Obese Polycystic Ovary Syndrome Group Research Articles

Association Between rs2278426 Polymorphism of the ANGPTL8 Gene and Polycystic Ovary Syndrome.

To study the relationship between the single nucleotide polymorphism (SNP) rs2278426 in the angiopoietin-like protein 8 gene (ANGPTL8) and polycystic ovary syndrome (PCOS). A total of 122 patients with PCOS and 108 controls were recruited for comparison of glucose, lipid, insulin, sex hormone, and ANGPTL8 levels. Polymerase chain reaction (PCR) and gene sequencing were performed for comparison of the frequency of the CC, CT, and TT rs2278426 genotypes and the rs2278426 allele distributions between the PCOS and control groups and between the obese and non-obese subgroups of the PCOS and control groups. The frequency of the T allele was significantly higher in the PCOS group than that in the controls (P = 0.037). In the dominant genetic model, the proportion of the CT+TT genotype in the PCOS group was significantly higher than that in the controls (P = 0.047). Subgroup analysis demonstrated that the T allele proportion was significantly higher in obese PCOS group than obese control group (P = 0.027). PCOS with the CT+TT genotype had significantly higher body mass index (BMI; P = 0.001), triglyceride (TG; P = 0.005), homeostasis model assessment of insulin resistance (HOMA-IR; P = 0.035), testosterone (P = 0.041), and ANGPTL8 (P = 0.037) levels and significantly lower high-density lipoprotein (HDL) levels (P = 0.025) than PCOS with the CC genotype. Obese PCOS group with the CT+TT genotype had significantly higher TG (P = 0.015), luteinizing hormone (LH; P = 0.030), fasting insulin (FINS; P = 0.039), HOMA-IR (P = 0.018), and ANGPTL8 (P = 0.049) levels than obese PCOS group with the CC genotype. Polymorphisms of rs2278426 may induce glycolipid metabolic disorders by affecting ANGPTL8 levels and functions in Han Chinese females with obesity from the Shandong region, increasing the risk of PCOS in this population.

Lipid accumulation product is an effective predictor of metabolic syndrome in non-obese women with polycystic ovary syndrome.

To explore the correlation of lipid accumulation product (LAP) with metabolic syndrome (MS) and to assess the predictive value of LAP for MS risk in polycystic ovary syndrome (PCOS) with different body mass index (BMI). A total of 242 PCOS patients and 150 controls were recruited and divided into normal-weight, overweight, and obese groups, then further divided into MS and without MS subgroups. Clinical and anthropometric variables and laboratory results were recorded. LAP was calculated from waist circumference (WC) and triglyceride using sex-specific formulae. Logistic regression analysis and receiver operating characteristic (ROC) curve were applied to determine and analyze the predictive value of LAP for MS. The prevalence of MS among PCOS patients was 45.04%, which was significantly higher than that of the controls (10%). Stratified by BMI, the incidence of MS in the normal-weight, overweight, and obese PCOS groups were 15.58%, 41.43%, and 71.58%, respectively. Logistic regression analysis indicated that LAP was an independent risk factor for MS in both normal-weight and overweight groups; however, the results were not significant in the obese group. ROC curve analysis showed that LAP had an outstanding discrimination index for MS in normal-weight (AUC=0.960, cut-off value=42.5) and overweight (AUC=0.937, cut-off value=47.93) PCOS patients, with a sensitivity of 0.917/0.931 (normal-weight/overweight) and a specificity of 0.969/0.854 (normal-weight/overweight), respectively. Normal-weight and overweight PCOS patients also have a fairly high incidence of MS and should receive as much attention as obese patients. Compared to applying multiple clinical indicators, LAP is more convenient and facilitates acquiring early and accurate diagnoses of MS among non-obese PCOS patients using fewer MS markers.

Evaluation of sestrin 2 and tribbles homolog 3 levels in obese and nonobese women with polycystic ovary syndrome.

This study was designed to evaluate the relationship of two new biomarkers [tribbles homolog 3 (TRB3) and sestrin 2 levels], which were previously associated with obesity, with metabolic parameters in obese and nonobese women with polycystic ovary syndrome (PCOS). This cross-sectional case control study was conducted between September 2017 and August 2019 in the gynecology department of a tertiary referral hospital. The values of the plasma sestrin 2, TRB3, insulin, fasting plasma glucose, lipid profile, and homeostasis model assessment of insulin resistance (HOMA-IR) were compared in 90 obese women with PCOS (BMI > 30), 90 women with nonobese PCOS (BMI < 30), and 90 control patients (BMI < 30). The mean age of the study group consisting of all PCOS patients (26.11 ± 4.64 years) and the mean age of the control group (26.3 ± 4.4 years) were statistically similar (p = 0.239). The serum sestrin 2 values of the obese PCOS group were found to be statistically significantly lower than the control and non-obese PCOS groups (p = 0.001, p = 0.0001), while the sestrin 2 values of the nonobese PCOS group were found to be statistically significantly lower than the control group (p = 0.0001). The TRB3 values of the control group were found to be statistically significantly lower than the obese and nonobese PCOS groups (p = 0.0001), while the TRB3 values of the nonobese PCOS group were found to be statistically significantly lower than the obese PCOS group (p = 0.0001). A negative correlation was observed between the sestrin 2 level and BMI (r = -0.272 p = 0.0001), insulin (r = -0.261 p = 0.0001), and HOMA-IR levels (r = -0.250 p = 0.0001). A positive correlation was observed between the TRB3 values and TG (r = 0.248 p = 0.0001), and LDL-C values (r = 0.235 p = 0.0001). According to the findings in this study, low sestrin 2 and high TRB3 levels may be related to impaired metabolic status in the obese PCOS group. Thus, it may be promising for the development of treatment of PCOS and associated metabolic disorder in the future.

Controlled attenuation parameters to assess liver steatosis in obese patients with polycystic ovary syndrome.

This study was performed to investigate the changes and influencing factors of liver controlled attenuation parameter (CAP) in obese patients with polycystic ovary syndrome (PCOS), and to determine the prevalence and risk factors of nonalcoholic fatty liver disease (NAFLD) in PCOS patients with obesity. Forty-one PCOS patients with obesity and twenty age- and body mass index (BMI)-matched control women without PCOS were enrolled in this study. General data, body composition, biochemical parameters, sex hormones, and liver CAP in the two groups were collected and compared. Liver CAP was measured using transient elastography. NAFLD was more common in the Obese PCOS group than in the control group (75.61% vs. 45.00%, P=0.018). Compared to the control group, the obese PCOS group showed apparent increases in alanine transaminase (ALT), aspartate transaminase (AST), CAP, triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), totle testosterone (TT), free androgen index (FAI), fasting insulin (FIns), and homeostasis model assessment-insulin resistance (HOMA-IR), along with lower high-density lipoprotein cholesterol (HDL-C) and sex hormone binding globulin (SHBG) levels. In addition, as shown by Spearman analysis, liver CAP in PCOS patients with obesity had a positive correlation with ALT, AST, TG, TT, FAI, FIns, and HOMA-IR, and a negative correlation with SHBG. Logistic regression analysis showed that TG, TT, FIns, and HOMA-IR were risk factors for NAFLD, while TT was an independent risk factor for NAFLD in PCOS patients with obesity. PCOS patients with obesity had a significantly higher prevalence of NAFLD. Furthermore, in PCOS patients with obesity, liver CAP was associated with disorders of lipid metabolism, insulin resistance, and hyperandrogenemia, with elevated testosterone levels being an independent risk factor for NAFLD in PCOS patients with obesity.

Serum Obestatin Levels in PCOS and its Relation with Homa-IR

Background: Is to investigate the level of Obestatin in PCOS patients and compare with controls and also see the correlations between the serum Obestatin levels and HOMA-IR.&#x0D; Patients and methods: We analyzed 30 patients with PCOS and 20 normal women as controls. PCOS patients were divided into two groups based on obese group and non-obese group Serum Obestatin levels, Insulin Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) determined and compared among both groups.&#x0D; Results: Serum Obestatin levels were significantly lower in obese PCOS group than non-obese and control.

Correlation between kisspeptin and biochemical markers in obese and non-obese women with polycystic ovary syndrome

Introduction The purpose of this study was to determine the association between kisspeptin levels and obesity in patients with polycystic ovary syndrome (PCOS) or in healthy controls and to explore the correlation between levels of kisspeptin and various endocrine and metabolic indices in each group. Methods From August 2020 to December 2021, the clinical data of 78 patients with polycystic ovary syndrome and 78 healthy individuals were collected. The two groups were further divided into obese and non-obese groups based on a BMI cutoff of 25. Serum kisspeptin levels were measured using enzyme linked immunosorbent assay (ELISA). Pearson’s correlation analysis was used to determine the correlation between PCOS and kisspeptin levels. Results The weight, body mass index (BMI), and waist circumference (WC), estradiol (E2), and testosterone (T) of the obese PCOS group were significantly higher than those of the study group (p < .05). WC, kisspeptin, triglycerides (TG), glucose (GLU), alanine amiotransferase (ALT), blood urea nitrogen (BUN), uric acid (UA), E2, luteinizing hormone (LH), prolactin (PRL), and T in the non-obese PCOS group were higher than those in the control group, and the difference was statistically significant (p < .05). Levels of E2 and TG in the obese PCOS group were significantly higher than those in the non-obese PCOS group (p < .05). Kisspeptin levels in the PCOS group exhibited a significant positive correlation with LH, T, and AMH levels; kisspeptin level positively correlated with T in the non-obese PCOS group and with anti-Müllerian hormone (AMH) in the obese PCOS group. Conclusion Serum kisspeptin levels are associated with hormone levels in patients with PCOS. Kisspeptin correlates with distinct biochemical indices in obese versus non-obese groups, indicating that kisspeptin may play a role in the prognostication, treatment, and clinical evaluation of patients with varying BMI.

Short-chain fatty acid-butyric acid ameliorates granulosa cells inflammation through regulating METTL3-mediated N6-methyladenosine modification of FOSL2 in polycystic ovarian syndrome

Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by chronic low-grade inflammation. Previous studies have demonstrated that the gut microbiome can affect the host tissue cells’ mRNA N6-methyladenosine (m6A) modifications. This study aimed to understand the role of intestinal flora in ovarian cells inflammation by regulating mRNA m6A modification particularly the inflammatory state in PCOS. The gut microbiome composition of PCOS and Control groups was analyzed by 16S rRNA sequencing, and the short chain fatty acids were detected in patients’ serum by mass spectrometry methods. The level of butyric acid was found to be decreased in the serum of the obese PCOS group (FAT) compared to other groups, and this was correlated with increased Streptococcaceae and decreased Rikenellaceae based on the Spearman’s rank test. Additionally, we identified FOSL2 as a potential METTL3 target using RNA-seq and MeRIP-seq methodologies. Cellular experiments demonstrated that the addition of butyric acid led to a decrease in FOSL2 m6A methylation levels and mRNA expression by suppressing the expression of METTL3, an m6A methyltransferase. Additionally, NLRP3 protein expression and the expression of inflammatory cytokines (IL-6 and TNF-α) were downregulated in KGN cells. Butyric acid supplementation in obese PCOS mice improved ovarian function and decreased the expression of local inflammatory factors in the ovary. Taken together, the correlation between the gut microbiome and PCOS may unveil crucial mechanisms for the role of specific gut microbiota in the pathogenesis of PCOS. Furthermore, butyric acid may present new prospects for future PCOS treatments.

Serum Phoenixin-14 levels of women with polycystic ovary syndrome increase proportionally with BMI.

This study aimed to compare serum PNX-14 values of women with PCOS classified as lean or overweight according to the BMI values. Fifty lean or overweight women diagnosed with PCOS according to the revised Rotterdam criteria were included in the study. They were divided into two groups according to their BMI values. Thirty patients with BMI values of 18.5-24.9 kg/m2 constituted the normal-weight PCOS group. Twenty patients with BMI values of 25-29.9 kg/m2 formed the overweight PCOS group. Thirty patients with regular menstrual cycles who did not exhibit clinical and laboratory findings of PCOS were selected as the control group. The patients in the control group were also divided into two different groups as normal weight (n=17) and overweight (n=13). In anovulatory PCOS group, blood samples were collected on the third day of progesterone withdrawal bleeding. Both in ovulatory PCOS and control groups, blood samples were collected on the third day of spontaneous menstrual cycle. In addition to basal hormonal parameters, serum phoenixin-14 concentrations were measured by enzyme-linked immunosorbent assay. LH values of the overweight or lean PCOS group were significantly higher than the overweight or lean non-PCOS group (p<0.01). The LH/FSH ratios of the lean and obese PCOS groups were significantly higher than the non-PCOS control group (p<0.01). Testosterone levels of both lean and obese PCOS groups were significantly higher than non-PCOS groups (p<0.02). The HOMA-IR value of the obese PCOS group was significantly higher than the lean PCOS group (p<0.03). The HOMA-IR values of the patients in the PCOS group were significantly higher than the non-PCOS controls. Phoenixin-14 levels of the obese PCOS group were approximately three times higher than the lean PCOS group (p<0.01). Phoenixin-14 levels of the obese non-PCOS group were also three times higher than the lean non-PCOS group (p<0.01). Serum Phoenixin-14 levels of patients in the lean PCOS group were significantly higher than in the lean non-PCOS group (9.11±2.09 pg/mL vs. 2.04±0.11 pg/mL, p<0.01). Serum Phoenixin-14 levels of the patients in the obese PCOS group were significantly higher than in the obese non-PCOS group (27.4±3.04 pg/mL vs. 6.44±1.09 pg/mL, p<0.01). A positive and significant correlation was found between serum PNX-14 levels and BMI, HOMA-IR, LH, and testosterone levels in both lean and obese PCOS patients. This study showed for the first time that serum PNX-14 levels are significantly increased in lean and obese PCOS patients. The increase in PNX-14 showed a proportional trend with BMI levels. Serum PNX-14 levels were correlated positively with serum LH, testosterone, and HOMA-IR.

Up-regulation of miR-133a-3p promotes ovary insulin resistance on granulosa cells of obese PCOS patients via inhibiting PI3K/AKT signaling

BackgroundMicroRNAs are a type of non-coding single-stranded RNA, which is involved in the regulation of ovary insulin resistance (IR). This study aims to explore the underlying mechanisms of miR-133a-3p regulating ovary IR in obese polycystic ovary syndrome (PCOS).MethodsGranulosa cells (GCs) were extracted from follicular fluids of PCOS patients (obese PCOS group and non-obese PCOS group) and healthy women (control group). The expression of miR-133a-3p in GCs was detected by qRT-PCR. The targets and pathways of miR-133a-3p were predicted by bioinformatics analyses. The protein levels of PI3K, p-AKT, GLUT4, p-GSK-3β, and p-FOXO1 were measured by Western blotting.ResultsMiR-133a-3p was highly expressed in GCs from PCOS patients, especially in obese PCOS patients. The protein levels of PI3K and p-AKT was downregulated in GCs from PCOS patients. There were 11 target genes of miR-133a-3p enriching in PI3K/AKT signaling pathway. miR-133a-3p mimic downregulated the expression of PI3K, p-AKT, and GLUT4, and upregulated the protein levels of p-GSK-3β and p-FOXO1. miR-133a-3p inhibitor presented the opposite effect of miR-133a-3p mimic.ConclusionMiR-133a-3p promotes ovary IR on GCs of obese PCOS patients via inhibiting PI3K/AKT signaling pathway. This study lays a foundation for further research on the mechanism of ovary IR in obese PCOS patients.

Assessment of neutrophil to lymphocyte ratio, C-reactive protein, mean platelet volume in obese, and nonobese patients with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is associated with low-grade chronic inflammation.This was a retrospective case–control study.In the present study, the risk coefficients of neutrophil to lymphocyte ratio (NLR), high-sensitive C-reactive protein (hs-CRP), and mean platelet volume (MPV) in obese patients with PCOS were determined. This study was designed to investigate NLR, hs-CRP, and MPV levels in 68 obese patients with PCOS and 44 nonobese patients with PCOS, and our study group was matched with 47 obese and 43 nonobese controls, respectively.PCOS group had higher MPV, NLR, insulin, glucose, and HOMA-IR rates than those of the controls. Subgroup analyses revealed that the obese PCOS group had higher NLR, hs-CRP, and MPV levels compared to those of controls. The obese PCOS group had higher NLR, hs-CRP, and MPV levels compared to those of the nonobese PCOS group. The odds ratios and 95% confidence intervals of those variables (NLR, hs-CRP, MPV) were found significant (P < .05). NLR, hs-CRP, and MPV variables were found statistically significant in the analysis of receiver operating characteristics.Our study demonstrated that NLR, hs-CRP, and MPV levels are increased in patients with obese PCOS.

Serum kisspeptin, leptin, neuropeptide Y, and neurokinin B levels in adolescents with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is characterized by ovarian dysfunction, clinical and/or biochemical hyperandrogenism, and polycystic ovaries. Its pathogenesis is still unclear. This study aimed to investigate the relationship between kisspeptin, leptin, neuropeptide Y (NPY), and neurokinin B (NKB) levels for evaluating the pathogenesis of PCOS. Levels of these parameters were analyzed in 20 patients with PCOS, and 16 healthy adolescents. Serum NPY levels were significantly higher in the obese and non-obese PCOS group (p<0.01). There was a negative correlation between the kisspeptin and the NKB levels (p<0.01) in the PCOS group but not in the control group. This negative correlation was also found in both PCOS groups (p<0.01). In the obese PCOS group, serum kisspeptin levels were significantly lower than the control and non-obese PCOS groups (p<0.05) although serum leptin and NPY levels were significantly higher in the obese PCOS group (p<0.01). The high NPY levels in both obese and non-obese patients with PCOS indicate that NPY plays a role in the pathogenesis independently from obesity. Significantly high leptin and low kisspeptin levels in the obese PCOS group suggested that they may be associated with obesity rather than PCOS.

Role of Oxidative Stress in Obese and Nonobese PCOS Patients.

Objective The aim of this study was to evaluate the relationship between the oxidant-antioxidant status, endothelial dysfunction, lipid metabolism, and metabolic syndrome risk in women with polycystic ovary syndrome (PCOS). Materials and Methods Forty-five obese (BMI >30 kg/m2) woman diagnosed with PCOS in the study, forty-five nonobese (BMI <30 kg/m2) PCOS diagnosis working groups, and forty-nine healthy control groups were created with patients. Serum malondialdehyde (MDA) levels with antioxidant activities, such as SOD, GSH, GPx, and CAT activities, were measured by spectrophotometry. Results There was a statistically significant difference in the mean serum MDA level in the obese PCOS group compared to the nonobese group and the control group (p < 0.001). When the antioxidant parameters, such as SOD, GPx, GSH, and CAT, were compared with the healthy control group, nonobese, and obese PCOS groups, the difference between the groups was statistically significant (p < 0.001). A positive correlation was observed between MDA and BMI, triglyceride, LDL, SBP, DBP, and HOMA-IR in the PCOS patient group. Conclusion Oxidative stress and decreased antioxidant parameters in PCOS patients were correlated with hyperinsulinemia, hypertension, and dyslipidemia findings, and we think that this oxidative stress condition may contribute to metabolic syndrome and cardiovascular diseases in PCOS patients.

Decreased serum profile of the interleukin-36α in polycystic ovary syndrome

ObjectiveThe aim of this study was to determine the serum adiponectin and interleukin-36 alpha (IL-36α) levels in polycystic ovary syndrome (PCOS), and their relationship with obesity. Materials and methodsThis observatory study included 80 PCOS patients and 58 controls. The clinical, biochemical, and hormonal parameters, and serum adiponectin and IL-36α levels of the patients were evaluated. ResultsThe serum IL-36α levels of the PCOS patients were significantly lower when compared to the control group, despite a similar mean body mass index (BMI) (P = 0.000). The adiponectin levels were significantly lower in the obese PCOS group when compared to the obese control group (P = 0.03). The plasma IL-36α level was positively correlated with adiponectin level, but negatively correlated with the serum LH level (P = 0.000 and P = 0.004, respectively). Using receiver operating characteristic analysis, the cut-off value of IL-36α was calculated as 0.815 for PCOS. In the multiple binary logistic regression analysis, IL-36α (OR [95% CI] 0.432 [0.303, 0.616], P < 0.001) and adiponectin (OR [95% CI] 1.044 [1.005, 1.084], P = 0.028) were determined to be significantly associated with PCOS. ConclusionA reduced IL-36α level may play a role in the pathogenesis of ovulatory disfunction and insulin resistance in PCOS patients. Further studies are needed to understand the pathogenic and clinical significance of the IL-36 system in PCOS.

Analysis of Endocrine and Metabolic Indexes in Non-Obese Patients with Polycystic Ovary Syndrome and Its Compare with Obese Patients.

PurposeTo compare the endocrine and metabolic indexes of obese and normal body mass index (BMI) polycystic ovary syndrome (PCOS) patients, and explore factors affecting the pathogenesis and progression of PCOS.MethodsThis study included obese (n=79) and normal BMI (n=40) PCOS patients, and obese (n=30) and normal BMI (n=30) non-PCOS controls. Blood glucose, insulin (INS), blood lipids, sex hormones, and other metabolic and endocrine indicators were measured, and the correlations between the indicators were analyzed.ResultsHOMA-IR, 0min INS, 60min INS, 120min INS, 180min INS, FAI, TG, TC, LDL-C and sd-LDL in obese PCOS group were higher, while SHBG, LH, LH/FSH and HDL-C were lower than those in normal weight PCOS group (P <0.05). 120min PBG, HOMA-IR, FAI, T, LH, LH/FSH, AMH, TC and LDL-C in obese PCOS group were higher than those in obese control group (P <0.05). 0min PBG, 60min PBG, 120min PBG, 180min PBG, 0min INS, 60min INS, 120min INS, 180min INS, HOMA-IR, LH, LH/FSH and T in normal weight PCOS group were higher than those in normal weight control group (P <0.05). In both normal weight group and obesity group, HOMA-IR entered the regression equation with FAI as dependent variable, and the absolute value of HOMA-IR standardized partial regression coefficient was higher than that of hs-CRP and AMH. In PCOS patients, FAI in the obese and non-obese PCOS groups was positively correlated with HOMA-IR.ConclusionEndocrine metabolic disorders in women with PCOS were more obvious than that in women with non-PCOS with matched BMI. The abnormality of glucose and lipid metabolism in obese PCOS patients is more serious than that in PCOS patients with normal BMI. Both obese and normal BMI PCOS patients were affected by hyperinsulinemia, and IR may play a key role in the pathogenesis and development of PCOS.

Serum X-box-binding protein 1 levels in PCOS patients

Objective X-box binding protein-1 (XBP1) is a possible indicator of metabolic syndrome and diabetes. This study aimed to evaluate the relationship between serum XBP1 levels and polycystic ovary syndrome (PCOS). Method A prospective observational study was conducted with 88 patients. The first group was defined as the control group with ovulatory and normal-BMI patients (n = 28). The second group comprised of nonobese PCOS patients (n = 30). The third group included overweight/obese patients with PCOS (n = 30). Fasting plasma glucose, serum lipids, follicle stimulating hormone, luteinizing hormone, total testosterone, dehydroepiandrosterone and XBP1 levels l were evaluated in all groups. Results There was a significant difference in XBP1 levels between the study groups, and higher levels were observed both in the nonobese and obese PCOS groups than in the healthy controls (p < .001). The median level of XBP1 was 73.7 pg/ml in the control group, 114.11 pg/ml in the nonobese PCOS group, and 151.61 pg/ml in the overweight/obese PCOS group. A cutoff level of XBP1 at 95.79 pg/ml level was determined with a significant AUC (area under the curve) level of 99% and high specificity and sensitivity rates to predict PCOS. Also, a significant positive correlation was observed between XBP1 levels and BMI, waist circumference, fasting plasma glucose and triglyceride levels (p < .05). Conclusions XBP1 levels were significantly higher in PCOS patients, particularly in overweight/obese PCOS patients, than in the controls. Also, the parameters associated with metabolic syndrome were related to XBP1 levels.

Comparison of clinical, metabolic, and hormonal parameters in lean vs. obese women with polycystic ovary syndrome: a single-center study from Bangladesh

A bi‑directional relationship exists between obesity and polycystic ovary syndrome (PCOS). Although most of the patients with PCOS are obese, normal-weight patients still account for a certain proportion of PCOS who have lesser degrees of insulin resistance and fewer metabolic risk factors. This study was conducted to compare the clinical, metabolic, and endocrine parameters of the two categories of PCOS: lean and obese PCOS. We evaluated 523 women with PCOS attending the Endocrinology outpatient department of a tertiary hospital in Bangladesh. PCOS patients with body mass index (BMI) <23 kg/m2 were categorized as lean PCOS and those with BMI ≥23 kg/m2 as obese PCOS. Out of 523 women with PCOS studied, the frequencies of lean- and obese PCOS were 23.3% and 76.7%, respectively. Age, systolic blood pressure (BP), diastolic BP, fasting plasma glucose, plasma glucose 2-hour after oral glucose tolerance test, serum triglyceride, total cholesterol, low-density lipoprotein cholesterol, total testosterone, and thyroid-stimulating hormone were higher in obese PCOS group; serum prolactin was higher in the lean PCOS group; modified Ferriman-Gallwey score and high-density lipoprotein cholesterol were similar in the two groups. Acanthosis nigricans (89.3% vs. 45.9%), prediabetes (24.4% vs. 13.1%), diabetes (6.7% vs. 1.6%), pre-hypertension (22.2% vs. 9.8%), hypertension (8.7% vs. 0.8%), metabolic syndrome (61.3% vs. 14.8%), and biochemical hyperandrogenism (27.7% vs. 11.5%) were more frequent in the obese group than the lean group. The two groups had similar frequencies of menstrual irregularity, hirsutism, a family member with type 2 diabetes, and dyslipidemia. Though metabolic abnormalities are more frequently observed when obesity is associated with PCOS, both lean and obese have adverse metabolic consequences. All patients with PCOS should be screened for metabolic abnormalities irrespective of BMI category.

Expression of PGC-1ɑ in Ovarian Tissue of PCOS Rat Model

To investigate the expression of peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) in the ovarian tissue of polycystic ovary syndrome (PCOS) rat model and obese PCOS rat model, and the possible mechanism of PCOS. Thirty SD rats were randomly divided into control group, PCOS rat model group and obese PCOS rat model group. DHEA dissolved in 0.2 mL soybean oil was injected daily into the rats of two PCOS groups for 21 d. Rats in obese PCOS model group were added with high-fat diet based on DHEA modeling, and each group had 10 rats. Body mass were measured before and on the 22 nd day after modeling. The serum testosterone (T) levels were measured by abdominal aortic blood, and the ovarian tissues of rats were taken for histological changes were observed by HE staining, immunohistochemical staining and Western blot to detect PGC-1ɑ protein expression. The body mass of rats in each group increased after modeling, and the body mass of rats in PCOS group and obese PCOS group increased significantly ( P<0.05). The serum T concentration of two PCOS model groups was higher than that of control group ( P<0.01). The serum T concentration in obese PCOS model group was higher than that in the PCOS group ( P<0.05). The results of HE staining of rat ovarian tissue showed that there were follicles and a small amount of corpus luteum at different developmental stages in the control group, and the granulosa cells were arranged in 4-6 layers. The number of immature small follicles in the two PCOS groups was significantly increased. The granulosa cells were arranged in 1-3 layers, relatively looser, and some follicles were atresia. In the obese PCOS group, the diameter of ovarian atretic follicles increased, the number of granulocyte layers decreased, and oocytes disappeared more obviously. Immunohistochemical staining showed that the PGC-1ɑ protein was mainly expressed in the cumulus and granulosa cells of ovarian tissue in the control group. The mean gray level of PGC-1ɑ protein expression in PCOS group (0.53±0.06) and obese PCOS group (0.36±0.03) was lower than that of the control group (0.75±0.03), with the statistical difference ( P<0.05). PGC-1ɑ expression in the obese PCOS group was lower than that in the PCOS group ( P<0.01). The results of Western blot were consistent with those of immunohistochemical staining. PGC-1ɑ is associated with damage of ovarian granulosa cells in high-fat environment. The decrease of PGC-1ɑ expression in granulosa cells of ovarian follicles may be an important cause of PCOS development.

Correlation Between Fecal Metabolomics and Gut Microbiota in Obesity and Polycystic Ovary Syndrome.

Objective: This study aimed to explore the relationship between the fecal metabolites and gut microbiota in obese patients with PCOS and provide a new strategy to elucidate the pathological mechanism of obesity and PCOS.Methods: The fecal samples of obese patients with PCOS (n = 18) and obese women without PCOS (n = 15) were analyzed by 16S rRNA gene sequencing and untargeted metabolomics. The peripheral venous blood of all subjects was collected to detect serum sex hormones. The association among fecal metabolites, gut microbiota, and serum sex hormones was analyzed with the R language.Results: A total of 122 named differential fecal metabolites and 18 enrichment KEGG pathways were obtained between the groups. Seven fecal metabolites can be used as characteristic metabolites, including DHEA sulfate. The richness and diversity of gut microbiota in the obese PCOS group were lower than those in the control group. Lachnoclostridium, Fusobacterium, Coprococcus_2, and Tyzzerela 4 were the characteristic genera of the obese patients with PCOS. Serum T level significantly and positively correlated with the abundance of fecal DHEA sulfate (p < 0.05), and serum DHEAS level significantly and negatively correlated with the abundance of fecal teasterone (p < 0.05).Conclusion: Specific fecal metabolites may be used as characteristic metabolites for obese patients with PCOS. The closely relationship among gut microbiota, fecal metabolites, and serum sex hormones may play a role in the related changes caused by hyperandrogenemia.

Copeptin and Obestatin Levels in Polycystic Ovary women and their Relation to Obesity, insulin metabolism and Cardiovascular diseases

Objective: is to investigate the correlations between the serum levels of copeptin and obestatin, carotid artery intima-media thickness (CIMT), and brachial artery flow mediated dilatation (FMD) in obese and non-obese women with PCOS. Design: Prospective randomized study. Setting: Obstetrics and Gynecology Department, El-Hussein and Sayed Galal University Hospitals, Al-Azhar University. Patient(s): We analyzed 54 patients with PCOS and 20 normal women as controls. PCOS patients were divided into two groups based on body mass index (BMI): obese group (BMI > 30 kg/m2, n = 28) and non-obese group (BMI < 30 kg/m2, n = 26). Serum Copeptin and Obestatin levels, Insulin Homeostasis Model Assessment for Insulin Resistance (HOMA-IR), CIMT and brachial artery FMD were determined and compared among both groups. Result(s): Serum Obestatin levels were significantly lower in obese PCOS group than non-obese and control. While Serum Copeptin levels were significantly higher in obese PCOS group than non-obese and control. Brachial artery FMD was lower in the PCOS groups than control. Obestatin was positively correlated with cardiovascular risk factor (FMD), whereas Copeptin was negatively correlated with FMD Conclusion(s): Obestatin and Copeptin may provide useful information regarding future cardiovascular risk in PCOS patients as Obestatin was negatively correlated and Copeptin was positively correlated with cardiovascular risk factor (FMD). Keywords: Cardiovascular diseases, Copeptin, Insulin resistance, Obesity, Obestatin, Polycystic ovary

Variation analysis of Ghrelin gene in Chinese patients with obesity, having polycystic ovarian syndrome

Association of single-nucleotide polymorphisms (SNPs) of the ghrelin gene with polycystic ovary syndrome (PCOS)is unclear. However, their correlation with PCOS-related obesity has been observed. The objective of this study was to evaluate the effects of ghrelin gene SNPs on PCOS-related obesity in Chinese women. The full-length sequence of the ghrelin gene was determined to explore the relationship of the SNPs with PCOS-related obesity in Chinese women. The gene was sequenced, including all exons, introns and exon–intron boundaries in 230 Han Chinese women with PCOS and 162 normal women. Significant genotypic and allelic differences were observed between the obese PCOS group and obese control group at rs35681 locus (p = .013 and .017). The genotypic analysis of obese and non-obese people in the PCOS group showed that the proportion of A allele in the obese PCOS group (10.9%) was higher than that of the G allele (3.6%). This study revealed that ghrelin rs35681 might be related to the occurrence of obesity associated with PCOS, and allele A was found to increase the risk of obesity in PCOS.