster Analysis indicated that LDS was superior to metformin and the combination therapy in ameliorating PCOS symptoms. The findings suggest that there is little to no benefit in adding metformin to LDS for the clinical management of PCOS. Although these results are from preclinical studies, further case-controlled, randomized placebo studies on a larger patient sample are necessary to confirm these findings in clinical settings.

Polycystic ovary syndrome (PCOS) represents the most prevalent endocrine disorder among women of reproductive age, affecting approximately 5-18% of females worldwide. Characterized by irregular ovulation, hyperandrogenism, and polycystic ovaries, hyperandrogenism is the defining feature. Recent evidence highlights that, in addition to its notable reproductive and metabolic consequences, PCOS may also contribute to an elevated risk of renal complications. This increased risk is attributed to chronic low-grade inflammation, hormonal dysregulation, and disturbances in lipid metabolism inherent to the condition. However, the pathological mechanisms, clinical manifestations, and progression of secondary renal damage in this cohort remain insufficiently studied. This review consolidates current understanding of the relationship between PCOS and chronic kidney disease (CKD), aiming to clarify potential mechanisms by which PCOS may induce secondary renal dysfunction, encompassing both direct renal impairment and indirect damage mediated through systemic alterations. Furthermore, it advocates for comprehensive management strategies to mitigate renal risks in patients with PCOS, emphasizing the necessity of multidisciplinary approaches and further research to address these critical gaps.

Sleep problems like obstructive sleep apnea (OSA) are common in polycystic ovary syndrome (PCOS), although the underlying mechanisms are not well understood. We aimed to determine the prevalence of sleep problems, synthesise and appraise studies analysing the associations between serum sex hormones, sex hormone-binding globulin (SHBG) and sleep problems in females with PCOS.

Systematic review and meta-analysis.

A systematic search using MEDLINE, Embase, PsycInfo, CINAHL, Scopus, and Google Scholar was performed till 3 August 2024. Studies that examined serum sex hormones, SHBG or hyperandrogenism with sleep disorders and/or sleep disturbances in PCOS were eligible. Random effects meta-analyses of sex hormones and SHBG among females with PCOS with compared to without OSA were conducted.

From 4487 screened studies, 24 were included, with nine suitable for meta-analyses. Among females with PCOS, 46.0% had OSA and 56.0% had other sleep disturbances. SHBG levels were significantly lower in women with PCOS and OSA compared to those without OSA (standardised mean difference = -0.62; 95% CI = -0.82 to -0.42; I2 = 0%; 179 participants; p < 0.00001), but no differences were seen in total and free testosterone, dehydroepiandrosterone sulfate, androstenedione, and oestradiol. No significant associations between serum sex hormones, SHBG or hyperandrogenism with sleep disturbances in PCOS were observed.

SHBG, rather than hyperandrogenism, may play a more important mechanistic role for OSA in PCOS, while other sleep disturbances exhibit a less severe SHBG profile. These findings enhance comprehension of underlying pathophysiology of sleep problems in PCOS. Further validation across PCOS populations is warranted.

Adiponectin (ApN) is an antidiabetic and anti-inflammatory protein synthesized by adipose tissue. It is essential in regulating insulin sensitivity, glucose, and lipid metabolism by controlling AMPK, PPARα, and MAPK signals. It is an anti-inflammatory property that protects pancreatic β-cells. Often, low levels of ApN are linked to obesity, type II diabetes and the development of PDAC. However, changes in lifestyle and the use of certain drugs can improve ApN function and insulin sensitivity. PDAC is a highly aggressive cancer linked to obesity, type II diabetes, and insulin resistance. ApN plays a complex role in PDAC progression and can suppress PDAC development by weakening β-catenin signaling. Decreases in ApN levels are associated with increased PDAC risk in diabetic patients. PDAC and diabetes are interconnected through the development of insulin resistance, islet dysfunction, change in immunological response, inflammation, oxidative stress, and altered hormone secretion. Genetic studies highlight specific genes like HNF4G and PDX1 that influence both conditions and miRNAs such as miR-19a promote tumor progression through the PI3K/AKT pathway. This review discusses the role of ApN in diabetes and PDAC and the interrelation between diabetes and PDAC.

Cardiovascular disease (CVD) remains the leading cause of mortality among people with type 1 diabetes (T1D), with cardiovascular mortality rates 2-5 times higher than in the general population. A concerning sex disparity exists within this high-risk population, as the cardioprotective advantage typically observed in women without diabetes appears attenuated or eliminated in individuals with T1D. This disparity is evident across the CVD spectrum, including coronary artery disease, stroke, heart failure, and cardiovascular mortality, with women consistently experiencing an excess burden of disease. These differences are particularly pronounced in women with early-onset T1D, leading to a substantial loss of life-years-approximately 18 years for women compared to 14 for men. Several factors may contribute to this sex disparity. First, the effect of hyperglycemia on CVD appears to have a sex-based differential impact and women with T1D often demonstrate more difficulties to achieve optimal glycemic control. Second, although women with T1D generally exhibit a more favorable CVD risk factor profile than men with T1D, the presence of hypertension, smoking or diabetic kidney disease seem to have a strong impact on CVD in women. Diabetes also appears to diminish sex-based differences in lipid metabolism, and a trend towards increased obesity rates among women with T1D has been observed. Lastly, female-specific factors, which are more prevalent in T1D, exacerbate cardiovascular risk. These include premature menopause, pregnancy-related disorders (such as preeclampsia), polycystic ovary syndrome, and autoimmune diseases, which disproportionately affect women. This narrative review examines the epidemiological evidence highlighting the aspects regarding the excess risk of CVD in women with T1D and evaluates sex disparities in both traditional and female-specific risk factors. Finally, we include a sex-based analysis from the Catalan Registry, which highlights the critical need for greater awareness and enhanced early detection and management of CVD risk factors in this population.

Studies have associated obesity with peripubertal hyperandrogenemia. However, these studies were performed in academic centers and could have been influenced by selection bias.

To investigate if free testosterone levels are elevated in peripubertal girls with obesity.

We analyzed data from the National Health and Nutrition Examination Survey 2013-2016 databases.

1299 girls aged 6-18 years residing in the United States.

Mean free testosterone concentration (calculated from total testosterone and SHBG).

Among girls aged 6 to 9 years, mean (95% confidence interval) free testosterone was 0.33 pg/mL (0.28-0.38) in healthy-weight girls vs 0.86 pg/mL (0.67-1.05) in girls with obesity. Among girls aged 10 to 14 years, free testosterone was 2.29 pg/mL (2.05-2.53) in healthy-weight girls vs 4.10 pg/mL (3.60-4.60) in girls with obesity. Among girls aged 15 to 18 years, free testosterone was 3.33 pg/mL (2.96-3.70) in healthy-weight girls and 5.64 pg/mL (4.93-6.36) in girls with obesity. Girls with obesity in all age groups had higher free testosterone levels compared to healthy-weight girls. In each age group, the 95% confidence intervals for free testosterone did not overlap between healthy weight vs obesity subgroups. A multiple regression model accounted for 42% of the variance in free testosterone (R2 = 0.42), and both weight and age categories were independent predictors of free testosterone (P < .0001 for each).

In a nationally representative sample of US girls, obesity is associated with elevated free testosterone, suggesting an important relationship between obesity and peripubertal hyperandrogenemia.

Non-Hispanic Black women (BW) have a greater risk of type 2 diabetes (T2D) and insulin resistance (IR) compared to non-Hispanic White women (WW). The mechanisms leading to these differences are not understood, and it is unclear whether synergistic effects of race and obesity impact disease risk. To understand the interaction of race and weight, hepatic and peripheral IR were compared in WW and BW with and without obesity.

Hepatic and peripheral IR were measured by a labeled, hyperinsulinemic-euglycemic clamp in BW (n = 32) and WW (n = 32) with and without obesity. Measurements of body composition, cardiorespiratory fitness, and skeletal muscle (SM) respiration were completed. Data were analyzed by mixed model ANOVA.

Subjects with obesity had greater hepatic and peripheral IR and lower SM respiration (P < .001). Despite 14% greater insulin (P = .066), BW tended to have lower peripheral glucose disposal (Rd; P = .062), which was driven by women without obesity (P = .002). BW had significantly lower glucose production (P = .005), hepatic IR (P = .024), and maximal coupled and uncoupled respiration (P < .001) than WW. Maximal coupled and uncoupled SM mitochondrial respiration was strongly correlated with peripheral and hepatic IR (P < .01).

While BW without obesity had lower Rd than WW, race and obesity did not synergistically impact peripheral IR. Paradoxically, WW with obesity had greater hepatic IR compared to BW. Relationships between SM respiration and IR persisted across a range of body weights. These data provide support for therapies in BW, like exercise, that improve SM mitochondrial respiration to reduce IR and T2D risk.

Polycystic ovary syndrome (PCOS) is a common reproductive and metabolic disorder in the reproductive-age women. The international evidence-based guideline for the assessment and management of PCOS 2023 now suggests raising the follicle number per ovary (FNPO) threshold from 12 to 20 to define its key feature, polycystic ovarian morphology (PCOM). However, understanding of low- and high-FNPO PCOS cases defined in this cutoff is very limited. Given that the measures of lipoprotein subfractions are the biomarkers of several common diseases, this study aims to explore clinical characteristics and lipoprotein subfractions in low- and high-FNPO PCOS, and develop a diagnostic model.

A total of 1918 women including 792 low- and 182 high-FNPO PCOS cases, met the international evidence-based guideline 2023, and 944 controls were collected for clinical data analysis. Plasma samples of 66 low-FNPO and 24 high-FNPO PCOS cases and 22 controls matched with BMI and age were utilized for the measurement of 112 lipoprotein subfractions by nuclear magnetic resonance spectroscopy. Partial least squares discriminant analysis (PLS-DA) and logistic regression analysis were used to identify key lipoprotein subfractions. Ten machine learning algorithms and recursive feature elimination with logistic regression were used to construct the effective model to predict PCOM based on the new guideline. Models were validated with bootstrap resampling.

High-FNPO PCOS cases presented worse lipid parameters compared with low-FNPO cases and controls. Based on the results of PLS-DA and logistic regression analysis, seven key lipoprotein subfractions were selected, including V2TG, V3TG, V4TG, V2CH, V3CH, V3PL, and V4PL. The addition of them into the anti-Müllerian hormone (AMH) models for predicting high-FNPO PCOS resulted in a significantly improved model performance (AUC increased from 0.750 to 0.874). Even if the only V3TG was added into the AMH model, the AUC increased to 0.807.

Lipid metabolism, particularly seven key lipoprotein subfractions, has been identified as a major risk factor for high-FNPO PCOS cases. Among these, V3TG subfraction warrants special attention, both from the perspective of disease risk and precision diagnosis. Due to the lack of effective external validation at this stage, validation of larger sample sizes is necessary before generalizing the application.

Polycystic ovary syndrome (PCOS) is a metabolic and hormonal disorder that affects physical and emotional well-being. The aim of this cross-sectional study was to assess associated factors like sleep disturbance, obstructive sleep apnea (OSA), anxiety and depression in a German-speaking population with PCOS.

We designed an anonymous online survey with items from validated questionnaires, including the Hospital Anxiety and Depression Scale (HADS), the Generalized Anxiety Disorder (GAD-7), the Pittsburgh Sleep Quality Index (PSQI) and the STOP-Bang questionnaire to screen for OSA. The survey was mainly distributed via social media in Austria, Germany and Switzerland. Data from 587 questionnaires were analyzed.

Based on the STOP Bang questionnaire, 19.5% of women had a high probability for OSA. BMI and insulin resistance were identified as independent associated factors with OSA (both p < 0.001). Overall, the median anxiety score (GAD-7) was in the moderate range (Median 10.0, Interquartile range (IQR) 8.0). According to the HADS, association with moderate to severe anxiety (HADS-A) was 52.0% and with moderate to severe depression (HADS-D) 27.8%. There was a significant positive correlation between HADS-A/ HADS-D and BMI (r = 0.122, (HADS-A)/ r = 0.223 (HADS-D), both p < 0.01). According to the PSQI, 60.5% had mild sleep disturbance and 29.7% had chronic sleep disturbance. Chronic sleep disturbance was associated with anxiety disorders and depression, as well as a high probability of OSA (p < 0.001) after adjustment for age.

Our study highlights the probability of depression, anxiety and sleep disorders, including OSA, in women with PCOS and their association with BMI and insulin resistance.

Type 2 diabetes (T2D) is increasingly becoming a major global health challenge. However, research on T2D in non-elderly populations remains insufficient.

We analyzed data from the Global Burden of Disease (GBD) study in 2021, focusing on diabetes-related indicators among individuals aged 15 to 59 across 204 countries and regions. This included prevalence, incidence, mortality, and Disability-Adjusted Life Years (DALYs), categorized into 21 GBD regions according to the Sociodemographic Index (SDI). We employed join-point regression and Bayesian Age-Period-Cohort models to assess trends from 1990 to 2021 and forecast from 2021 to 2050.

The global age-standardized incidence rate increased from 196.3 per 100,000 (95 % UI, 145.2-257.4) in 1990 to 361.1 per 100,000 (95 % UI, 275.2-458.4) in 2021. The prevalence, mortality rate, and DALYs exhibit a similar upward trend. Although both men and women have experienced rises in prevalence, incidence, mortality rate, and DALYs, men continue to lead these metrics across nearly all age groups. Low-middle SDI countries bear the most severe disease burden. A high body mass index is a major risk factor in this population. It is estimated that by 2050, approximately 1.195 billion non-elderly individuals worldwide will have T2D, with epidemiological changes being the primary driver of this disease burden.

This study on the burden of T2D reveals that its prevalence among non-elderly individuals is steadily increasing and is projected to affect over a billion people worldwide by 2050. Targeted measures are crucial to tackle this global health challenge for this population.

Polycystic ovarian syndrome (PCOS) is a common endocrine condition in women. Studies have shown that PCOS is associated with poor quality of life, anxiety, sadness, dissatisfaction with one's appearance, and sexual dysfunction.

This study was conducted to determine whether a strong psycho-pathological personality is related to PCOS and whether this personality is related to the hyperandrogenic state.

Anthropometric, metabolic, hormonal, clinical, and psychological characteristics were examined in 90 Bahraini women with PCOS. After confirming the diagnosis of PCOS via Rotterdam criteria, including ovarian ultrasound, each patient was evaluated via the following questionnaires: 1) the GAD-7 (General Anxiety Disorder-7) to measure the severity of anxiety; 2) the Patient Health Questionnaire-9 (PHQ-9) to confirm and measure the severity of depression; 3) the Barratt Impulsiveness Scale (BIS-11) to measure aggression; and 4) the McLean Screening Instrument to identify borderline personality disorders (MSI-BPDs). The study was approved by the Institutional Review Board.

Compared to controls, PCOS patients exhibited significantly higher rates of severe depression (8% vs. 0%, p < 0.001), severe anxiety (7% vs. 0%, p < 0.001), impulsivity (BIS-11: 39.43 ± 9.69 vs. 26.64 ± 2.92, p < 0.001), and borderline personality traits (McLean: 2.41 ± 2.44 vs. 1.2 ± 0.94, p < 0.001). Metabolic comorbidities, including obesity (BMI 28.88 vs. 20.27, p < 0.001) and hypothyroidism (48% vs. 0%, p < 0.001), were prevalent in PCOS. Hyperandrogenism correlated weakly with psychiatric outcomes (all p > 0.05).

Women with PCOS demonstrate markedly elevated psychiatric and medical burdens compared to healthy controls. While hyperandrogenism showed limited direct associations, metabolic dysfunction (e.g., obesity) may mediate psychiatric risk. These findings underscore the need for multidisciplinary care integrating psychological and endocrine management, particularly in populations where cultural norms exacerbate PCOS-related distress.

Polycystic Ovary Syndrome (PCOS) is a common health condition related to a woman's hormonal problems. Hormonal imbalance, metabolic disorders, and an increased insulin level mainly characterize the ailment. This detailed review focuses on dietary strategies, macromolecules, macromolecules, and herbal interventions that exception-ally work in PCOS treatment. Research has shown that Mediterranean, low-glycemic index, and ketogenic diets that are modified with individuals in mind are the best ways to resolve insulin resistance, obesity, and lack of ovulation. The other nutrients shown to affect glucose metabolism and play a role in hormone regulation are the macromolecules, such as increased protein and reduced refined carbs. Among the different micronutrients, vitamin D, omega-3 fatty acids, and inositol were shown to be the most vital supplements in the treatment of PCOS-induced oxidative damage, hyperandrogenism, and infertility. Not to mention, cinnamon, curcumin, sage, fennel, and traditional Chinese herbal medicine are among some of the herbal remedies that so far show good potential to be the perfect complementary therapy tools as they create better glycemic control, inflammation reduction, and menstrual cycle regularization. Even though the findings are promising, the current supply of clinical trials for standardizing these nutritional and herbal protocols is lacking. Overall, this report stresses the fact that a customized, holistic diet regime is the best treatment for women with PCOS to make them feel well and live a long and healthy life.

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder in women of reproductive age that encompasses a multitude of signs and symptoms, including hyperandrogenism, polycystic ovarian morphology, ovulatory dysfunction, and insulin resistance. The study aims to explore the role of aromatic amino acid (AAA) disorders in the syndrome. A systematic search on the databases Scopus, PubMed, and Google Scholar until 20 July 2024 over the past 5 years regarding metabolomic studies on PCOS patients' blood and the status of AAAs resulted in 12 related papers. Our review showed that AAA metabolic pathways are dysregulated, and their levels in the blood serum and plasma of PCOS patients in most studies are elevated due to inflammation and oxidative stress which, assisted by gut dysbiosis, give rise to insulin resistance that develops into PCOS. AAA abnormalities can also directly induce the defining symptoms of the syndrome through diminished neurotransmitter availability and impaired signaling. According to our review, AAA perturbations are detected in every stage of PCOS pathophysiology, making them valuable biomarkers for early diagnosis and management of the syndrome. Further investigation of the biological function, role, and impact of AAAs, probably alongside other metabolites, including BCAAs, could lead to the discovery of new tools for preventing and managing PCOS symptoms.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder in women of reproductive age. This condition is associated with various hormonal, reproductive and metabolic alterations, including androgen excess, ovulatory disorders and a hyperinsulinemic state. A personalized therapeutic approach is necessary to improve PCOS, focusing on patients' main concerns, with the goal of addressing ovarian dysfunction, reducing hyperandrogenism and improving metabolic alterations, particularly through weight reduction. The therapeutic class of glucagon-like peptide-1 receptor analogues (GLP-1 RAs) represents an attractive option for PCOS due to its various beneficial effects, such as weight loss. In this review, we discuss the clinical and pathological aspects of PCOS, as well as the data and potential roles of GLP-1 RAs in managing this condition.

The Polycystic ovary syndrome (PCOS), a prevalent endocrine disorder affecting women's reproductive and metabolic health, faces diagnostic challenges due to heterogeneous clinical presentations and the absence of reliable biomarkers. This study investigates the role of Glucosaminyl (N-acetyl) transferase 2 (GCNT2) in modulating sex hormone-binding globulin (SHBG) and its potential as a therapeutic target in PCOS pathophysiology.

A prospective cohort of 103 PCOS patients treated with oral contraceptives (2021-2024) was established. Bidirectional Mendelian randomization (MR) was employed to assess genetic associations and causal relationships between PCOS and SHBG. Molecular docking studies evaluated cryptotanshinone's binding affinity to key proteins (COL1A1, COL4A2, COL6A2) in the PI3K/Akt pathway. GCNT2's regulatory effects on collagen synthesis and extracellular matrix pathways. Pharmacokinetic profiling validated therapeutic viability.

Bidirectional MR revealed significant genetic associations (P < 0.001) and causal links between PCOS and SHBG, implicating GCNT2 as a key modulator. Cryptotanshinone exhibited strong binding affinity to PI3K/Akt signaling pathway proteins and favorable pharmacokinetic properties. Enrichment analyses highlighted GCNT2's role in collagen biosynthesis (FDR < 0.05) and extracellular matrix regulation.

This study identifies GCNT2 as a critical mediator of PCOS pathophysiology through SHBG modulation and collagen remodeling. Cryptotanshinone emerges as a promising therapeutic candidate, targeting PI3K/Akt signaling pathway with high specificity. These findings advance the understanding of PCOS mechanisms and provide a foundation for biomarker-driven diagnostics and precision therapeutics. Further validation in clinical trials is warranted to translate these insights into practice.

Polycystic ovary syndrome (PCOS), a reproductive endocrine disorder with quintessential features of metabolic dysfunction, affects millions of women worldwide. Hyperinsulinemia (i.e., elevated insulin without hypoglycemia) is a common metabolic feature of PCOS that worsens its reproductive symptoms by exacerbating pituitary hormone imbalances and increasing levels of bioactive androgens. Hyperinsulinemia in PCOS is often attributed to insulin resistance, based on the concept that impaired insulin-mediated glucose disposal would induce compensatory insulin hypersecretion. However, it is challenging to define the sequential relationship between insulin sensitivity and insulin secretion, as they are tightly interlinked, and evidence suggests that hyperinsulinemia can alternatively precede insulin resistance. Notably, other drivers of hyperinsulinemia (outside of insulin resistance) may be highly relevant in the context of PCOS. For instance, high androgen levels can augment both hyperinsulinemia and insulin resistance, generating a self-perpetuating cycle of reproductive and metabolic dysfunction. In this review, we evaluate the cause-and-effect relationships between insulin resistance and hyperinsulinemia in PCOS. We examine evidence for the prevailing theory of insulin resistance as the primary defect that causes secondary compensatory hyperinsulinemia, and an alternative framework of hyperinsulinemia as the earlier defect that perpetuates reproductive and metabolic features of PCOS. Considering the heterogeneous nature of PCOS, it is improbable that its metabolic characteristics always follow the same progression. Comprehensively examining all mechanistic regulators of hyperinsulinemia and insulin resistance in PCOS might thereby lead to improved prevention and management strategies, and address critical knowledge gaps in the progression of PCOS pathogenesis.

Several studies suggest a linkage between PCOS and autoimmunity with a high frequency of chronic autoimmune thyroiditis (AIT) reported in PCOS patients, however, this subject remains controversial. The aim of this study was to investigate the prevalence of AIT in PCOS women and identify parameters that would serve as independent predictors of AIT.

Two hundred fifty seven (257) PCOS patients according to the NIH criteria and one hundred forty three (143) controls, women with normal menstrual cycles and without clinical or biochemical hyperandrogenism, were recruited for the study. Anthropometric characteristics and a complete family history for AIT were recorded. Thyroid hormones, antithyroid antibodies, androgen, glucose and insulin levels were measured. Thyroid gland structure was evaluated by ultrasound scan.

Patients and controls did not differ in age, BMI as well as genetic predisposition for AIT (p > 0.05). Women with PCOS presented higher levels of androgens and HOMA-IR index, as expected. AIT prevalence did not differ between women with PCOS and controls (4.8 vs 9.3%, p = 0.13). However, the subgroup of PCOS patients with AIT presented a significantly stronger predisposition for AIT (33.3 vs 4.7%, p = 0.004) compared to patients without AIT. In a multivariate regression model, a positive family history of AIT was proved to be the strongest independent predictor of AIT in the PCOS group (OR 7.06, 95% CI 1.04-47.79, R2 = 0.39).

The prevalence of AIT in the PCOS patients does not differ from the general population when family predisposition to AIT is taken into account.

New concepts have emerged regarding how interrelationships of hyperandrogenism and hyperinsulinemia from systemic insulin resistance contribute to the origins of polycystic ovary syndrome (PCOS). Although these androgen-insulin interrelationships are associated with several reproductive and metabolic variables, their specific cause and effect relationships remain unclear. This review examines specific causal relationships between hyperandrogenism and hyperinsulinemia from systemic insulin resistance to understand how these complex interactions contribute to the phenotypic expression of PCOS.

Clinical interventions for the treatments of hyperandrogenism and hyperinsulinemia from systemic insulin resistance as well as in-vitro studies of androgen and insulin actions on critical target tissues are examined to understand why androgen-insulin interrelationships are central to the origins of PCOS.

Bidirectional interrelationships between hyperandrogenism and hyperinsulinemia from systemic insulin resistance in normal-weight PCOS women may have originally evolved as an ancient metabolic adaptation to simultaneously favor fat storage and energy utilization for survival and reproduction during famine. These androgen-insulin interactions in PCOS now predispose to metabolic diseases and pregnancy complications in today's obesogenic environment and, therefore, require improved preventive healthcare to optimize the long-term health of PCOS women and their children.

To investigate influences of Dingkun Pill on granulosa cell proliferation and apoptosis (P&A) in polycystic ovary syndrome (PCOS) mice and its association with the TGF-β1/Smad2 signaling pathway (SPW) activity. Forty-eight female SD mice were rolled into experimental group (EG, Dingkun Pill), control group (CG, metformin), model group (MG, distilled water), and normal group (NG, distilled water), with 12 mice per group. The Beloosesky method was employed to establish the PCOS mouse model. Serum hormone (follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone (T)), expression of vascular endothelial growth factor (VEGF) in rat ovarian tissue and expression of HOXA10 in endometrial tissue, cell P&A, and expression level (EL) of TGF-β1 and Smad2 were compared among groups. Compared to the MG, the EG and CG exhibited significantly reduced levels of FSH, LH, and testosterone, while estradiol levels were significantly elevated. Furthermore, granulosa cell proliferation was notably enhanced, and the apoptosis rate was significantly decreased (P < 0.05). In addition, the expression of VEGF in ovarian tissue, as well as the expression of TGF-β1 and Smad2, was significantly lower in EG and CG compared to MG, while the expression of the HOXA10 gene in the endometrium was significantly increased (P < 0.05). Compared to CG, EG showed higher ovarian VEGF expression and lower HOXA10 gene expression (P < 0.05).Dingkun Pill notably improves serum hormone in a PCOS mouse model, inhibits granulosa cell apoptosis, and enhances granulosa cell proliferation activity. This effect is likely mediated through the inhibition of the TGF-β1/Smad2 SPW, suggesting a protective role of Dingkun Pill in PCOS.

Polycystic ovary syndrome (PCOS) is strongly associated with metabolic abnormalities, with 50-70% of patients exhibiting insulin resistance (IR), which significantly impacts the reproductive health of women in their reproductive years. Growth differentiation factor 15 (GDF15), a hormone responsive to nutritional stress, has been implicated in several diseases. This study sought to clarify the relationship between GDF15 levels and IR condition in PCOS patients. Based on the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), patients were categorized into an IR-PCOS group (n = 124) and a non-insulin-resistant group (non-IR-PCOS group, n = 109). Fasting blood samples were collected to measure GDF15 concentrations. To assess metabolic complications in relation to GDF15 levels, patients were also classified into high and normal GDF15 groups. Serum GDF15 levels were significantly higher in IR-PCOS patients (median 772.94 pg/ml) compared to non-IR-PCOS patients (median 575.80 pg/ml, P < 0.05). The high GDF15 group showed more severe metabolic and lipid abnormalities than the normal GDF15 group. Spearman correlation analysis revealed a correlation between increased GDF15 levels and impaired glucose metabolism. Logistic regression analysis identified GDF15, HDL-C, and prolactin as risk factors for IR in PCOS, and the fully adjusted regression coefficient for GDF15 levels and IR prevalence was 4.490 (95% CI 1.541 to 13.088). Restricted cubic spline analysis confirmed a positive association between GDF15 levels and IR within a specific range. The combined predictive probability of GDF15, prolactin, and HDL-C for IR was 0.763 (95% CI 0.701 to 0.826) according to ROC analysis. Elevated GDF15 levels may be associated with IR in PCOS patients, suggesting a potential role for GDF15 in the pathophysiology of IR in this condition.

Polycystic ovary syndrome (PCOS) is a multifaceted endocrine disorder with reproductive and metabolic dysregulation. PCOS has been associated with inflammation and metabolic syndrome (MetS); however, the moderating effects of inflammation as measured by C-reactive protein (CRP) and menopause on the PCOS-MetS association have not been studied in Hispanic/Latinas with PCOS who have a higher metabolic burden.

We studied the cross-sectional association between PCOS and (1) MetS in 7316 females of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), (2) subcomponents of MetS including impaired fasting glucose (IFG) and elevated triglycerides (TGL), and (3) effect modification by menopausal status and CRP.

The HCHS/SOL is a multicenter, longitudinal, and observational study of US Hispanic/Latinos. Our study sample included females from visit 2 with self-reported PCOS and MetS (ages 23-82 years).

PCOS (prevalence = 18.8%) was significantly associated with MetS prevalence [odds ratio [odds ratio (OR) = 1.41 (95% confidence interval: 1.13-1.76)], IFG and TGL (OR = 1.42 (1.18-1.72), OR = 1.48 (1.20-1.83), respectively]. We observed effect modification by menopausal status (ORpre = 1.46, Pint= .02; ORpost = 1.34, Pint= .06) and CRP (ORelevated = 1.41, Pint= .04; ORnormal = 1.26, Pint= .16) on the PCOS-MetS association. We also observed a superadditive interaction between CRP and PCOS, adjusting for which resulted in an attenuated effect of PCOS on MetS (OR = 1.29 [0.93-1.78]).

Hispanic/Latino females with PCOS had higher odds of MetS, IFG, and elevated TGL than their peers without PCOS. Interaction analyses revealed that the odds of MetS are higher among PCOS females who have premenopausal status or high inflammation. Interventions in Hispanic/Latinas should target these outcomes for effective management of the disease.

Background/Objectives: Among the therapeutic options available for managing PCOS, metformin improves insulin sensitivity, reduces androgen levels, and helps restore menstrual regularity and ovulation. While primarily used for its metabolic effects, metformin therapy may also influence reproductive parameters, including AMH levels, which are pivotal in improving ovarian function and predicting therapeutic outcomes in PCOS. The aim of this study was to search the scientific literature and analyze the correlation between AMH levels and metformin hydrochloride therapy in women with PCOS and IR. Methods: A systematic review of the scientific literature was conducted using the following keywords: polycystic ovarian syndrome, anti-Mullerian hormone, insulin resistance, metformin, treatment, biomarker, and metabolic syndrome. This review was aimed at investigating the potential of AMH as a biomarker of the effectiveness of metformin therapy in patients with PCOS and IR. Results: Metformin treatment in PCOS patients has shown significant reductions in serum AMH levels with prolonged therapy. As an insulin sensitizer, metformin improves insulin sensitivity, reduces hyperinsulinemia, and suppresses hyperandrogenism. This process inhibits the growth of antral follicles, which is reflected in decreased AMH levels. Conclusions: Reductions in AMH levels and improvements in insulin sensitivity can serve as indicators of treatment efficacy and enhancements in reproductive function for these patients. AMH could be considered a prognostic marker for evaluating the effectiveness of metformin therapy. A decrease in AMH levels following treatment may indicate improved ovarian function and a reduction in polycystic morphology. However, further research is necessary to confirm these findings and to determine the optimal dosages and duration of treatment.

Polycystic ovary syndrome (PCOS) has been associated with a high prevalence of obstructive sleep apnea syndrome (OSAS). However, the impact of OSAS on the PCOS symptom profile remains unclear. This systematic review and meta-analysis, which informed the 2023 International Evidence-based PCOS Guideline, aims to assess the prevalence and related symptoms of OSAS among females with and without PCOS.

A systematic search using databases (MEDLINE, Embase, EBM Reviews, PsycInfo and CINAHL) was performed until 16th May 2024. Random-effects restricted maximum likelihood meta-analyses compared OSAS and related symptoms between PCOS and non-PCOS groups. OSAS outcomes were categorized as apnea-hypopnea index (AHI)≥5 only, AHI≥5 with symptoms, AHI≥10 with symptoms and composite OSA (i.e., all AHI cut-offs with and/or without symptoms). Subgroup analyses by body mass index (BMI), age, PCOS diagnostic criteria and ethnicity were performed. Risk of bias and certainty of evidence by the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework were conducted.

From 4438 records, 3205 titles/abstracts were screened and 40 were eligible for full-text screening. Eight cross-sectional studies met inclusion criteria and meta-analysis. The pooled prevalence of OSA was 37.0% in PCOS (29.0% adolescents; 40.0% adults) and 6.0% in non-PCOS. Compared with non-PCOS, those with PCOS showed higher risk for composite OSA (odds ratio (OR): 9.52; 95% CI: 3.90 to 23.26; I 2 = 54.5%; 8 studies, n=942; P<0.001) and more pronounced OSAS risk with increasing symptom severity in PCOS (AHI≥5 OR: 3.90; 95% CI: 1.63 to 9.34; AHI≥5 with symptoms OR: 17.95; 95% CI: 6.17 to 52.22; AHI≥10 with symptoms OR: 30.61; 95% CI: 7.99 to 117.25, all P ≤ 0.0023). Subgroup results showed significantly higher risk of OSAS overall in overweight/obesity, adults and white ethnicity compared with normal weight, adolescent and Asian subgroups, respectively (all P<0.001), but independent of PCOS diagnostic criteria.

The prevalence of OSA was higher in PCOS compared with non-PCOS groups, with the risk of OSAS increasing with worse symptom severity. Adults and those of higher BMI and of white ethnicity were at increased risk of OSAS. Hence, identifying and treating OSAS symptoms in PCOS may be beneficial, but further validation of findings is warranted.

Insulin resistance (IR) is regarded as a significant role in the pathophysiology of Polycystic Ovary Syndrome (PCOS), hence early identification of IR in PCOS patients is crucial for their treatment. Recent researches indicate that Waist-to-Height Ratio (WHtR) differs in patients with PCOS accompanied by IR compared to those with PCOS alone; however, a consensus has yet to be reached. This research presents a meta-analysis of current data to propose a straightforward new index for diagnosing PCOS with insulin resistance.

This study aims to assess the correlation between WHtR and insulin resistance in individuals with polycystic ovarian syndrome by meta-analysis and the synthesis of research information. This study will offer prognostic insights into the onset of insulin resistance in individuals with polycystic ovaries.

This systematic review has finalized registration (CRD42025638798) on the PROSPERO platform. We conducted a search of prominent databases, including PubMed, Embase, Web of Science, The Cochrane Library, and performed manual searches. Observational studies of relevance (cohort, case-control, or cross-sectional) published before January 13, 2025, were considered. The methodological quality of case-control studies and cohort studies was evaluated using the NOS tool. Simultaneously, AHRQ criteria were employed to evaluate cross-sectional research. The study outcomes were reported as mean ± sd. The aggregated data was analyzed using StataMP17.0.

A meta-analysis encompassing nine studies with 3012 participants identified a significant correlation between an increased WHtR and the onset of insulin resistance in individuals with polycystic ovarian syndrome (SMD: 1.07, 95% CI: 0.81, 1.32, p = 0.000).

Patients with PCOS and insulin resistance will exhibit a greater WHtR compared to those with PCOS without insulin resistance. Thus, the incidence of insulin resistance in patients with polycystic ovary syndrome can be anticipated by monitoring the WHtR.

https://www.crd.york.ac.uk/PROSPERO/view/CRD42025638798, identifier CRD42025638798.

Polycystic ovary syndrome (PCOS) is a heterogeneous familial disorder affecting up to one in five women. The aetiology remains unclear, but available evidence suggests it is a polygenic disorder with epigenetic, developmental, and environmental components. The diagnostic criteria for PCOS are based on reproductive features, and the syndrome is categorized into several phenotypes that can vary by race and ethnicity. Insulin resistance and metabolic dysfunction have a crucial role in the pathogenesis of the syndrome and contribute to many adverse metabolic outcomes that place a substantial burden on the health of women with PCOS across their lifespan. Metabolic abnormalities like those identified in women with PCOS are also present in their female and male first-degree relatives. Overall, more emphasis is required on defining PCOS as a metabolic disorder in addition to a reproductive one. This approach could affect the management and future treatment options for the syndrome. The rationale of the current review is to identify and analyse existing evidence for PCOS as a metabolic, as well as a reproductive, disease.

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age, with a prevalence of 8-13% depending on diagnostic criteria. Its pathophysiology is linked to insulin resistance and resulting chronic inflammation. This study compares serum levels of fractalkine and high-sensitivity C-reactive protein (hs-CRP), markers of chronic inflammation, in PCOS patients before and after metformin therapy.

Thirty women with PCOS were recruited from gynecology and dermatology OPDs. Their serum fractalkine and hs-CRP levels were measured before starting metformin. The patients were then administered metformin, beginning with 500 mg once daily and increasing to 500 mg three times daily over four months, followed by repeat measurements of serum fractalkine and hs-CRP.

Post-metformin therapy, a significant reduction in serum fractalkine levels was observed (from 0.52 ± 0.29 to 0.38 ± 0.21 ng/ml, p = 0.001). Similarly, hs-CRP levels decreased significantly (from 0.71 ± 0.37 to 0.58 ± 0.27 ng/ml, p = 0.016). Clinical improvements in hirsutism, acne, acanthosis, and BMI were also noted, alongside a significant reduction in insulin resistance parameters.

Chronic inflammation in PCOS contributes to insulin resistance. Metformin therapy, by improving insulin resistance, reduces hyperinsulinemia and hyperglycemia, leading to decreased production of reactive oxygen species and amelioration of chronic inflammation. This is evidenced by lowered serum fractalkine and hs-CRP levels and improved insulin resistance parameters in this study.

PCOS is characterized by ovarian hyperandrogenism and insulin resistance (IR), which give rise to symptoms of hyperandrogenism and central obesity, which in turn may cause depression, lower self-esteem, and deteriorate coping strategies in stressful situations.

to examine the mental condition, self-esteem, and ways of coping with stress in women with PCOS compared to age and BMI-matched healthy controls and to correlate them with clinical and laboratory hyperandrogenism, central obesity, and IR.

42 women with PCOS and 39 controls were assessed for the above-mentioned psychological measures and correlated with serum hormonal and metabolic parameters.

Compared to controls, women with PCOS had more symptoms of depression (p = 0.026), a higher level of tension induction (p = 0.032), were more prone to alcohol consumption (p = 0.015), and were less likely to use the strategy of active coping in stressful situations (p = 0.014) and to seek instrumental (p = 0.048) and emotional support (p = 0.043). The presence of hirsutism correlated negatively with the level of emotional induction (R = -0.32, p < 0.05), and androgenic alopecia positively with the hedonistic tone (R = 0.36, p < 0.05). Serum testosterone (TST) correlated positively with the likelihood of seeking instrumental support in stressful situations (R = 0.31, p < 0.05) and with emotional focus (R = 0.34, p < 0.05). Serum androstenedione (A4-dione) correlated negatively with the escape behavior (R = -0.32, p < 0.05). No correlations were found between waist circumference and IR with the studied psychological measures.

Women with PCOS are characterized by depression, higher levels of tension induction, and impaired coping strategies in stressful situations, which correlate with clinical and laboratory indices of hyperandrogenism and not with central obesity and IR.

Despite certain studies indicating hearing impairments in individuals with polycystic ovary syndrome (PCOS), the correlation between PCOS and sensorineural hearing loss (SNHL) remains inconclusive. This study aimed to investigate the association between PCOS and SNHL.

A systematic literature search was conducted using PubMed, MEDLINE, EMBASE, and the Cochrane Library from inception to June 24, 2024.

This meta-analysis included cross-sectional, case-control, or cohort studies examining the association between PCOS and SNHL without language or regional restrictions. Case reports, case series, animal studies, and in vitro studies were excluded. We adhered to Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines and utilized the Newcastle-Ottawa Scale to assess the risk of bias in the included studies.

After performing the systematic review, we conducted a meta-analysis that included 489 patients from 5 studies: 349 patients with PCOS and 140 age- and sex-matched controls without PCOS. The meta-analysis compared the mean differences in frequency-specific pure-tone thresholds between patients with PCOS and matched controls, providing 95% confidence intervals for these differences. Given the expected clinical heterogeneity, we employed the DerSimonian and Laird random-effects model. Our results revealed significant hearing loss at specific frequencies (1000, 4000, 8000, 10,000, 12,000, 14,000, 16,000, 18,000, and 20,000 Hz) in the PCOS group compared to the control group (P < .05). Furthermore, the degree of hearing loss is greater at higher frequencies.

This meta-analysis demonstrated an association between PCOS and SNHL, particularly at higher frequencies.

Polycystic ovary syndrome (PCOS) represents a multifaceted endocrine, reproductive, and metabolic disorder characterized by hyperandrogenism and hyperinsulinemia-induced insulin resistance (IR). Recent studies reported that the etiology of PCOS is likely correlated with genes involved in steriodogenesis, IR and glucose metabolism. Among the candidate genes in insulin signaling pathways, RAB5B, a small GTPase involved in vesicle trafficking, significantly impacts cellular pathways in ovarian follicular cells, leading to clinical and endocrine changes among women with PCOS. Additionally, RAB5B is crucial for insulin-mediated glucose uptake and is involved in PI3K, AKT, and MAPK/ERK pathways, affecting LHCGR-stimulated steroidogenesis. Despite extensive research, the precise molecular mechanisms underlying RAB5B mediated IR in PCOS remained elusive.

The study aimed to explore the potential link between RAB5B gene expression and IR among women with PCOS.

A total of age matched 270 subjects were enrolled in this study including 135 PCOS women and 135 apparently healthy controls. These study participants were subjected to detailed medical history, clinical and physical examination. All subjects were further evaluated for biochemical, hormonal and RAB5B gene expression estimation. Expression levels of RAB5B gene were analyzed using gene-specific primers and the SYBR® Green PCR Kit (Qiagen, Germany) and their qPCR reaction mix, according to the manufacturer's guidelines. Student t-test and ANOVA were used to evaluate the differences in the means of various parameters.

The HOMA-IR (2.28 ± 1.4 vs. 1.36 ± 0.73) was significantly elevated among women with PCOS than controls (p < 0.05). We also found that the QUICKI (0.35 ± 0.04 vs. 0.37 ± 0.04), MATSUDA (12.59 ± 4.71 vs. 15.47 ± 4.33) and FGIR (11.56 ± 7.06 vs. 14.32 ± 8.66) were higher in controls than women with PCOS (p < 0.05). We also observed that women with PCOS had elevated levels of RAB5B mRNA levels when compared with apparently healthy controls. Bivariate correlation analysis among HOMA-IR stratified PCOS and control subjects revealed strong negative correlation between IR+ PCOS and IR- PCOS (r = -0.61, P < 0.05) and IR- control (r = -0.37, p < 0.05) subjects respectively.

Our study demonstrated that there is potential link between RAB5B gene expression and IR specifically in the context of IR indices among women with PCOS.

Although recent studies indicate a high prevalence of subclinical hypothyroidism (SCH) in women with polycystic ovary syndrome (PCOS), the reported prevalence rates vary widely. Therefore, we conducted this study to estimate the pooled prevalence of SCH among women with PCOS. Additionally, emerging evidence suggests that SCH may negatively impact insulin resistance in PCOS. Thus, we examined its effect on insulin resistance indices as our secondary objective.

We searched PubMed, Web of Science, Scopus, and Embase from their inception to February 25, 2024. Observational studies reporting the prevalence of SCH among women with PCOS were included. Joanna Briggs Institute's (JBI) critical appraisal checklist for prevalence studies was adopted for the risk of bias assessment. The random-effects model was employed to estimate the pooled prevalence with its 95% confidence intervals (CI). The weighted mean difference (WMD) was used to compare the insulin resistance indices between PCOS patients with and without SCH.

Twenty-nine studies comprising 5765 women with PCOS were included. The meta-analysis demonstrated that 19.7% (95% CI: 16.1%; 23.5%) of women with PCOS have SCH. PCOS patients with SCH had significantly higher HOMA-IR (WMD = 0.78, 95% CI: 0.34; 1.22) and fasting insulin (WMD = 2.38, 95% CI: 0.34; 4.42) levels than those without SCH. Differences in fasting plasma glucose and 2-hour postprandial glucose did not reach statistical significance.

This systematic review and meta-analysis found that approximately 20% of women with PCOS have SCH. This underscores the need for regular thyroid function testing in these patients. The prevalence of SCH is influenced by the TSH cut-off used for diagnosis, highlighting the need for establishing a standardized TSH cut-off value. Furthermore, SCH significantly elevates the HOMA-IR index and fasting insulin levels, highlighting its potential impact on insulin resistance. Whether these metabolic changes are clinically important and put these individuals at higher risk of developing type 2 diabetes mellitus and cardiovascular disease requires further investigation.

CRD42024510798.

Not applicable.

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder affecting reproductive-age women, characterized primarily by hyperandrogenism, ovulatory dysfunction, and metabolic abnormalities. In recent years, the gut microbiota has garnered widespread attention for its potential role as a key regulator of host metabolism in the pathogenesis of PCOS. Studies have shown that PCOS patients exhibit dysbiosis in their gut microbiota, characterized by reduced microbial diversity, an imbalance in the ratio of Firmicutes to Bacteroidetes, changes in the abundance of specific taxa, and abnormal levels of metabolic products. These alterations may exacerbate metabolic dysfunction in PCOS through multiple mechanisms, including influencing host energy metabolism, disrupting lipid and bile acid metabolism, and inducing chronic inflammation. Addressing gut dysbiosis through the modulation of patients' microbiomes-such the use of, prebiotics, fecal microbiota transplantation, and optimizing diet lifestyle-may offer strategies for improving metabolic abnormalities and alleviating clinical symptoms in PCOS. Additionally, the gut microbiome promises as a potential marker, aiding in the precise diagnosis and personalization of PCOS. Although our current understanding of how the gut microbiota influences PCOS is still limited, research is needed to explore the causal relationships and mechanisms involved, providing a more reliable theoretical basis for clinical. This review aims summarize the research progress on the relationship between gut microbiota and PCOS, and to suggest future directions to promote the development of prevention and treatment strategies for PCOS.

Polycystic ovary syndrome (PCOS) is linked to non-alcoholic fatty liver disease (NAFLD). Biochemical, sex hormonal, and anthropometric indicators have been explored for screening NAFLD in PCOS patients. However, the accuracy of NAFLD screening using these indicators in PCOS patients remains uncertain. This study aimed to identify biochemical, sex hormonal, and anthropometric indicators associated with NAFLD in overweight and obese PCOS patients and assess the diagnostic efficacy of combined indicators.

This cross-sectional study (Clinical trial number ChiCTR1900020986; Registration date January 24th, 2019) involved 87 overweight or obese women with PCOS (mean age 29 ± 4 years). Measurements included anthropometric indices, biochemistry, sex hormone levels, and liver proton density fat fraction (PDFF). Correlation analysis, intergroup comparisons, and logistic regression analysis were used to identify risk factors for NAFLD (PDFF > 5.1%). The receiver operating characteristic curve, area under the curve (AUC), sensitivity, specificity, positive predictive value, and negative predictive value were used to determine cut-off values and evaluate diagnostic accuracy.

Liver PDFF was 7.69% (3.93%, 14.80%) in overweight and obese PCOS patients, with 67.8% diagnosed with NAFLD. NAFLD was associated with increased body mass index (BMI), abdominal circumference (AC), and triglyceride, total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), glucose, insulin, and free testosterone (FT) levels, and with decreased high-density lipoprotein-cholesterol (HDL-C) and sex hormone-binding globulin (SHBG) levels (P < 0.05). Risk factors for NAFLD in PCOS included BMI > 26.8 kg/m2, AC > 88.3 cm, triglyceride > 1.57 mmol/L, TC > 4.67 mmol/L, LDL-C > 3.31 mmol/L, glucose > 4.83 mmol/L, insulin > 111.35 pmol/L, FT > 7.6 pg/mL and SHBG < 25 nmol/L (β = 1.411-2.667, P < 0.005). A multi-indicator model including triglycerides, LDL-C, glucose, insulin, and SHBG showed higher diagnostic accuracy (AUC = 0.899, P < 0.001) for screening NAFLD in PCOS patients than single indicators (AUC = 0.667-0.761, P < 0.05).

Overweight and obese PCOS patients have higher incidences of liver PDFF and NAFLD. A multi-indicator model including triglycerides > 1.57 mmol/L, LDL-C > 3.31 mmol/L, glucose > 4.83 mmol/L, insulin > 111.35 pmol/L, and SHBG < 25 nmol/L is highly accurate for screening NAFLD in overweight and obese PCOS patients.

Polycystic Ovary Syndrome (PCOS) is a prevalent endocrine disorder characterized by hyperandrogenism, insulin resistance, and menstrual irregularities, leading to infertility in many women. Emerging evidence suggests intermittent fasting (IF), particularly time-restricted feeding (TRF), may improve reproductive and metabolic outcomes in women with PCOS by addressing core pathophysiological mechanisms. This systematic review examines the impact of IF on fertility and reproductive hormones in women with PCOS.

A systematic search was conducted in PubMed, Scopus, and Cochrane Library using predefined search terms related to intermittent fasting, fertility, and PCOS. Eligible studies published between 2014 and 2024 were identified following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Inclusion criteria targeted primary research evaluating the effects of IF on reproductive outcomes, menstrual irregularities, and metabolic parameters in women with PCOS. Data extraction and quality assessment were performed using the Caldwell framework.

Three studies were included in the review. TRF interventions led to significant improvements in menstrual regularity, with 33-40 % of participants reporting normalized cycles. Reductions in total testosterone, free androgen index, anti-Müllerian hormone (AMH), and luteinizing hormone (LH) levels were observed, alongside increased sex hormone-binding globulin (SHBG). TRF also improved insulin sensitivity, reduced body weight, and decreased inflammatory markers, all of which contribute to enhanced reproductive outcomes. Key outcomes included a 9 % reduction in testosterone levels, 26 % reduction in the free androgen index (FAI), and significant improvements in menstrual regularity (33-40 %).

Intermittent fasting, particularly TRF, shows potential as a non-pharmacological intervention to improve reproductive health and fertility in women with PCOS. By targeting hyperandrogenism, insulin resistance, and menstrual irregularities, TRF offers a promising lifestyle approach. However, larger randomized controlled trials with long-term follow-up are needed to confirm these findings and establish IF as a standard therapeutic option for PCOS management.

Vitamin D receptor (VDR) gene polymorphisms have been implicated in polycystic ovary syndrome (PCOS). Despite VDR gene polymorphisms importance and their risk for PCOS, they have not been extensively studied. The main objective was to evaluate the associations between VDR gene polymorphisms and risk for PCOS.

The current systematic review and meta-analysis examined VDR gene polymorphisms with PCOS in case-control and cohort studies. Relevant keywords were used to search Scopus, Web of Science, PubMed, MEDLINE, ScienceDirect, and Google Scholar for peer-reviewed publications until July 1, 2024. Selected papers were assessed for risk bias and quality using the Modified Newcastle-Ottawa scale. A meta-analysis was conducted using a random-effect model. The association between VDR gene polymorphism(s) and PCOS in women was reported as odds ratios (ORs) with 95 % confidence intervals (CIs).

Twenty eligible studies, including 5618 subjects, were included in systematic review and meta-analysis. This study revealed a significant association between ApaI (rs7975232; OR = 1.18, 95 % CI = 1.06-1.30, p < 0.01), BsmI (rs1544410; OR = 1.22, 95 % CI = 1.08-1.37, p < 0.01), Cdx2 (rs11568820; OR = 1.15, 95 % CI = 0.97-1.38, p < 0.01), and TaqI (rs731236; OR = 1.25, 95 % CI = 1.13-1.39, p < 0.01). However, there was no significant association in the FokI (rs22228570; OR = 1.01, 95 % CI = 0.91-1.112, p = 0.12) polymorphism with PCOS risk.

The present systematic review and meta-analysis shows that women with ApaI, BsmI, Cdx2, and TaqI VDR gene polymorphisms may have a higher risk of PCOS. This study was registered on the Prospective International Registry of Systematic Reviews (PROSPERO) with registration number CRD42024564851.

Polycystic ovary syndrome (PCOS) is one of the commonest gyneco-endocrine disorders amongst women of reproductive age. Whether PCOS and cardiometabolic traits in PCOS patients are associated with shortened telomere length (TL) or relative leukocyte telomere length (rLTL) remains unclear.

214 women with PCOS and 214 age-matched women were recruited. rLTL was measured with an updated quantitative real-time PCR protocol and reported as ΔΔCt between telomere and a single-copy gene encoding β-globin relative to a normalisation control. A two-way Mendelian randomization analysis using the UK Biobank Resource was performed to assess the causal relationship between rLTL and PCOS.

Women with PCOS had significantly shortened rLTL (PCOS: 0.5 ± 0.7; control: 0.8 ± 0.6; p < 0.001). Longer rLTL was associated with a lower risk of PCOS after adjusting for age, history of smoking and other cardiometabolic traits (OR: 0.503; 95% CI: 0.342-0.730; p < 0.001). Longer rLTL was associated with reduced risk of dyslidpidemia (OR: 0.563; 95% CI: 0.450-0.968; p = 0.042) in PCOS patients. PCOS subjects with rLTL shorter than mean of the rLTL of control subjects had an elevated risk of dysglycemia (OR: 2.09; 95% CI: 1.04-4.29; p = 0.040). No causal relationships were found between rLTL and PCOS in the Mendelian randomization study.

Women with PCOS have significantly reduced rLTL and shorter LTL may be associated with cardiometabolic risk factors in PCOS subjects. There are no causal relationship between genetically determined PCOS and TL or vice versa.

Obesity and metabolic syndrome are significant contributors to infertility in women and are closely associated with insulin resistance (IR). The metabolic score for insulin resistance (METS-IR) is a new, non-insulin-based fasting index used to measure IR. However, the potential of METS-IR as a predictive indicator of female infertility risk has not been established. This study aimed to explore the association between METS-IR and the risk of female infertility.

This cross-sectional study used data from the National Health and Nutrition Examination Survey (NHANES) from 2013 to 2018. We conducted multivariate logistic regression, restricted cubic spline (RCS), and threshold effect analyses to investigate the relationship between METS-IR and female infertility.

According to the self-reported data, 188 (12.20%) participants were classified as infertile. A significantly higher proportion of participants with elevated METS-IR were found to have infertility. Multivariable logistic regression analysis revealed that METS-IR was significantly associated with increased risk of female infertility, irrespective of the independent variable analysis by continuous variables or tertiles in the fully adjusted model (Model 3, continuous variable: OR = 1.02, 95% confidence interval (CI):1.01-1.04, p = 0.005; tertile 3 vs. tertile 1: OR = 2.00, 95% CI = 1.21-3.28, p = 0.0128, p for trend =0.0126). RCS analysis indicated a linear correlation between METS-IR and the risk of infertility (p = 0.121), and threshold effect analysis further supported this linear association (p = 0.136). Moreover, above the inflection point of 32.94, the risk of infertility significantly increased with increasing METS-IR level (p < 0.0001).

Our results suggest that high levels of the METS-IR index are positively associated with infertility among reproductive-aged females in the United States.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder among women of reproductive age. Diagnosing adolescent PCOS is challenging due to the overlap between adult PCOS diagnostic criteria and normal physiological changes in adolescence. This review examines the diagnosis and treatment strategies for adolescent PCOS. The diagnosis of adolescent PCOS should meet two primary criteria-ovulatory dysfunction and biochemical or clinical hyperandrogenism-after excluding other causes. Defining these criteria accurately aids in early diagnosis and management of adolescent PCOS. However, due to limited research, age-specific diagnostic standards remain lacking. Once diagnosed, timely interventions-such as lifestyle, exercise, and dietary changes, along with targeted treatments like metformin and antiandrogens-should be initiated. In addition, the management of adolescent PCOS presents several challenges, including the absence of standardized medication guidelines, adolescent psychological factors that may impede adherence to dietary and exercise recommendations, and parental concerns about the long-term effects of medication on bone health and metabolism. Therefore, additional research is required to establish optimal management protocols to enhance patients' quality of life and prevent complications.