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PubMed2005

Cardiovascular risk in women with polycystic ovarian syndrome (PCOS).

AIMS: Studies have suggested that polycystic ovary syndrome (PCOS) is associated with increased cardiovascular risk. The aim of this study was to examine cardiovascular risk profiles in women with PCOS compared with healthy age and weight matched control subjects using novel biochemical and biophysical markers. METHODS: After ethics committee approval, 11 women with PCOS and 12 controls were recruited (mean age, 32; SD, 6.5 years; mean body mass index (BMI), 33.1; SD, 5.9 kg/m2). Serum was analysed for lipid and lipoprotein profile (total and high density lipoprotein cholesterol, triglycerides, apolipoprotein B-100, apolipoprotein A1, lipoprotein (a)), and sialic acid, fibrinogen, homocysteine, and C reactive protein (CRP) concentrations. Endothelial function was also assessed by a standard venous occlusion plethysmography technique to measure reactive hyperaemic forearm blood flow (RH), and expressed as per cent increase from baseline. RESULTS: There were no significant differences in glucose, lipid, or lipoprotein concentrations between the two groups. Furthermore, sialic acid (PCOS: mean, 70.5; SD, 149 mg/litre; controls: mean, 71.3; SD, 112 mg/litre), fibrinogen (PCOS: mean, 3.1; SD, 1.0 g/litre; controls: mean, 3.3; SD, 0.7 g/litre), CRP (PCOS: mean, 4.6; SD, 4.2 mg/litre; controls: mean, 5.41 SD, 5.5 mg/litre), and RH (PCOS: mean, 158.7; SD, 135.5%; controls: mean, 200.1; SD, 114.2%) were similar. CONCLUSIONS: There were no differences in surrogate markers of the processes linked to enhanced cardiovascular risk between patients with PCOS and weight matched controls.

Adolescent↗
PubMed2004

Insulin resistance in the skeletal muscle of women with PCOS involves intrinsic and acquired defects in insulin signaling.

Insulin resistance in polycystic ovary syndrome (PCOS) is due to a postbinding defect in signaling that persists in cultured skin fibroblasts and is associated with constitutive serine phosphorylation of the insulin receptor (IR). Cultured skeletal muscle from obese women with PCOS and age- and body mass index-matched control women (n = 10/group) was studied to determine whether signaling defects observed in this tissue in vivo were intrinsic or acquired. Basal and insulin-stimulated glucose transport and GLUT1 abundance were significantly increased in cultured myotubes from women with PCOS. Neither IR beta-subunit abundance and tyrosine autophosphorylation nor insulin receptor substrate (IRS)-1-associated phosphatidylinositol (PI) 3-kinase activity differed in the two groups. However, IRS-1 protein abundance was significantly increased in PCOS, resulting in significantly decreased PI 3-kinase activity when normalized for IRS-1. Phosphorylation of IRS-1 on Ser312, a key regulatory site, was significantly increased in PCOS, which may have contributed to this signaling defect. Insulin signaling via IRS-2 was also decreased in myotubes from women with PCOS. In summary, decreased insulin-stimulated glucose uptake in PCOS skeletal muscle in vivo is an acquired defect. Nevertheless, there are intrinsic abnormalities in glucose transport and insulin signaling in myotubes from affected women, including increased phosphorylation of IRS-1 Ser312, that may confer increased susceptibility to insulin resistance-inducing factors in the in vivo environment. These abnormalities differ from those reported in other insulin resistant states consistent with the hypothesis that PCOS is a genetically unique disorder conferring an increased risk for type 2 diabetes.

Adult↗
PubMed2002

Decreased insulin receptor (IR) autophosphorylation in fibroblasts from patients with PCOS: effects of serine kinase inhibitors and IR activators.

Insulin resistance is characteristic of many patients with polycystic ovary syndrome (PCOS). Several studies have suggested that a decrease in insulin receptor (IR) autophosphorylation is a significant component of this resistance. In this study, we have used a highly sensitive ELISA to measure IR tyrosine phosphorylation in fibroblasts from patients with PCOS and healthy control women. After the stimulation of intact fibroblasts with insulin, IR tyrosine phosphorylation in cells from the PCOS patients was decreased by approximately 40% when compared with controls. However, when IR were first immunocaptured from fibroblasts and then stimulated with insulin, neither basal nor insulin-stimulated IR autophosphorylation was different between the two groups, suggesting that a factor independent of the IR was involved. To examine the role of increased serine kinase activity in decreased IR autophosphorylation in PCOS, fibroblasts from PCOS patients were pretreated with inhibitors of serine kinases before insulin stimulation. Pretreatment with H7, a nonspecific protein kinase inhibitor, completely reversed the decrease in insulin-stimulated IR autophosphorylation. Pretreatment with H89, an inhibitor of protein kinase A, partially reversed this function, whereas pretreatment with Gö6983, an inhibitor of protein kinase C, was without effect. We next studied the effects of two small molecule activators of the IR tyrosine kinase: TLK16998 and Merck L7. Both TLK16998 and Merck L7 were able to reverse the impaired insulin-stimulated IR autophosphorylation. In summary, a factor(s) extrinsic to the IR cause impaired IR signaling in fibroblasts from patients with PCOS. Reversal of the impaired IR signaling by inhibitors of serine kinase activity suggests that serine kinase-mediated pathways may be involved in the insulin resistance. Moreover, the observation that TLK16998 and Merck L7 improved IR tyrosine phosphorylation in fibroblasts from patients with PCOS suggests that specific pharmacological therapies might be developed to treat the insulin resistance in PCOS.

Adolescent↗
PubMed2005

Approach to adolescent polycystic ovary syndrome (PCOS) in the pediatric endocrine community in the U.S.A.

OBJECTIVE: Polycystic ovarian syndrome (PCOS) is the most common endocrinopathy in adult women, and is emerging as a common cause of menstrual disturbances in the adolescent population. Insulin resistance, which is considered one of its underlying causes, has increased substantially in the past decade, putting more adolescent girls at risk for PCOS and its complications. Our objective was to survey pediatric endocrinologists' approach to diagnosis and treatment of PCOS in the adolescent population, as there is presently no structured recommended approach to this emerging problem. DESIGN/METHODS: A questionnaire survey was sent to 839 members of the Lawson Wilkins Pediatric Endocrine Society (LWPES). A total of 176 (21%) responses was received and analyzed. REDULTS: The majority of the participants would consider initiating work-up in an adolescent with oligomenorrhea or secondary amenorrhea 12-24 months after menarche. The following work-up was selected as a baseline for a teenager with oligomenorrhea or secondary amenorrhea by more than 50% of participants: LH and FSH, total and free testosterone, prolactin, 17-OH-progesterone, DHEAS and glucose/insulin measurements. For treatment of PCOS, the majority of surveyed endocrinologists suggested estrogen/progesterone combination. Metformin was considered appropriate treatment in the general adolescent population with PCOS by 30% and in obese teenagers with PCOS by 68% of surveyed endocrinologists. CONCLUSIONS: Our findings indicate the trend among pediatric endocrinologists towards earlier work-up of menstrual irregularities in adolescents--unlike the traditional practice of waiting for 2 years after menarche. Most pediatric endocrinologists would consider evaluation for insulin resistance using glucose/insulin measurement, but only a small percentage considers performing OGTT in these patients. Even though using estrogen/progesterone combination is the preferred therapeutic approach, 30% of surveyed endocrinologists consider metformin therapy for the general adolescent population with PCOS, and 68% would consider using it in obese adolescents with PCOS.

Adolescent↗
PubMed1998

Adrenal androgenic response to 2-hour ACTH stimulation test in women with PCOS.

Adrenal function may be abnormal in women with polycystic ovary syndrome (PCOS). This study aims to evaluate adrenal steroid response to the adrenocorticotropic hormone (ACTH) stimulation test and to find out the effect of high serum testosterone levels on adrenal response. We have also investigated any subtle enzyme deficiency by extending blood sampling to 2 h with 30 min intervals following ACTH administration. Twenty-eight women with PCOS and 18 healthy controls without hirsutism and oligomenorrhea were included in the study. After determining their serum basal levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, dehydroepiandrosterone sulfate (DHEAS), 17-hydroxyprogesterone (17-OHP), and progesterone, ACTH stimulation test was performed. The change in serum 17-OHP and the summed rate of change in serum 17-OHP and progesterone levels were estimated and 95th percentile for each value was computed. Women with PCOS were heavier and more hirsute than controls (p < 0.01, p < 0.001, respectively). Serum basal LH, LH:FSH ratio, testosterone (p < 0.001, for all), DHEAS (p < 0.01), and 17-OHP (p < 0.05) were higher in women with PCOS. All of the 17-OHP measurements, including basal and each 30 min interval after the administration of ACTH, were higher in women with PCOS than those of healthy controls (p < 0.05, p < 0.002, p < 0.001, p < 0.015, p < 0.018, respectively). However, the incremental changes in serum 17-OHP30-0, 17-OHP60-0, 17-OHP90-0, 17-OHP120-0, and the summed rate of change in serum 17-OHP and progesterone in women with PCOS were not different from those in healthy controls. The incremental response in terms of serum progesterone, DHEAS, and testosterone levels to the ACTH stimulation test for each 30 min interval was not different in women with PCOS than in healthy controls. We were not able to show any critical value for serum basal testosterone and DHEAS levels that would effect response to ACTH stimulation in terms of 17-OHP levels. We have concluded that extending the duration of blood sampling up to 2 h has no advantage in evaluating adrenal steroid response to ACTH stimulation. Since serum 17-OHP levels remain within normal limits in response to ACTH stimulation, the origin of elevated serum basal 17-OHP levels may be polycystic ovaries. Elevated serum testosterone level does not have any adverse effect on adrenal function. Serum progesterone measurement seems to have no place in the diagnosis of 21-hydroxylase deficiency. Adrenal androgenic response to ACTH stimulation is normal in women with PCOS.

17-alpha-Hydroxyprogesterone↗
PubMed2006

Endometrium in PCOS: Implantation and predisposition to endocrine CA.

Polycystic ovarian syndrome (PCOS) is a common endocrinopathy characterized by oligo/anovulatiaon and elevated circulating androgens or evidence of hyperandrogenism after all known potential causes have been excluded. In addition, insulin resistance and accompanying hyperinsulinemia commonly occur in women with PCOS. There is increasing evidence that the endocrinologic and metabolic abnormalities in PCOS may have complex effects on the endometrium, contributing to the infertility and endometrial disorders observed in women with this syndrome. Androgen receptors and steroid receptor co-activators are over-expressed in the endometrium of women with PCOS. Also, biomarkers of endometrial receptivity to embryonic implantation-such as alpha(v)beta3-integrin and glycodelin-are decreased, and epithelial expression of estrogen receptor alpha (ERalpha) abnormally persists in the window of implantation in endometrium in women with PCOS. In addition to being responsive to the steroid hormones estradiol, progesterone, and androgens, the endometrium is also a target for insulin, the receptor for which is cyclically regulated in normo-ovulatory women. In vitro, insulin inhibits the normal process of endometrial stromal differentiation (decidualization). In addition, insulin-like growth factors (IGFs) and their binding proteins are regulated in and act on endometrial cellular constituents, and hyperinsulinemia down-regulates hepatic IGFBP-1, resulting in elevated free IGF-I in the circulation. Thus, elevated estrogen (without the opposing effects of progesterone in the absence of ovulation), hyperinsulinemia, elevated free IGF-I and androgens, and obesity all likely contribute to endometrial dysfunction, infertility, increased miscarriage rate, endometrial hyperplasia, and endometrial cancer common in women with PCOS. The potential mechanisms underlying these disorders, specifically in women with PCOS, are complex and await additional transdisciplinary research for their complete elucidation.

Abortion, Spontaneous↗
PubMed2001

Polycystic ovarian syndrome (PCOS) and insulin resistance.

OBJECTIVES: Polycystic ovary syndrome (PCOS) presents a high risk of developing type 2 diabetes mellitus. We studied a group of women with PCOS and evaluated this defect in insulin action. METHODS: The study population consisted of nine PCOS women, six obese type 2 diabetic patients, and five controls whose body mass index (BMI) was similar to that of the nine PCOS women. The 75-g oral glucose tolerance test (OGTT) and the hyperinsulinemic euglycemic glucose clamp test were performed. Clinical characteristics and the metabolic profiles, including the insulin sensitivity index (ISI), were compared. RESULTS: PCOS women showed significantly elevated insulin responses during OGTT, but their blood glucose levels were comparable with the controls. The subjects with PCOS had more insulin resistance than the other groups. There was no difference among the groups in terms of clinical characteristics and metabolic profiles, except age, luteinzing hormone (LH), testosterone, and sex hormone binding globulin (SHBG). CONCLUSION: We conclude that PCOS women have significant insulin resistance which is independent of adiposity.

Adult↗
PubMed2004

PCOS: a diagnostic challenge.

Useful research and diagnostic criteria for PCOS arose from a conference in 1990, whereby PCOS could be defined by: (i) clinical and/or biochemical hyperandrogenism, (ii) chronic anovulation, and (iii) exclusion of related disorders. The presence of "polycystic ovaries" was not included in this definition, which created significant concern since many women with PCOS have polycystic ovaries on ultrasound, and conversely women with this ovarian morphology have a higher prevalence of androgen excess and insulin resistance. More recently, at an expert meeting in 2003 in Rotterdam, it was recommended that PCOS be defined when at least two of the following three features were present, after exclusion of other aetiologies: (i) oligo- or anovulation, (ii) clinical and/or biochemical hyperandrogenism, or (iii) polycystic ovaries. These newer criteria effectively create additional phenotypes of PCOS (e.g. women with hyperandrogenism and polycystic ovaries but normal ovulatory function, and women with ovulatory dysfunction and polycystic ovaries but no clinical or biochemical evidence of hyperandrogenism). It remains to be demonstrated whether these phenotypes actually represent patients with PCOS. Nonetheless, the trend towards the use of uniform diagnostic criteria in studies of PCOS will increase the comparability and potentially the value of published research.

Female↗
PubMed2001

Lipids and lipoprotein subfractions in women with PCOS: relationship to metabolic and endocrine parameters.

OBJECTIVE: Women with polycystic ovary syndrome (PCOS) exhibit an abnormal lipoprotein profile, characterized by raised concentrations of plasma triglyceride, marginally elevated low density lipoprotein (LDL)-cholesterol, and reduced high density lipoprotein (HDL)-cholesterol. However, a normal LDL-cholesterol level may be misleading since LDL exists as subpopulations of particles differing in size and atherogenic potential. Smaller LDL particles are more atherogenic and high concentrations often occur in association with elevated circulating triglyceride concentrations (but frequently normal total LDL-cholesterol), increased hepatic lipase activity (HL) and insulin resistance. Information on LDL subclasses and HL activity in women with PCOS is sparse. The aim of this study was to determine the concentrations of small, dense LDL (LDL-III) in women with PCOS relative to body mass index (BMI)-matched controls. We also examined the association of lipoprotein subfraction concentrations with endogenous sex hormone concentrations, since existing literature suggested that androgens up-regulate and oestrogens down-regulate HL activity, a key determinant of LDL subfraction distribution. DESIGN: Cross sectional study. PATIENTS: Fifty-two women with oligomenorrhoea and polycystic ovaries determined by ultrasound and BMI matched women with normal menstrual rhythm (NMR) and normal ovarian appearances (n = 14) were recruited from gynaecology clinics. Anthropometric data and fasting blood samples were obtained for metabolic, hormonal and LDL subfraction estimation and a heparin provocation test was used to estimate HL activity. RESULTS: Subjects with PCOS demonstrated higher waist:hip ratio (WHR), testosterone, triglyceride, VLDL-cholesterol concentrations, and HL activity (P < 0.05), whereas SHBG concentrations were significantly lower than controls. PCOS women had higher concentrations (38.0 vs. 25.0 mg/l; P = 0.026) and proportions (12.8 vs. 8.2%; P = 0.006) of small, dense LDL (LDL III), relative to controls. Within the PCOS group, plasma triglyceride and HL activity were the strongest univariate predictors of LDL III mass. They remained as independent predictors in multivariate analysis, and together accounted for 37% of its variability (P = 0.0002). Independent predictors of plasma triglyceride and HL in turn, were measures of fat distribution (waist circumference or WHR) and fasting insulin concentration. Serum testosterone concentration was not associated either in univariate or multivariate analysis with any of the measured lipid, lipoprotein or subfraction parameters, nor with HL activity in the women with PCOS. CONCLUSION: We conclude that women with polycystic ovary syndrome have increased hepatic lipase activity and mass and percentage of small, dense low density lipoprotein relative to body mass index-matched controls with normal menstrual rhythm and normal ovaries. Further, these metabolic perturbances appear related more closely to adiposity/insulin metabolism than to circulating androgen levels.

Adult↗
PubMed2002

Clinical manifestations and insulin resistance (IR) in polycystic ovary syndrome (PCOS) among South Asians and Caucasians: is there a difference?

OBJECTIVE: Polycystic ovary syndrome (PCOS) is more prevalent in South Asian women residing in the UK than in Caucasians. Insulin resistance (IR) is central to the pathogenesis of PCOS, while type 2 diabetes is commoner in South Asians. We aimed to determine a possible ethnic difference in the clinical and biochemical characteristics of South Asian vs. Caucasian women with PCOS. PATIENTS AND DESIGN: A case-control cross-sectional observational study of consecutive women with anovular PCOS (47 South Asians, 40 Caucasians) and their age-matched controls (11 South Asians and 22 Caucasians). MEASUREMENTS: Index subjects: a questionnaire-based interview on clinical symptoms and family history; anthropometric measurements, clinical observations of the presence and degree of acne, hirsutism and acanthosis nigricans; transvaginal pelvic ultrasound; biochemical analyses of fasting blood sugar, fasting plasma insulin, fasting lipids, testosterone, and SHBG concentrations. CONTROL GROUP: age- and weight-matched unrelated women from the same ethnic backgrounds without PCOS seeking treatment for male infertility were studied by similar methods to those used with the index subjects. RESULTS: South Asians with PCOS presented at a younger age (age 26 +/- 4 vs. 30.1 +/- 5 years, P = 0.005). Body mass index (BMI) and waist : hip ratios were similar in the two affected cohorts. More South Asians had oligomenorrhoea commencing at a younger age. Hirsutism (Ferriman Gallwey score 18 vs. 7.5, P = 0.0001), acne, acanthosis nigricans and secondary infertility were significantly more prevalent in South Asians. The fasting glucose was similar (4.52 +/- 0.08 vs. 4.62 +/- 0.09 mmol/l, P = 0.25), the fasting insulin higher (89.4 +/- 8.9 vs. 48.6 +/- 4.8 pmol/l, P = 0.0001) and insulin sensitivity (IS) lower (0.335 +/- 0.005 vs. 0.357 +/- 0.002, P = 0.0001) among South Asians. Serum SHBG was significantly less in South Asians (35 +/- 3.3 vs. 55 +/- 9.4 nmol/l, P = 0.02), while serum testosterone was similar (2.69 +/- 0.11 vs. 2.64 +/- 0.13 nmol/l, P = 0.37). CONCLUSIONS: We conclude that South Asians with anovular PCOS seek treatment at a younger age, have more severe symptoms, and have higher fasting insulin concentrations and lower insulin sensitivity than Caucasians.

Adult↗
PubMed2005

Endometrial fluid visualized through ultrasonography during ovarian stimulation in IVF cycles impairs the outcome in tubal factor, but not PCOS, patients.

BACKGROUND: The aim of the present study was to examine the impact of the presence of endometrial fluid (seen through ultrasound) on the outcome of IVF cycles and its association with the aetiology of infertility, in tubal and polycystic ovary syndrome (PCOS) cases specifically. METHODS: We retrospectively evaluated the charts of all PCOS and tubal factor infertility patients that underwent IVF between June 1, 2001 and May 31, 2002. Twenty-four PCOS and 14 tubal factor infertility patients in whom endometrial fluid was detected were compared with 94 PCOS and 160 tubal factor patients whose stimulation cycles did not show any fluid collection. The main outcome measures were implantation and pregnancy rates. RESULTS: Implantation rates were lower in the tubal factor patients in the presence of endometrial fluid (6.12% and 21.4%, respectively) in comparison with all other tubal factor infertile patients in whom no fluid accumulation inside the cavity was detected. In PCOS cycles there was no significance in patients with presence of endometrial fluid in comparison with the all other PCOS cycles without any fluid accumulation. CONCLUSIONS: When fluid collection inside the endometrial cavity is first seen during ovarian stimulation of PCOS patients undergoing IVF, embryo transfer can be performed safely if the fluid has disappeared and not returned by the day of embryo transfer. However, in tubal factor cycles one should think of either cancellation of the cycle or cryopreservation of all embryos.

Adult↗
PubMed2006

Adiponectin and resistin in PCOS: a clinical, biochemical and molecular genetic study.

BACKGROUND: We conducted a cross-sectional case-control study to evaluate the possible involvement of adiponectin and resistin in the pathogenesis of polycystic ovary syndrome (PCOS). METHODS: Seventy-six PCOS patients and 40 non-hyperandrogenic women matched for BMI and degree of obesity were included. Serum adiponectin and resistin levels, anthropometrical and hormonal variables, the 45 T-->G and 276 G-->T polymorphisms in the adiponectin gene, and the -420 C-->G variant in the resistin gene, were analysed. RESULTS: Serum adiponectin concentrations were reduced in PCOS patients compared with controls (P = 0.038) irrespective of the degree of obesity, whereas serum resistin levels were increased in overweight and obese women compared with lean subjects (P = 0.016), irrespective of their PCOS or controls status. The adiponectin and resistin polymorphisms were not associated with PCOS and did not influence serum levels of adiponectin, resistin and other clinical and hormonal variables. In a multiple regression model, the waist-to-hip ratio, free testosterone levels and age, but not insulin resistance, were the major determinants of hypoadiponectinaemia. CONCLUSIONS: PCOS patients present with hypoadiponectinaemia, in relation with abdominal adiposity and hyperandrogenism. Our present results suggest that hyperandrogenism and abdominal obesity, by reducing the serum levels of the insulin sensitizer adipokine adiponectin, might contribute to the insulin resistance of PCOS.

Adiponectin↗
PubMed2001

Defects in insulin receptor signaling in vivo in the polycystic ovary syndrome (PCOS).

Women with polycystic ovary syndrome (PCOS) are insulin resistant secondary to a postbinding defect in insulin signaling. Sequential euglycemic glucose clamp studies at 40 and 400 mU. m(-2). min(-1) insulin doses with serial skeletal muscle biopsies were performed in PCOS and age-, weight-, and ethnicity-matched control women. Steady-state insulin levels did not differ, but insulin-mediated glucose disposal was significantly decreased in PCOS women (P < 0.05). Insulin receptor substrate (IRS)-1-associated phosphatidylinositol 3-kinase (PI 3K) activity was significantly decreased in PCOS (n = 12) compared with control skeletal muscle (n = 8; P < 0.05). There was no significant difference in the abundance of IR, IRS-1, or the p85 regulatory subunit of PI 3K in PCOS (n = 14) compared with control (n = 12) muscle. The abundance of IRS-2 was significantly increased (P < 0.05) in PCOS skeletal muscle, suggesting a compensatory change. We conclude that there is a physiologically relevant defect in insulin receptor signaling in PCOS that is independent of obesity and type 2 diabetes mellitus.

Adult↗
PubMed1990

The role of inhibin in women with polycystic ovary syndrome (PCOS).

Human follicular fluids from normal women and from women with polycystic ovary syndrome (PCOS) were collected at various stages of the menstrual cycle, and inhibin and steroid contents were determined by rat anterior pituitary cell monolayer bioassay system and specific RIAs, respectively. Inhibin contents in viable follicles were significantly higher than those in atretic and in cystic follicles. Preovulatory and luteal phase follicles had lower inhibin levels than viable follicles in normal women. A significant inverse correlation was found between inhibin contents and androstenedione to estrogen ratios. The inhibin contents in PCOS follicles were not significantly different from those of viable follicles of normal women at the early follicular phase, but they were significantly higher than in atretic follicles. Since PCOS ovaries often contain more antral follicles than normal ovaries, it could be that this potential source of inhibin may be greater than in normal ovaries. Furthermore, 9 out of 10 follicles in any ovary of normal women are atretic and contribute less inhibin production, whereas PCOS ovaries contain many follicles capable of secreting considerable amounts of inhibin. Therefore, PCOS ovaries totally may secrete more inhibin than normal ovaries. This higher potency of PCOS ovaries to secrete inhibin along with higher serum estrogen levels may be responsible for the disparity between basal LH and FSH levels in PCOS.

Animals↗
PubMed1990

Impaired glucose tolerance in patients with polycystic ovary syndrome (PCOS).

Fasting insulin concentration and the insulin response to an oral glucose tolerance test were measured in 15 women with polycystic ovary syndrome (PCOS) and 6 weight-matched normal women. The fasting insulin concentrations were not increased in PCOS in comparison to normal women. Insulin response to an oral glucose test was significantly decreased (p less than 0.05) in PCOS at 30 min, although 63% of these women had mild impairment of glucose tolerance. The glucose response did not differ between the obese PCOS patients and those with nonobesity. No correlations were demonstrated between the fasting serum insulin concentrations and insulin response at 30 min, and both androgens and the luteinizing hormone. These findings suggest that (1) hyperinsulinemia is not a feature of PCOS in Japan; (2) only obese PCOS patients have a tendency of abnormalities in insulin secretion; (3) it is evident that PCOS represents an inadequately characterized disorder of insulin action and a novel paradigm in which to investigate the relationship between reproductive functions and carbohydrate metabolism.

Adult↗
PubMed2006

Insulin resistance in PCOS.

Polycystic ovary syndrome (PCOS) is the commonest endocrinopathy affecting women of reproductive age, manifested with a variety of clinical signs, none of which is pathognomonic. The association of insulin resistance and reproductive abnormalities with clinical hyperandrogenism in a woman was first demonstrated by Achard and Thiers in the "diabetes of bearded woman." The link of PCOS with insulin resistance was subsequently established by clinical studies characterizing the profound insulin resistance in obese and lean PCOS patients. Insulin resistance, hyperinsulinemia, and beta-cell dysfunction are very common in PCOS, but are not required for the diagnosis. The numerous in vivo and in vitro data supporting the central role of insulin resistance in the pathogenesis of PCOS found a broad clinical application in the management of the syndrome, where the regulation of cycle abnormalities and the facilitation of pregnancy in obese PCOS patients was assisted by co-administration of agents such as the well-known insulin sensitizers. The documentation of the presence of insulin resistance contributed substantially to unravel several metabolic components present in the syndrome. Today our knowledge about PCOS appears to have broader health implications and to have profoundly altered our view of the gravity of this condition.

Diabetes Mellitus, Type 2↗
PubMed2006

Oxidised low-density lipoprotein concentration - early marker of an altered lipid metabolism in young women with PCOS.

OBJECTIVE: Women with polycystic ovary syndrome (PCOS) are assumed to be at increased risk for cardiovascular diseases. This study examined the variations in oxidised low-density lipoprotein (OxLDL) concentration in relation to insulin levels in young women with PCOS. DESIGN: Cross-sectional clinical study in tertiary cares research hospitals. A total of 179 women with PCOS (79 overweight) and 56 age- and body mass index-matched controls were examined. METHODS: Blood samples were collected in follicular phase of the cycle for the basal glucose, total-, high-density lipoprotein-cholesterol (HDL-C) and LDL-cholesterol, OxLDL, triglycerides, apolipoprotein-A1 (Apo-A1) and B (Apo-B), lipoprotein (a), insulin, testosterone and sex hormone-binding globulin (SHBG). Homeostatic model index (HOMA) and free androgen index (FAI) were determined. RESULTS: Overweight and normal weight women with PCOS had higher concentrations of OxLDL than their control counterparts (P = 0.007 and 0.003 respectively). Both the basal insulin (P = 0.003) and HOMA values (P < 0.001) were significantly higher in overweight than normal weight patients. Testosterone and FAI were higher in patients than in the respective controls (P < 0.001). The only independent predictor of increased OxLDL concentration in normal weight patients was Apo-B-to-Apo-A1 ratio (P < 0.001, odds ratio (OR) 6.1; 95% confidence interval (CI) 2.3-16.4), while in obese PCOS, it was total cholesterol-to-high-density lipoprotein cholesterol ratio (P < 0.001, OR 2.8; 95% CI 1.6-4.9). CONCLUSION: Young normal weight and overweight PCOS women have similarly increased OxLDL levels. Our results may indicate the presence of primary alteration in lipid metabolism in patients with PCOS. To answer the question whether the alteration in LDL particle size can by itself pose a higher cardiovascular risk, a careful follow-up of these women is needed.

Adult↗
PubMed2001

Cardiovascular risk in adolescent and young adult obese females with polycystic ovary syndrome (PCOS).

Women with polycystic ovary syndrome (PCOS) could have associated risk for cardiovascular disease. The aim of the present study was to investigate the relationship between age and metabolic factors on cardiovascular risk in obese women with PCOS. Obese patients with PCOS were divided into an adolescent group (n=11; age 16.90 +/- 0.45 yr; BMI 35.04 +/- 1.70 kg/m2), and an adult group (n=18; age 29.66 +/- 1.31; BMI 34.57 +/- 1.46). We determined basal values of glucose, insulin, lipid and fibrinolytic parameters from blood samples taken in all patients and matched controls. Significantly different concentrations between the groups with PCOS were obtained for glucose, total cholesterol, triglycerides, LDL-cholesterol and Apo-B. Elevated concentrations of insulin (20.63 mU/l), both insulin sensitivity indexes--G:I ratio (7.52 mg/10(-4) U) and HOMA model (4.11 mmol/l x U/l(2))--and PAI-1 (5.49 U/ml) were obtained in the adolescent group with PCOS compared to controls, with further increase in the adult group with PCOS. It seems that the youngest obese population with PCOS represents a cohort with potential cardiovascular disease in adulthood.

Adolescent↗