Although polycystic ovary syndrome (PCOS) is associated with high body mass index (BMI), less is known about the cardiometabolic manifestations of PCOS without excess adiposity. Among female adolescents enrolled in the Project Viva longitudinal prebirth cohort, we characterized growth, adiposity, and cardiometabolic biomarkers among those with vs without PCOS, stratified by BMI category. We defined PCOS at the mid-teen visit (mean age 17.7 years) as self-reported diagnosis or oligo-anovulation with clinical/biochemical hyperandrogenism. We obtained anthropometric and dual x-ray absorptiometry measurements. Within each BMI category (≥85th percentile vs < 85th percentile), we used unadjusted linear regression to compare growth trajectories, adiposity, and cardiometabolic biomarkers among those with vs without PCOS. We used mixed effects models to visually represent estimated BMI and linear growth trajectories. Among 358 females with data at the mid-teen visit, n = 51 (14%) participants met our criteria for PCOS. Among females with BMI <85th percentile, those with PCOS (n = 27) had earlier age at peak height velocity [β = -.57 years; 95% confidence interval (CI) -0.96, -0.18], higher Homeostatic Model Assessment of Insulin Resistance (β = .77, 95% CI 0.23, 1.30), and lower adiponectin-leptin ratio (β = -.35, 95% CI -0.65, -0.06) vs without PCOS. Females with BMI ≥85th percentile had similar biomarkers by PCOS status. Adiposity measures did not differ by PCOS status within either BMI category. Within this population-based cohort, adolescents with PCOS and BMI <85th percentile had greater insulin resistance and adipose tissue dysfunction vs without PCOS. PCOS-associated metabolic dysfunction exist even among adolescents with BMI <85th percentile.

Adverse reproductive outcomes remain a significant concern for women of reproductive age with polycystic ovary syndrome (PCOS), yet the role of the lower genital tract (LGT) microenvironment has been largely overlooked. This study aimed to investigate the association between the LGT microbiome and the outcomes of in vitro fertilization and frozen embryo transfer (IVF-FET) in women with PCOS. A total of 191 reproductive-aged women undergoing assisted reproductive technology (ART) treatment between December 2018 and October 2021 were recruited. The LGT microbiota was profiled using 16S rRNA sequencing and analyzed in relation to ART outcomes and clinical parameters. Furthermore, cervical transcriptome sequencing was performed in a subset of PCOS patients to investigate whether LGT microbiota alterations were associated with functional changes in mucosal epithelial cells. The results demonstrate significant dysbiosis of the LGT microbiome in patients with PCOS, characterized by a reduction in Lactobacillus abundance. Among 72 PCOS patients undergoing IVF-FET, those with a relative Lactobacillus abundance of ≥50% (n = 57) exhibited significantly improved reproductive outcomes compared to those with Lactobacillus abundance &amp;lt;50% (n = 15). Elevated testosterone levels were identified as the most significant factor associated with a reduced abundance of Lactobacillus in PCOS patients. Transcriptomic analysis further revealed that the LGT microbiota was associated with maintaining mucosal epithelial barrier integrity and immune homeostasis in PCOS. In conclusion, the findings highlight that dysbiosis of the LGT microbiota may significantly influence reproductive outcomes in PCOS patients, emphasizing the importance of targeting the LGT microenvironment to improve ART success rates.

Sexual function in women with Polycystic Ovary Syndrome: the role of psychological factors.

Background Polycystic Ovary Syndrome (PCOS) and Recurrent Pregnancy Loss (RPL) are reproductive disorders frequently linked to psychological distress. This study compared the severity of depression, anxiety, and stress levels between women with PCOS and RPL and assessed their association with years of marriage. Materials and methods A cross-sectional study conducted a random sampling method on 157 women (PCOS: 70; RPL: 87) attending the Obstetrics and Gynecology OPD at IMS BHU, Varanasi. Psychological status was assessed using the DASS-21 scale, a reliable tool widely used in reproductive health research. Chi-square test and independent sample t-tests were used for statistical analysis. Results Mean scores were significantly higher in RPL than in PCOS: depression (10.7 ± 3.5 vs. 8.8 ± 4.3, p = 0.003), anxiety (13.3 ± 3.8 vs. 10.7 ± 5.5, p = 0.001), and stress (12.3 ± 4.4 vs. 10.3 ± 6.1, p = 0.007). Marriage duration was significantly longer among women with severe depression (RPL: 8.4 ± 5.2 yrs.; PCOS: 6.3 ± 3.1 yrs), anxiety (RPL: 8.6 ± 5.1 yrs.; PCOS: 7.1 ± 3.3 yrs), and stress (RPL: 9.0 ± 5.2 yrs.; PCOS: 6.3 ± 3.1 yrs), all p &amp;lt; 0.05. Age was higher in RPL patients (p = 0.024); LH was higher in PCOS (p = 0.000). No significant differences were observed in AMH or BMI. Psychological symptoms were more severe among women with RPL, and a longer duration of marriage was associated with greater symptom severity. Marriage duration was significantly higher in women classified with severe depression, anxiety, and stress based on DASS-21 scores, indicating a correlational rather than causal relationship. Conclusion Routine psychological assessment is recommended for women with PCOS and RPL. Early identification of psychological distress may help improve overall reproductive and emotional health outcomes in these patients.

Polycystic Ovary Syndrome(PCOS) is a lifestyle disorder which is seen in girls of reproductive age. Absence or irregular periods ,hirsutism ,fertility issues, weight gain are symptoms shown by the individual. Insulin resistance, dyslipidemia, hyperandrogenism are the common feature of PCOS. Alternation happens in secretion of hormone like luteinizing hormone and follicle-stimulating hormone. Sedentary lifestyle and unhealthy eating habits is the primary reasons for the causes of PCOS in girls .Hence lifestyle modification is first step for solving. Aim of study: Management of PCOS is possible through diet and physical activity Material and methods: Data from Science direct and Google scholar Result and Conclusions: Diet therapy and regular physical exercise is the treatment for PCOS management. Blood glucose level and insulin resistance and weight loss can be modified through diet. High fibre, high protein and low carb are the prescribed diet. There is no specific diet for this condition. It also involve the combination of proper mental health. Keywords: Polycystic Ovary Syndrome, Diet, Physical Activity, Mental Health

Correction to: “Risk of Type 2 Diabetes, MASLD and Cardiovascular Disease in People Living With Polycystic Ovary Syndrome”

Disordered eating behaviors are linked to reproductive health and are more common in women with polycystic ovary syndrome (PCOS). However, it remains unclear whether they are risk factors for PCOS. To investigate the associations of disordered eating behaviors during adolescence and PCOS in adulthood. Prospective, longitudinal cohort (1996-2021). United States. Female participants (n = 6208) from the Growing Up Today Study. Disordered eating behaviors were self-reported on repeated questionnaires during follow-up. Physician-diagnosed PCOS was reported on each questionnaire starting in 2010. Multivariable logistic regression with generalized estimating equations to calculate the adjusted odds ratios (aOR) and 95% confidence intervals (CIs) for the association between past-year frequency of binge eating, laxative use, and self-induced vomiting and PCOS. We identified 410 cases (7%) of PCOS. Binge eating was the most common behavior, with 2331 (38%) girls binge eating at least once during follow-up. Additionally, 1103 (18%) girls reported self-induced vomiting and 701 (11%) reported using laxatives for weight control at least once. Compared to girls who never binge ate, cumulative binge eating more than monthly was associated with higher odds of PCOS (aOR: 1.59, 95% CI: 1.09, 2.33). Cumulative laxative use less than monthly was associated with lower odds of PCOS (aOR: 0.45, 95% CI: 0.29, 0.72) while at least monthly laxative use was associated with higher odds of PCOS (aOR: 1.67, 95% CI: 0.89, 3.14). Self-induced vomiting was not associated with PCOS. Girls who binge eat during adolescence may have increased odds of developing PCOS.

Aims: Polycystic ovary syndrome (PCOS) may confer increased risk for cardiovascular disease (CVD) and may also be common among women with type 1 diabetes. We examined whether PCOS confers increased risk of vascular damage among women with type 1 diabetes. Methods: Participants (n = 853) included women with type 1 diabetes enrolled in SEARCH, a large prospective population-based study of diabetes in youth, who underwent at least one assessment of arterial stiffness and responded to questions about a physician diagnosis of PCOS at approximately 17 years of age and again at approximately 22 years of age. Using generalized estimating equations, which accounted for repeated measures, we examined whether PCOS was associated with higher odds of arterial stiffness before and after adjustment for cardiovascular risk factors. Results: Among women with type 1 diabetes, arterial stiffness was more frequent among those reporting a physician diagnosis of PCOS versus those without a physician diagnosis of PCOS (24.4% vs. 7.9%, p = 0.0001). After adjustment for cardiovascular risk factors, including age, race/ethnicity, diabetes duration, waist circumference, mean arterial pressure, and cigarette use, PCOS remained strongly associated with arterial stiffness (odds ratio: 2.08, 95% confidence interval: 1.09, 3.99). Conclusions: In a large cohort of youth-onset type 1 diabetes, arterial stiffness is observed as early as the 3rd decade of life among women, placing them at risk for premature CVD. Women with type 1 diabetes and PCOS have greater risk of vascular damage compared to women with type 1 diabetes who do not have PCOS.

Polycystic ovary syndrome (PCOS) affects both obese and normal-weight women, with limited treatment options available for the nonobese population. Metformin (MET), an insulin sensitizer, is used to ameliorate insulin resistance and associated reproductive endocrine metabolic dysfunctions in PCOS patients. The efficacy of chiglitazar, a peroxisome proliferator-activated receptor (PPAR) pan-agonist used for type 2 diabetes treatment, is undefined in PCOS patients. In this randomized controlled trial, the effects of metformin versus chiglitazar on insulin resistance and reproductive endocrine metabolism are assessed in normal-weight women with PCOS. Fifty-five normal-weight women with PCOS aged 18 to 45 years were included. Patients were randomly assigned to receive either chiglitazar (32mg once daily) or MET (500mg twice daily). Anthropometric measurements, menstrual cycle changes, sex hormone characteristics, and an oral glucose-insulin release test (OGIRT) were performed after three months of continuous use. Following 12 weeks of treatment with chiglitazar, there were notable improvements in insulin and blood glucose levels at the 120-minute mark of the OGIRT, and the peak insulin levels were significantly earlier than those at baseline, indicating a more pronounced effect than that in the MET group. Moreover, both the chiglitazar and MET treatments led to significant improvements in menstrual cyclicity, and luteinizing hormone (LH) and testosterone (Testo) levels, with no significant differences detected between the two groups. Prolactin (PRL) levels were significantly elevated in the Chiglitazar group compared with the MET group. There was also no significant difference in the efficacy of the two treatments for PCOS in subgroups with different baseline IR0 values. In normal-weight PCOS patients, chiglitazar is similar to MET with regard to improving menstrual frequency and total testosterone (TT) and LH levels. Compared with MET, chiglitazar significantly improves fasting insulin levels, insulin and blood glucose levels at 120min of the OGIRT and advances the insulin peak. This single-center, open-label, 1:1 randomized controlled trial is registered with ClinicalTrials (NCT06125587, ClinicalTrials.gov) on 2023-11-05.

The pelvic pain bias assessment: a new assessment of interpretation bias specific to pelvic pain.

Meal timing is increasingly recognized as a critical determinant of metabolic health, alongside diet quality and caloric intake. Late-night eating—particularly dinner consumed close to sleep onset—has been associated with obesity, impaired glucose metabolism, and features of metabolic syndrome. This study investigated the relationship between late dinner habits and metabolic outcomes in young adults, integrating evidence from a cross-sectional survey and a comprehensive literature review. A survey with 30 adult volunteers, from Skopje, North Macedonia, aged 28–35 years, with a validated questionnaire, assessing dinner timing, dietary patterns, and self-reported health conditions; anthropometric data was completed. Among participants, 70% reported eating dinner after 21:00. Late eaters had higher prevalence of overweight (67% vs. 22% in early eaters) and metabolic conditions, including diabetes, elevated cholesterol, fatty liver, hypertension, and polycystic ovary syndrome. Most late eaters (85%) consumed high-fat or high-sugar meals. These observations align with extensive human studies showing that late meals are linked to higher body mass index, reduced insulin sensitivity, impaired glucose tolerance, dyslipidaemia, and altered energy expenditure, independent of total energy intake. Mechanistic evidence implicates circadian misalignment, disrupted secretion of appetite-regulating hormones, impaired diet-induced thermogenesis, and perturbation of gut microbiome rhythms. Behavioral and social factors such as skipping breakfast, irregular work schedules, and evening social activities further contribute to delayed meal timing. Collectively, these findings indicate that late dinner consumption is a modifiable behavioral risk factor with clinically meaningful implications. Promoting earlier, balanced dinners and aligning meal timing with the body’s circadian rhythm may support metabolic health, prevent obesity, and reduce the risk of metabolic syndrome in young adults and the general population.

Demographics, clinical characteristics, polycystic ovarian syndrome phenotypes, and factors associated with anti-mullerian hormone levels among women with PCOS at a Fertility Center in Ghana: a 5-year retrospective study

MicroRNA mediated downregulation of HSD17B1 impairs estrone-to-estradiol conversion in polycystic ovarian syndrome.

Metformin-loaded Chitosan nanoparticles alleviate insulin resistance in the polycystic ovarian syndrome rat model through modulation of PI3K/AKT/ GLUT4 in ovarian tissue.

Polycystic ovary syndrome (PCOS) is associated with an increased risk of cerebrovascular disease, but the effects on cerebrovascular function are unknown. In this pilot study, we sought to compare cerebrovascular perfusion, pulsatility, reactivity and metabolism between women with PCOS and healthy volunteers using MRI, and investigated the influence of testosterone and insulin resistance on these parameters. Case-control pilot study. Fifteen patients with PCOS (age: 32.0 ± 7.4 years; body mass index [BMI]: 31.8 ± 5.7 kg/m2) and 12 healthy controls (HC) (age: 30.7 ± 6.4 years; BMI: 30.2 ± 5.8 kg/m2). We used 3T magnetic resonance imaging (MRI) to assess several aspects of cerebrovascular function: (1) perfusion (cerebral blood flow [CBF] and arterial arrival time [AAT]; PCOS N = 15; HC N = 12), (2) pulsatility index (PCOS N = 15; HC N = 12), (3) breath-hold induced cerebrovascular reactivity (CVR; PCOS N = 15; HC N = 10), and (4) global oxygen metabolism (oxygen extraction fraction [OEF] and cerebral metabolic rate of oxygen [CMRO2]; PCOS N = 9; HC N = 8). Linear regression models investigated the contribution of PCOS status, serum testosterone and Homeostatic Model Assessment for Insulin Resistance (HOMA2-IR). Regional analysis underwent false discovery rate (FDR) correction for multiple comparisons. Overall baseline CBF was not statistically different in PCOS patients compared to controls after adjustment for other variables (χ2(1) = 3.29; p = 0.07) but did show evidence for regional reduction with PCOS status in the transverse temporal gyrus (χ2(84) = 110.31; p = 0.03; -29.05 mL/100 g/min ± 7.26 [standard error; SE]). Similarly, while PCOS status was not associated with overall CVR (χ2(1) = 0.78; p = 0.38), there was evidence of a regional interaction (χ2(84) = 154.25; p < 0.001) in the parahippocampus (1.37% signal change ± 0.27 [SE]) and pericalcarine cortex (1.04% signal change ± 0.26 [SE]). Neither testosterone nor HOMA2-IR was associated with any outcome measure. We observed regional reduction in cerebral blood flow and regional increase in cerebrovascular reactivity in women with PCOS compared to healthy controls. However, due to the limited statistical power and unclear menstrual timing in this pilot study, these results require further replication.

NLRP3 inflammasome activation in PCOS: A novel target for managing insulin resistance and metabolic dysregulation.

Effects of the need for in-vitro fertilization to conceive on pregnancy risks in women with the polycystic ovary syndrome. Evaluation of a population database and a matched cohort.

Elevated level of platelet factor 4 in follicular fluid is associated with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder caused by hyperandrogenism, estrogen imbalance, and insulin resistance. It is a chronic condition that affects hormonal balance, but genetic and environmental factors are believed to play an important role in its development. There is no evidence that PCOS directly affects the pancreas and its enzymes. The aim was to understand the effect of PCOS on the pancreas from a physiological and histological perspective. Twenty-four female rats were divided into three groups (eight rats in each group). The first group was the control group, consisting of healthy rats that did not receive any medication. The second group was given 0.2 mg/kg of letrozole orally to induce PCOS. The third group was injected with 0.7 mg/kg of estradiol to also induce PCOS. At the end of the experiment, blood samples were used to assess levels of hormones such as testosterone, estradiol, and insulin, as well as enzymes such as amylase. Ovarian and pancreatic organs were also taken for histological sectioning. The results showed a significant increase in testosterone concentrations in the letrozole-treated group and a significant decrease in estradiol concentrations, in contrast to the estradiol- treated group, where testosterone concentrations decreased and estradiol concentrations increased. Regarding enzymes, a decrease in amylase concentrations was observed in the letrozole-treated group, in contrast to the estradiol-treated group, where amylase concentrations increased. Increased insulin concentrations were also observed in both groups. As for histological sections, ovarian sections from female mice in which polycystic ovary syndrome was induced using letrozole and estradiol showed numerous cystic follicles on the ovarian surface with a thin granular layer, dissolution of the corpus luteum, and the disappearance of primordial, primary, secondary, and Graafian follicles. As for histological sections of the pancreas from female mice induced with letrozole, changes such as alpha cell proliferation and capillary dilation were observed. Pancreatic cells and islets of Langerhans were normal, and the effect of PCOS in this group was mild. Compared to the other group in which PCOS was induced with estradiol, we observed more significant changes and effects, such as islet cell hyperplasia, endothelial cell hyperplasia, capillary congestion, acinar cell necrosis, and beta cell degeneration. The study summarizes the effect of PCOS on the pancreas, which leads to pathological changes there, leading to decreased activity.

Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder characterized by hyperandrogenism and frequently associated with insulin resistance (IR), a key pathogenic factor in PCOS. However, insulin sensitizers commonly used to treat PCOS are often recommended off-label and may cause side effects. This study investigated the therapeutic effects of pancreastatin inhibitor 8 (PSTi8), an insulin sensitizer, in a PCOS rat model. The PCOS rat model was established by daily feeding with a high-fat diet and administering subcutaneous injections of dehydroepiandrosterone at a dose of 60 mg/kg body weight for 21 days and further, followed by 21 days of treatment with PSTi8 (10 mg/kg) and metformin (300 mg/kg). Body weight, estrous cycle, glucose, and insulin tolerance test results were monitored. Ovarian morphology, estrous cycle changes, oxidative stress and inflammatory markers, steroidogenic hormone levels and protein expression, and insulin signaling pathway were assessed to evaluate the therapeutic effectiveness of PSTi8 in PCOS rats. This study found that PSTi8 improved IR and reduced body weight in PCOS rats. PSTi8 lowered serum levels of insulin (27%), testosterone (56%), estradiol (2-fold), progesterone (21%), sex hormone-binding globulin (7.5%), and luteinizing hormone/follicle stimulating hormone ratio (57%). Additionally, PSTi8 helped to restore ovarian morphology, estrous cycle, and improve dyslipidemia. PSTi8 treatment also reduces the oxidative stress level of total superoxide ismutase (16%), glutathione peroxidase (26%), and inflammation in PCOS rats. Furthermore, PSTi8 restores the steroidogenic protein expression and increases PI3K/Akt phosphorylation in PCOS rats. These findings demonstrate PSTi8 exhibited comparable efficacy to metformin in ameliorating IR and ovarian dysfunction in the studied PCOS model. SIGNIFICANCE STATEMENT: Polycystic ovary syndrome (PCOS) increases risk of reproductive and metabolic disorders, partly due to systemic inflammation. This study combined dehydroepiandrosterone with high-fat diet and successfully induced PCOS-like features in rats. PSTi8, a pancreastatin inhibitor known for insulin-sensitizing effects in various disease models, effectively reversed PCOS-associated pathophysiology. PSTi8 improves insulin sensitivity by activating the PI3K/AKT signaling pathway and ameliorates oxidative stress and inflammation in PCOS rats. Additionally, PSTi8 treatment normalized steroidogenesis protein expression and reduced circulating biomarkers linked to cardiovascular risk.