Nonobese PCOS Compared to Obese PCOS Have Similar Clinical Presentation, Hormonal Profile, and Insulin Resistance.

Objectives:The objective was to compare body composition, metabolic characteristics, and insulin resistance between obese (body mass index [BMI] ≥25 kg/m2) polycystic ovary syndrome (PCOS) and nonobese PCOS (BMI <25 kg/m2) women and their age- and BMI-matched controls.Materials and Methods:A total of 81 PCOS women (Rotterdam criteria) (obese – 42; nonobese – 39) and 86 controls (obese – 42; nonobese –44) were recruited in this cross-sectional study. All women underwent a detailed assessment of clinical, anthropometric, and metabolic parameters, insulin resistance indices, and body composition measurements with visceral adipose tissue assessment (VAT) (dual-energy X-ray absorptiometry scan).Results:Of PCOS women, 27% (80% – obese PCOS; 20% – nonobese PCOS) were diagnosed with metabolic syndrome (International Diabetes Federation criteria), 35% of PCOS women (46% – obese PCOS; 54% – nonobese PCOS) had impaired glucose tolerance, and 7% of PCOS women (2/3rd – obese PCOS; 1/3rd – nonobese PCOS) had diabetes mellitus. Insulin resistance was seen in about 80% in obese PCOS women and 20% in nonobese PCOS women based on various insulin resistance indices such as fasting insulin (≥12.2 μU/ml), Homeostasis Model Assessment-Insulin Resistance (≥2.5), and Quantitative Insulin Sensitivity Check Index (<0.33). Total body fat, estimated (Est.) VAT, and corrected Est. VAT (corrected for body weight) were significantly increased (P = 0.0001) in both obese and nonobese PCOS women when compared to those of their age- and BMI-matched controls. However, corrected Est. VAT (corrected for body weight) was not significantly different between obese and nonobese PCOS women.Conclusion:Both obese and nonobese PCOS women when compared with their age- and BMI-matched controls were metabolically worse and had more visceral adiposity. Nonobese PCOS poses similar risk as that of obese PCOS in having similar amount of VAT (corrected for body weight).

Upregulation of complement system factors are reported to be increased in polycystic ovary syndrome (PCOS) and may be due to obesity and insulin resistance rather than inherently due to PCOS. We directly compared complement factors from an obese, insulin-resistant PCOS population to a nonobese, non-insulin-resistant PCOS population in a proteomic analysis to investigate this. Plasma was collected from 234 women (137 with PCOS and 97 controls) from a biobank cohort and compared to a nonobese, non-insulin-resistant population (24 with PCOS and 24 controls). Slow off-rate modified aptamer (SOMA) scan plasma protein measurement was undertaken for the following complement system proteins: C1q, C1r, C2, C3, C3a, iC3b, C3b, C3d, C3adesArg, C4, C4a, C4b, C5, C5a, C5b-6 complex, C8, properdin, factor B, factor D, factor H, factor I, Mannose-binding protein C (MBL), complement decay-accelerating factor (DAF) and complement factor H-related protein 5 (CFHR5). The alternative pathway of the complement system was overexpressed in both obese and nonobese PCOS, with increased C3 (p < 0.05) and properdin (p < 0.01); additionally, factor B increased in obese PCOS (p < 0.01). For inhibitors of this pathway, factor I was increased (p < 0.01) in both slim and obese PCOS, with an increase in CFHR5 and factor H in obese PCOS (p < 0.01). Complement factors iC3b, C3d and C5a, associated with an enhanced B cell response and inflammatory cytokine release, were increased in both slim and obese PCOS (p < 0.05). C3a and its product, C3adesArg, were both significantly elevated in nonobese PCOS (<0.01) but not altered in obese PCOS. Hyperandrogenemia correlated positively with properdin and iC3b in obese PCOS (p < 0.05) but not in nonobese PCOS. There was no association with insulin resistance. BMI correlated positively in both groups with factor B, factor H and C5a. Additionally, in obese PCOS, BMI correlated with C3d, factor D, factor I, CFHR5 and C5a (p < 0.05), and in nonobese PCOS, BMI correlated with properdin, iC3b, C3, C3adesArg, C3a, C4, C5, C5a and C1q. In obese controls, BMI correlated with C3, C3desArg, C3a, C3d, C4, factor I, factor B, C5a and C5, whilst in nonobese controls, BMI only correlated negatively with C1q. Comparison of nonobese and obese PCOS showed that properdin, C3b, iC3b, C4A, factor D, factor H and MBL differed. The upregulation of the alternative complement pathway was seen in nonobese PCOS and was further exacerbated in obese PCOS, indicating that this is an inherent feature of the pathophysiology of PCOS that is worsened by obesity and is reflected in the differences between the nonobese and obese PCOS phenotypes. However, the increase in the complement proteins associated with activation was counterbalanced by upregulation of complement inhibitors; this was evident in both PCOS groups, suggesting that insults, such as a cardiovascular event or infection, that cause activation of complement pathways may be amplified in PCOS.

Polycystic ovary syndrome (PCOS) is a prevalent condition in women of reproductive age. It is characterized by androgen excess and chronic anovulation. Some trace elements, macroelements, and heavy metals have been linked to pathophysiological mechanisms of PCOS .&#x0D; To study the alterations in the serum levels of the trace element manganese (Mn), some macroelements, magnesium(Mg) and calcium (Ca), and the heavy metals cadmium (Cd) and lead (Pb), in obese and non-obese PCOS patients; and the association of these alterations with some of the hormonal changes occurring in PCOS.&#x0D; The study was carried out at Kamal Al-Samarrai Hospital (Center for Infertility treatment and in vitro Fertilization "IVF") Baghdad- Iraq. Eighty-two women were enrolled in the study. Fifty-four of them were diagnosed by a specialist gynecologist as PCOS patients; they were subdivided into two subgroups according to their body mass index (BMI); twenty-seven obese PCOS patients with BMI &gt; 30 kg/m2, and another twenty seven non obese patients PCOS with BMI &lt;30 kg/m2. Whereas, twenty-eight apparently healthy women with regular menstruation and of comparable age, were selected to serve as control groups; they were subdivided into, fourteen obese women with BMI &gt; 30kg/m2, and fourteen non obese women with BMI &lt;30 kg/m2.&#x0D; Blood lead and cadmium levels were significantly higher in both of the obese and the non-obese PCOS groups, than in their corresponding control groups. While, serum magnesium, calcium and manganese levels were significantly lower in both of the obese and the non-obese PCOS groups, as compared to their corresponding control groups. The results revealed no significant difference in the levels of the measured elements, between the obese PCOS group and the non-obese PCOS group. The serum FSH levels was significantly lower in obese PCOS patients than in the obese and non-obese control groups. There was a positive correlation between blood lead and serum TSH levels in non-obese PCOS women; and between serum total testosterone and cadmium levels in obese PCOS women. Finally, there was negative correlation between serum magnesium and serum LH levels in non-obese PCOS women.&#x0D; the study has demonstrated higher blood levels of lead and cadmium; and lower serum levels of magnesium, calcium and manganese in PCOS groups than control subject. There were no significant differences between obese PCOS women and non-obese PCOS women in the levels of the studied hormones, elements and heavy metals.

BackgroundAndrosterone glucuronide (ADTG) concentrations have been suggested as a marker of the effects of androgens at the target tissue level. As the mechanism for hyperandrogenemia in obese and nonobese polycystic ovary syndrome (PCOS) may differ, this study compared the different androgen parameters in non-obese compared to obese women with PCOS, and in normal subjects.MethodsEleven non-obese and 14 obese women with PCOS were recruited and compared to 11 control women without PCOS. Total testosterone, dehydroepiandrosterone sulphate (DHEAS), ADTG, and androstenedione were analysed using gold standard tandem mass spectrometry, and the free androgen index (FAI) was calculated.ResultsTotal testosterone, ADTG and androstendione levels did not differ between non-obese (body mass index (BMI) ≤25 kg/m2) and obese PCOS (BMI >25 kg/m2) but all were significantly higher than for controls (p < 0.01). The ADTG to DHEAS ratio was significantly elevated 39 ± 6 (p < 0.01) in obese PCOS in comparison to non-obese PCOS and controls (28 ± 5 and 29 ± 4, respectively). The free androgen index (FAI) and insulin resistance (HOMA-IR) were significantly higher in obese PCOS compared to non-obese PCOS and controls (p < 0.01). DHEAS was significantly higher in the non-obese versus obese PCOS (p < 0.01). All androgen parameters were significantly lower and sex hormone binding globulin (SHBG) significantly higher in normal subjects compared to those with obese and non-obese PCOS.ConclusionsThe ADTG:DHEAS ratio was significantly elevated in obese PCOS compared to non-obese PCOS and controls suggesting that this may be a novel biomarker discriminatory for obese PCOS subjects, perhaps being driven by higher hepatic 5α reductase activity increasing ADTG formation in these women.

Background:Insulin resistance has an important role in pathophysiology of polycystic ovarian syndrome (PCOS). Yet there are certain controversies regarding the presence of insulin resistance in non-obese patients. Objective:The aim was to compare the insulin resistance and various endocrine and metabolic abnormalities in obese and non-obese PCOS women.Materials and Methods: In this cross-sectional study which was performed from 2007-2010, 115 PCOS patients, aged 16-45 years were enrolled. Seventy patients were obese (BMI ≥25) and 45 patients were non-obese (BMI <25). Presence of insulin resistance and endocrine-metabolic abnormalities were compared between two groups. Collected data were analyzed with SPSS version 16.0 and p<0.05 was considered as statistically significant. Results:There was no significant difference in presence of insulin resistance (HOMA-IR >2.3) between two groups (p=0.357). Waist circumference (p<0.001), waist/hip ratio (p<0.001), systolic (p<0.001) and diastolic (p<0.001) blood pressures, fasting blood sugar (p=0.003) and insulin (p=0.011), HOMA-IR (p=0.004), total cholesterol (p=0.001) and triglyceride (p<0.001) were all significantly higher in obese PCOS patients. There was no significant difference in total testosterone (p=0.634) and androstenedione (p=0.736) between groups whereas Dehydroepiandrotendione sulfate (DHEAS) was significantly higher in non-obese PCOS women (p=0.018). There was no case of fatty liver and metabolic syndrome in non-obese patients, whereas they were seen in 31.3% and 39.4% of obese PCOS women, respectively.Conclusion:Our study showed that metabolic abnormalities are more prevalent in obese PCOS women, but adrenal axis activity that is reflected in higher levels of DHEAS was more commonly pronounced in our non-obese PCOS patients.

BackgroundPolycystic ovary syndrome (PCOS) is characterized by reproductive disorder and increased risk of metabolic syndrome. This study aimed to assess the metabolic parameters in the cord blood of neonate of mothers with obese PCOS and comparison with non-obese PCOS and controls.MethodsThis retrospective cohort study was conducted in Arash and Kamali Hospital in 2017–2018. The biochemical test was conducted on 78 neonates from obese PCOS mothers, 78 neonates from non-obese PCOS mothers, and 78 neonates from healthy mothers. Finally, cord blood lipid profile and insulin and blood sugar were determined by specific kits. Correlations between variables were compared with chi-square, Mann-Whitney’s U, Kruskal-Wallis H tests and regression model by SPSS 23 and P < 0.05 was considered significant.ResultsTriglycerides (TG) and high-density lipoprotein cholesterol (HDL) were higher in cord blood of newborn of obese PCOS women than non-obese PCOS and controls (P = 0.02, P < 0.001, respectively). Also, the mean insulin was higher in cord blood of neonate of non-obese PCOS women than in obese PCOS and controls (12.26 ± 12.79 vs. 11.11 ± 16.51 vs. 6.21 ± 10.66, P = 0.01). But in the study, there was no significant difference between the mean of umbilical cord low-density lipoprotein cholesterol (LDL), total cholesterol and blood sugar in three groups. The logistic regression model showed that metabolic parameters were related to PCOS.ConclusionsIn the present study, there was a significant difference between the mean of umbilical cord HDL, cholesterol, and the insulin level in the three groups. But, there was no significant association between the mean of blood sugar, LDL, and TG in the groups. The metabolic disorder in PCOS might affect cord blood lipid and insulin and adulthood health.

The basic tenet of this investigation was that obesity is not a prerequisite in the development of polycystic ovary syndrome (PCOS), as indicated by the fact that 50% of PCOS women are not obese. Further, obesity itself is a disease entity with the common manifestation of insulin resistance/hyperinsulinemia with PCOS. Given recent evidence that insulin and GH may have gonadotropin-augmenting effects, we have determined the common and distinguishing features of neuroendocrine-metabolic dysfunctions of lean [body mass index (BMI), < 23 kg/m2] and obese (BMI, > 30 kg/m2) women with the classical form of PCOS. Insulin sensitivity, as determined by rapid i.v. glucose tolerance testing; 24-h dynamics of insulin/glucose levels, somatotropic [GH/GH-binding protein/insulin-like growth factor I (IGF-I)/IGF-binding proteins (IGFBP)], and LH axes; and their downstream effects on ovarian steroids were simultaneously assessed in eight lean PCOS and eight obese PCOS patients and an equal number of BMI-matched normal cycling controls. Our results show that insulin sensitivity was reduced 50% (P < 0.01) in lean PCOS from that in lean controls. There was a further decrease in obese controls (P < 0.01) and a 2-fold greater reduction (P < 0.001) in obese PCOS than in obese controls, suggesting that insulin resistance (IR) is a common lesion in PCOS, and that obesity contributes an additional component to IR in obese PCOS. Consistent with the degree of IR, the manifestation of compensatory hyperinsulinemia in lean PCOS was incipient, being evident only in response to meals (P < 0.05), and became overt during the 24-h fasting/feeding phases of the day in obese control (P < 0.001) with a 2- to 3-fold greater elevation (P < 0.001) in obese PCOS. An enhanced early insulin response to glucose occurs equally in obese control (P < 0.01) and obese PCOS (P < 0.05), but not in their lean counterparts. Considering the more profound IR and the associated hyperglycemia in obese PCOS, the magnitude of the early insulin release is inadequate, suggesting that beta-cell dysfunction exists in obese PCOS. Remarkable differences in the somatotropic axis were also observed; although 24-h GH pulse frequency and levels of IGF-I and IGFBP-3 were unaltered by either PCOS or obesity, the 24-h mean GH pulse amplitude was increased by 30% (P < 0.01) in lean PCOS in the presence of normal levels of high affinity GHBP and normal GH response to GHRH. In distinct contrast, the somatotropic axis in both obese control and obese PCOS was profoundly modified, with attenuation of GH pulse amplitude (P < 0.001) and GH response to GHRH (P < 0.001), resulting in a state of hyposomatotropinism with a more than 50% reduction (P < 0.001) of 24-h mean GH levels. In addition, GHBP levels were elevated 2-fold and were correlated inversely with GH (r = -0.81) and positively with insulin (r = 0.75) concentrations. IGFBP-I levels were suppressed in both obese groups, with a 4-fold greater reduction in obese PCOS than that in obese controls. Thus, the downstream effects of hyperinsulinemia on the somatotropic axis may include up-regulation of hepatic production of GHBP, suppression of IGFBP-1 (r = 0.82) and sex hormone-binding globulin (r = -0.69) levels, and a more than 3-fold increase in ratios of IGF-I/IGFBP-1 and estradiol-testosterone/sex hormone-binding globulin, thereby increasing their bioavailabilities. In contrast, LH pulsatility was unaffected by obesity alone. An accelerated LH pulse frequency was evident in both lean and obese PCOS (P < 0.001), whereas the mean 24-h LH pulse amplitude was increased in lean (P < 0.001), but not obese, PCOS patients. These events resulted in a 3-fold increase in 24-h mean LH levels in lean PCOS and a 2-fold increase in obese PCOS. Thus, increased LH pulse frequency and augmented LH response to GnRH are characteristic of PCOS, independent of obesity, and the presence of obesity in PCOS is associated with an attenuated LH pulse amplitude, not accounted f

Do women with PCOS have a unique predisposition to obesity?

Objectives: To explore an association between CAPN10, SNP-44 (rs2975760) with IR condition in women with PCOS.&#x0D; Methods: A study included 120 participants of which 68 women have PCOS subdivide according to their body mass index (BMI) into 45 obese (BMI≥30) and 23 non-obese (BMI&lt;30). The remaining 52 represent the control group who were apparently healthy women with normal weight and normal menstrual cycle. Patients with PCOS were selected from the Infertility Department, Gynecology and Obstetrics Teaching Hospital, Kerbala Health Directorate / Kerbala-Iraq between Nov., 2021 and June, 2022. Diagnosis of PCOS is based on 2 of 3 findings: oligo/anovulation, hyperandrogenism, polycystic ovaries in ultrasound (Rotterdam criteria). Patients were interviewed and examined for weight, height, waist circumference, and hip circumference. Venous blood samples were collected at 9 AM after an overnight fast. IR was assessed by calculating homeostatic model assessment of insulin resistance (HOMA-IR) using the formula (fasting glucose mg/dl x fasting insulin µU/ml)/405, taking normal value &lt;2.7. Genotypes of CAPN10, SNP-44 has been identified using Allele-specific polymerase chain reaction (AS-PCR) technique.&#x0D; Results: The prevalence of IR based on HOMA-IR was (80%) in obese PCOS and (48%) in non-obese PCOS women. CAPN10, SNP-44 has been reconstructed and analyzed in patients and controls. Genotypes of 45 obese PCOS subjects (TT, N=26; TC, N=12; and CC, N=7), 23 non-obese PCOS subjects (TT, N=15; TC, N=6; and CC, N=2) and control subjects (TT, N=39; TC, N=11; and CC, N=2) were identified. The genotype distribution was statistically different between obese PCOS women and controls (OR=5.25, P=0.048). The association of SNP-44 allele with IR status was detected. HOMA-IR was greater in CC (10.54 ± 1.29, 9.88 ± 1.41) than in TT (3.30 ± 1.52, P&lt;0.001; 2.82 ± 1.45, P&lt;0.001) and TC (3.76 ± 1.58, P&lt;0.001; 4.10 ±1.57, P&lt;0.05) in obese PCOS and non-obese PCOS subjects respectively.&#x0D; Conclusion: In obese PCOS, the C allele was associated with higher insulin secretion and HOMA-IR compared with the T allele. The increased HOMA-IR is an indicator of IR. In this scenario, the C allele might be involved in the pathophysiology of insulin resistance in PCOS.

Aim: The aim of this study is to compare the metabolic and endocrinal parameters between obese and nonobese polycystic ovarian syndrome (PCOS) women with normal controls. Materials and Methods: The study was a cross-sectional comparative study. One-hundred PCOS women were randomized into two groups: Group I obese (n = 50) and Group II nonobese (body mass index [BMI] cutoff <23 kg/m 2 ). Fifty non-PCOS normal weight women formed the control Group III. Metabolic parameters (lipid profile, blood sugar profile, and serum insulin) and endocrinal parameters (serum luteinizing hormone [LH], follicle-stimulating hormone, and testosterone) were compared between the three groups. Results: Mean age of all the groups was comparable. A significantly higher waist circumference was seen in Group I; however, waist-hip ratio (WHR) was comparable between obese and nonobese PCOS groups. Between Groups I and II, mean fasting blood sugar, mean values of impaired glucose tolerance (IGT), and clinical hyperandrogenism were statistically comparable. Degree of insulin resistance (IR) in Group I versus Group II (44% vs. 36%) and of metabolic syndrome in Group I (20%) versus Group II (8%) was statistically comparable. Degree of hypertension (P = 0.001), IGT (P = 0.001), and dyslipidemia were higher in nonobese PCOS group versus normal group. Mean values of serum LH, serum fasting insulin, and serum testosterone were significantly different in nonobese PCOS women when compared with normal. Prevalence of IR (36% vs. 8%; P < 0.01) and metabolic syndrome was significantly higher in nonobese PCOS than normal controls. Conclusion: PCOS per se has evolved as a risk factor for endocrinal and metabolic derangements irrespective of the BMI status. Prevalence of IR and metabolic syndrome is high in nonobese PCOS as compared to normal controls, risks being as high as that in obese PCOS.

Visceral adiposity index (VAI) is a proposed parameter to evaluate visceral obesity instead of waist circumference (WC) in patients with polycystic ovary syndrome (PCOS). We aimed to evaluate VAI levels in overweight and/or obese, and non-obese PCOS patients and investigate the association between metabolic and inflammatory parameters. Seventy-six PCOS patients between 18 and 40, and 38 age- and BMI-matched controls were enrolled into the study. Both PCOS groups and controls were classified into two subgroups according to body mass index (BMI) <25 and ≥25kg/m2. In PCOS patients, waist/hip ratio (WHR) (p=0.023), diastolic blood pressure (DBP) (p=0.001), insulin (p=0.011), homeostasis of model assessment (HOMA-IR) (p=0.006) and uric acid (UA) (p=0.002) were higher than controls. In overweight and/or obese PCOS group, DBP (p<0.001), insulin (p=0.002), HOMA-IR (p=0.001), triglyceride (p=0.015) and VAI (p=0.031) were higher than overweight and/or obese controls. In non-obese PCOS group, WHR (p=0.016), WC (p=0.030), DBP (p=0.010) and UA (p<0.001) were higher than non-obese controls. Similar VAI levels were found in all PCOS and non-obese PCOS subgroups than peer controls. Overweight and/or obese PCOS group had higher VAI levels than non-obese PCOS group (p<0.001). VAI levels were positively correlated with WHR, glucose, HOMA-IR, high-sensitive CRP and UA in PCOS group. In controls, VAI levels were positively correlated with WHR, insulin and HOMA-IR. We found that VAI levels were higher in overweight and/or obese PCOS patients compared to peer controls and non-obese PCOS patients, and associated with some metabolic and inflammatory parameters.

Hyperinsulinemia secondary to a poorly characterized disorder of insulin action is a feature of the polycystic ovary syndrome (PCO). However, controversy exists as to whether insulin resistance results from PCO or the obesity that is frequently associated with it. Thus, we determined in vivo insulin action on peripheral glucose utilization (M) and hepatic glucose production (HGP) with the euglycemic glucose-clamp technique in obese (n = 19) and nonobese (n = 10) PCO women and age- and body-composition-matched normal ovulatory women (n = 11 obese and n = 8 nonobese women). None had fasting hyperglycemia. Two obese PCO women had diabetes mellitus, established with an oral glucose tolerance test; no other women had impairment of glucose tolerance. However, the obese PCO women had significantly increased fasting and 2-h glucose levels after an oral glucose load and increased basal HGP compared with their body-composition-matched control group. There were statistically significant interactions between obesity and PCO in fasting glucose levels and basal HGP (P less than .05). Steady-state insulin levels of approximately 100 microU/ml were achieved during the clamp. Insulin-stimulated glucose utilization was significantly decreased in both PCO groups whether expressed per kilogram total weight (P less than .001) or per kilogram fat free mass (P less than .001) or when divided by the steady-state plasma insulin (l) level (M/l, P less than .001). There was residual HGP in 4 of 15 obese PCO, 0 of 11 obese normal, 2 of 10 nonobese PCO, and 0 of 8 nonobese normal women. The metabolic clearance rate of insulin did not differ in the four groups. We conclude that 1) PCO women have significant insulin resistance that is independent of obesity, changes in body composition, and impairment of glucose tolerance, 2) PCO and obesity have a synergistic deleterious effect on glucose tolerance, 3) hyperinsulinemia in PCO is not the result of decreased insulin clearance, and 4) PCO is associated with a unique disorder of insulin action.

Characteristics of Polycystic Ovarian Syndrome and Relationship with Ghrelin in Adolescents

Polycystic Ovary Syndrome (PCOS) was originally described as a syndrome of amenorrhea, hirsutism and obesity associated with enlarged polycystic ovaries. There is increased androgen level and in some, insulin resistance (IR). Etiological relationship of androgen excess and IR in PCOS is not established. Influence of obesity on PCOS is controversial. This study was designed to see the androgen and insulin status in PCOS among obese and non-obese patients. It was a case-control study. Of total 80 study subjects, 60 primary infertile women suffering from PCOS were cases (30 obese and 30 non-obese). Age and BMI matched 20 healthy women having normal menstrual cycles were controls (10 obese and 10 non-obese). Age range of all were 20-40 years. Fasting plasma glucose, fasting S. Insulin and free Testosterone were measured. Insulin resistance (IR) was assessed by fasting glucose to insulin ratio (&lt;4.5). Subjects with DM or known endocrine disorders that may be associated with abnormal S.Insulin or plasma glucose concentration were excluded. No significant difference of fasting plasma glucose between PCOS (obese or non-obese) and respective controls (P&gt;0.5, in each) were observed. Significant difference of fasting S. Insulin and testosterone were observed between PCOS (both obese and non-obese) and respective controls (P&lt;0.01 in each), but there was no significant difference between obese and non-obese PCOS (P&gt;0.05). There was no significant difference of S.Testosterone between obese and non-obese PCOS(P&gt;0.05). There was also no significant difference of IR between obese and non-obese PCOS, but the ratio was &lt;4.5 (indicating IR in both). There were no significant correlation of S.Insulin with Testosterone in any group of PCOS (obese and non-obese) (P&gt;0.05). Increased S.Insulin and Testosterone was seen in PCOS irrespective of BMI. Further studies with larger sample size is recommended to assess etiological relationship between insulin and testosterone in PCOS. DOI: http://dx.doi.org/10.3329/bjmb.v3i1.13801 Bangladesh J Med Biochem 2010; 3(1): 11-15

Polycystic Ovary Syndrome (PCOS) was originally described as a syndrome of amenorrhea, hirsutism and obesity associated with enlarged polycystic ovaries. There is increased androgen level and in some, insulin resistance (IR). Etiological relationship of androgen excess and IR in PCOS is not established. Influence of obesity on PCOS is controversial. This study was designed to see the androgen and insulin status in PCOS among obese and non-obese patients. It was a case-control study. Of total 80 study subjects, 60 primary infertile women suffering from PCOS were cases (30 obese and 30 non-obese). Age and BMI matched 20 healthy women having normal menstrual cycles were controls (10 obese and 10 non-obese). Age range of all were 20-40 years. Fasting plasma glucose, fasting S. Insulin and free Testosterone were measured. Insulin resistance (IR) was assessed by fasting glucose to insulin ratio (&lt;4.5). Subjects with DM or known endocrine disorders that may be associated with abnormal S.Insulin or plasma glucose concentration were excluded. No significant difference of fasting plasma glucose between PCOS (obese or non-obese) and respective controls (P&gt;0.5, in each) were observed. Significant difference of fasting S. Insulin and testosterone were observed between PCOS (both obese and non-obese) and respective controls (P&lt;0.01 in each), but there was no significant difference between obese and non-obese PCOS (P&gt;0.05). There was no significant difference of S.Testosterone between obese and non-obese PCOS(P&gt;0.05). There was also no significant difference of IR between obese and non-obese PCOS, but the ratio was &lt;4.5 (indicating IR in both). There were no significant correlation of S.Insulin with Testosterone in any group of PCOS (obese and non-obese) (P&gt;0.05). Increased S.Insulin and Testosterone was seen in PCOS irrespective of BMI. Further studies with larger sample size is recommended to assess etiological relationship between insulin and testosterone in PCOS. DOI: http://dx.doi.org/10.3329/bjmb.v3i1.13801 Bangladesh J Med Biochem 2010; 3(1): 11-15