[Polycystic ovary syndrome (PCOS)].
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Adult↗
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Lecturing on polycystic ovary syndrome (PCOS)
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Androgens↗
Glucose intolerance, insulin resistance, and hyperandrogenemia in first degree relatives of women with polycystic ovary syndrome.
Polycystic ovary syndrome (PCOS) is associated with hyperinsulinemia, insulin resistance (IR), increased risk of glucose intolerance, and type 2 diabetes. Family studies have indicated a genetic susceptibility to PCOS. The aims of this study were 1) to assess glucose tolerance status, gonadotropins, and androgens in first degree relatives of patients with PCOS; and 2) to assess IR in normal glucose tolerant (NGT) family members. One hundred two family members of 52 patients with PCOS [Mothers(PCOS) (n = 34; mean age, 46.5 yr; mean body mass index (BMI), 28.8 kg/m(2)), Fathers(PCOS) (n = 24; mean age, 50.4 yr; mean BMI, 27.5 kg/m(2)), Sisters(PCOS) (n = 19; mean age, 25.1 yr; mean BMI, 22.9 kg/m(2)), and Brothers(PCOS) (n = 25; mean age, 23.7 yr; mean BMI, 22.5 kg/m(2))] and 82 unrelated healthy control subjects without a family history of diabetes or PCOS (4 age- and weight-matched subgroups, i.e. Control(MothersPCOS), Control(FathersPCOS), Control(SistersPCOS), and Control(BrothersPCOS)) were studied. Glucose and insulin (at baseline and during a 75-g, 2-h oral glucose tolerance test) were measured. IR was assessed by fasting insulin (FI), fasting glucose to insulin ratio (FGI), homeostatic model assessment (HOMA IR), and area under the curve for insulin during the oral glucose tolerance test (AUC(insulin)) in NGT Mothers(PCOS), Fathers(PCOS), Sisters(PCOS), Brothers(PCOS), and matched control subgroups. Including the prestudy-diagnosed 3 mothers and 2 fathers with diabetes, diabetes and impaired glucose tolerance (IGT) were noted in 16% and 30% of Mothers(PCOS) and 27% and 31% of Fathers(PCOS), respectively. There was no diabetes in Sisters(PCOS) and Brothers(PCOS). IGT was found in 5% of Sisters(PCOS). Impaired fasting glucose was found in 3% of Mothers(PCOS) and 4% of Brothers(PCOS). The analysis of NGT family members showed that Mothers(PCOS) had higher FI (P < 0.05), HOMA IR (P < 0.05), and AUC(insulin) (P < 0.01) and lower FGI (P < 0.05) than Control(MothersPCOS), whereas all IR parameters were comparable between Fathers(PCOS) and their matched control subgroup. Sisters(PCOS) had higher FI (P < 0.05), HOMA IR (P < 0.01), and AUC(insulin) (P < 0.05) and lower FGI (P < 0.01), and Brothers(PCOS) had higher AUC(insulin) (P < 0.01) than their matched control subgroups, respectively. Mothers(PCOS) had higher testosterone levels than Control(MothersPCOS) (P < 0.01 and P < 0.05 for pre- and postmenopausal women, respectively). Sisters(PCOS) had higher LH (P < 0.01), testosterone (P < 0.001), androstenedione (P < 0.01), and dehydroepiandrosterone sulfate (P < 0.05) levels than Control(SistersPCOS). There was no difference in gonadotropin and androgen levels in Fathers(PCOS) compared with Control(FathersPCOS) or in Brothers(PCOS) compared with Control(BrothersPCOS). Our results suggest that 1) first degree relatives of patients with PCOS may be at high risk for diabetes and glucose intolerance; 2) NGT female family members have insulin resistance; and 3) mothers and sisters of PCOS patients have higher androgen levels than control subjects. We propose that the high risks of these impairments warrant screening in first degree relatives of patients with PCOS.
Adult↗
Insulin, somatotropic, and luteinizing hormone axes in lean and obese women with polycystic ovary syndrome: common and distinct features.
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
Adolescent↗
Phenotypic variation in hyperandrogenic women influences the findings of abnormal metabolic and cardiovascular risk parameters.
In hyperandrogenic women, several phenotypes may be observed. This includes women with classic polycystic ovary syndrome (C-PCOS), those with ovulatory (OV) PCOS, and women with idiopathic hyperandrogenism (IHA), which occurs in women with normal ovaries. Where other causes have been excluded, we categorized 290 hyperandrogenic women who were seen consecutively for this complaint between 1993 and 2004 into these three subgroups. The aim was to compare the prevalence of obesity, insulin resistance, and dyslipidemia as well as increases in C-reactive protein and homocysteine in these different phenotypes with age-matched ovulatory controls of normal weight (n = 85) and others matched for body mass index (BMI) with women with C-PCOS (n = 42). Although BMI affected fasting serum insulin and the Quantitative Insulin-Sensitivity Check Index, these markers of insulin resistance were greatest in C-PCOS (n = 204), followed by OV-PCOS (n = 50) and then IHA (n = 33). Androgen levels were similar in OV-PCOS and IHA but were higher in C-PCOS, whereas gonadotropins were similar in all groups. Lipid abnormalities were highest in C-PCOS and OV-PCOS and were normal in IHA. C-reactive protein was elevated in C-PCOS and OV-PCOS but not IHA. Homocysteine was elevated only in C-PCOS. Overall, the prevalence of obesity (BMI > 30) was 29% in C-PCOS, 8% in OV-PCOS, and 15% in IHA and insulin resistance (Quantitative Insulin-Sensitivity Check Index < 0.33) was 68% in C-PCOS, 36% in OV-PCOS, and 26% in IHA. The prevalence of having at least one elevated cardiovascular risk marker was 45% in C-PCOS 38% in OV-PCOS and was not increased on IHA (6%). These results suggest that among hyperandrogenic women the prevalence of abnormal metabolic and cardiovascular risk parameters is greatest in C-PCOS, followed by OV-PCOS and then women with IHA. Moreover, in that in OV-PCOS and IHA, ages and weights were similar yet the prevalence of metabolic and cardiovascular risk was greater in OV-PCOS, the finding of polycystic ovaries may be a significant modifying factor.
Body Mass Index↗
Elevated serum levels of tumor necrosis factor alpha in normal-weight women with polycystic ovary syndrome.
Since an increase in tumor necrosis factor alpha (TNFalpha) expression has been associated with insulin resistance, this study was undertaken to determine the status of circulating TNFalpha and the relationship of TNFalpha with insulin levels, body weight, or both in women with polycystic ovary syndrome (PCOS). Fasting serum samples were analyzed in 34 subjects with PCOS, of whom 22 were obese (body mass index [BMI]>27 kg/m2), and in 40 normal control women, of whom 20 were obese. Women with PCOS exhibited a significantly (P<.02) higher mean serum TNFalpha concentration compared with the controls. The serum TNFalpha level and BMI were directly correlated in women with PCOS (r=.48, P<.005) and highly correlated in controls (r=.78, P<.001). When subjects were classified by body weight, the mean serum TNFalpha concentration was significantly (P<.001) elevated in normal-weight women with PCOS compared with normal-weight controls. On the other hand, mean serum TNFalpha concentrations in obese women with PCOS and obese controls were similar and significantly (P<.02) higher than in normal-weight women with PCOS. A direct correlation between serum fasting insulin and TNFalpha was evident in controls (r=.35, P<.03), but not in women with PCOS. However, in the subgroup of obese women with PCOS, fasting insulin directly correlated (r=.49, P<.03) with TNFalpha and the median fasting serum insulin concentration was significantly (P<.05) higher compared with the level in normal-weight women with PCOS and all controls. Fasting insulin and TNFalpha were no longer correlated in controls as a group and in obese women with PCOS when controlling for body weight. Serum TNFalpha did not correlate with luteinizing hormone (LH), testosterone (T), or dehydroepiandrosterone sulfate (DHEAS) in women with PCOS. However, serum insulin was significantly correlated (r=.49, P<.0004) with T and the BMI exhibited a trend for correlation with serum T (r=.33, P=.05) in women with PCOS. Finally, the mean serum LH concentration was significantly (P<.02) higher in normal-weight women with PCOS versus obese women with PCOS, and serum LH levels exhibited a trend for an inverse correlation with the BMI (r=.31, P=.09) in women with PCOS. We conclude that (1) serum TNFalpha is increased in normal-weight women with PCOS and is even higher in obese individuals regardless of whether they have PCOS; (2) factors other than obesity are the cause of elevated serum TNFalpha in normal-weight women with PCOS; and (3) whereas increased circulating TNFalpha may mediate insulin resistance in obesity, which may in turn promote hyperandrogenism in obese women with PCOS, it remains to be demonstrated whether this is also the case in normal-weight women with PCOS.
Adult↗
[Study on the relationship between serum adiponectin and insulin resistance in women with polycystic ovary syndrome].
OBJECTIVE: To study the relationship between serum adiponectin and insulin resistance in women with polycystic ovary syndrome (PCOS). METHODS: Forty women with PCOS and twenty five healthy women were divided into PCOS obese group [body weight index (BMI) > or = 25kg/m(2)], PCOS non-obese group (BMI < 25 kg/m(2)) and control group. There are 19 cases in PCOS obese group and 21 cases in PCOS non-obese group, 9 cases in obese control group and 16 in non-obese control group. Serum adiponectin levels of the four groups were detected by enzyme linked immunosorbent assay (ELISA) method, insulin by electrochemiluminescence immunoassay method, blood sugar by glucose oxidation enzyme method, tumor necrosis factor-alpha (TNF-alpha) by radioimmunoassay. Insulin sensitivity index (ISI) was calculated. RESULTS: (1) Serum adiponectin levels of PCOS obese group was (1.6 +/- 0.5) mg/L, of PCOS non-obese group was (3.0 +/- 0.6) mg/L. Their values were lower than obese control group (3.2 +/- 0.3) mg/L, and non-obese control group (4.9 +/- 0.5) mg/L (P < 0.05). (2) Fasting insulin levels of PCOS obese group was (17 +/- 6) mU/L, PCOS non-obese group was (14 +/- 6) mU/L. They were higher than obese control group (10 +/- 3) mU/L, and non-obese control group (7 +/- 3) mU/L (P < 0.05). (3) Fasting blood sugar level was (5.2 +/- 0.7) mmol/L in PCOS obese group, in PCOS non-obese group was (5.1 +/- 0.6) mmol/L, in obese control group was (5.4 +/- 0.5) mmol/L, and non-obese control group (4.8 +/- 0.6) mmol/L, without marked difference among four groups. (4) TNF-alpha levels of PCOS obese group was (1.32 +/- 0.14) microg/L, of PCOS non-obese group was (1.02 +/- 0.12) microg/L. They were higher than obese control group (0.93 +/- 0.15) microg/L, and non-obese control group (0.63 +/- 0.18) microg/L (P < 0.05). (5) ISI of PCOS obese group was -4.5 +/- 0.3, PCOS non-obese group was -4.1 +/- 0.4. Their values were lower than obese control group -3.6 +/- 0.3, and non-obese control group (-3.1 +/- 0.4) (P < 0.05). Serum adiponectin levels of the women with PCOS were correlated negatively with BMI (r = -0.56, P < 0.05), and correlated positively with ISI (r = 0.49, P < 0.05). CONCLUSION: Serum adiponectin levels of women with PCOS is decreased compared with healthy women, particularly in obese women with PCOS. The decrease is correlated with ISI.
Adiponectin↗
Gene by environment interaction effects on the metabolic subtype of Polycystic Ovary Syndrome in Hispanic Community Health Study/Study of Latinos.
Polycystic Ovary Syndrome (PCOS) is a common polygenic endocrine disorder that is heterogenous in clinical presentation across genetic ancestry groups. PCOS is characterized by an array of symptoms such as hyperandrogenism, impaired mental health, and metabolic dysregulation. Studying the interaction of environmental factors (such as diet, physical activity, anxiety, and depression) with genetic variants on PCOS and its subtypes in populations with high cardiometabolic burden, e.g., Hispanic/Latinas, could aid in unraveling pathophysiological and genetic pathways through which PCOS functions. We sought to study gene by environment interactions with PCOS and its metabolic subtype (mPCOS) in a sample of US Hispanic/Latina female adults from the Hispanic Community Heath Study/Study of Latinos. In this large community-based study, we derived PCOS using self-reported condition and menstrual cycle information. We classified females with PCOS as having mPCOS if they had high metabolic impairment (fasting glucose, fasting insulin, or body mass index higher than the 75th percentile). There were 451 individuals with PCOS and 221 of them had mPCOS in our sample. We found that PCOS and mPCOS were significantly associated with hyperglycemia and high triglycerides in this population. While a polygenic risk score derived in European ancestry did not generalize to Hispanic/Latina females with PCOS, we identified the best proxy genetic variants in this population in known PCOS regions and investigated their interactions with four environment variables (diet, physical activity, anxiety and depression). Associations with known PCOS loci were generalized in our study at STAG3L4 and CACNA1G genomic regions. We observed GxE interactions between variants in/near three genes and physical activity on PCOS and mPCOS, including FGGY, FAT1, and PTHLH. Additionally, we noted interactions between diet and a variant in FANCC on PCOS, and diet and a variant near CMAS on both PCOS and mPCOS. We also detected GxE interactions between anxiety and depression and a variant in FGGY on PCOS, and depression and a variant near FBP1 on mPCOS. Our results point to potential protective effects of physical activity in females with PCOS and could inform future research on the mitigating effects of lifestyle management on PCOS genetic risk in Hispanic/Latino populations.
GxE↗
Serum leptin levels in women with polycystic ovary syndrome: the role of insulin resistance/hyperinsulinemia.
Polycystic ovary syndrome (PCOS) is associated with chronic anovulation, hyperandrogenemia, insulin resistance (IR)/hyperinsulinemia, and a high incidence of obesity. Thus, PCOS serves as a useful model to assess the role of IR and chronic endogenous insulin excess on leptin levels. Thirty-three PCOS and 32 normally cycling (NC) women of similar body mass index (BMI) were studied. Insulin sensitivity (S(I)) was assessed by rapid ivGTT in a subset of 28 PCOS and 29 NC subjects; percent body fat was determined by dual-energy x-ray absorptiometry (DEXA) in 14 PCOS and 17 NC. Fasting (0800 h) and 24-h mean hourly insulin levels were 2-fold higher (P < 0.0001), and S(I) was 50% lower (P = 0.005) in PCOS than in NC, while serum androstenedione (A), testosterone (T), 17-alpha hydroxyprogesterone (17OHP), and estrone (E1) levels were elevated (P < 0.0001), and sex hormone-binding globulin (SHBG) levels were decreased (P < 0.01). Twenty-four hour LH pulse frequency, mean pulse amplitude, and mean LH levels were elevated in PCOS (P < 0.001) as compared with NC. Serum leptin levels for PCOS (24.1 +/- 2.6 ng/mL) did not differ from NC (21.5 +/- 3.5 ng/mL) and were positively correlated with BMI (r = 0.81) and percent body fat (r = 0.91) for the two groups (both P < 0.0001). Leptin levels for PCOS and NC correlated positively with fasting and 24-h mean insulin levels (r = 0.81, P < 0.0001 for both PCOS and NC) and negatively with S(I) and SHBG levels. Leptin concentrations for PCOS, but not NC, correlated positively with 24-h mean glucose levels and inversely with 24-h mean LH levels and 24-h mean LH pulse amplitude. Leptin levels were not correlated with estrogen or androgen levels for either PCOS or NC, although leptin levels were positively related to the ratios of E1/SHBG and E2/SHBG for both PCOS and NC and to the ratio of T/SHBG for PCOS only. In stepwise multivariate regression with forward selection, only 24-h mean insulin levels contributed significantly (P < 0.01) to leptin levels independent of BMI and percent body fat for both PCOS and NC. Given this relationship and the presence of 2-fold higher 24-h mean insulin levels in PCOS, the expected elevation of leptin levels in PCOS was not found. This paradox may be explained by the presence of adipocyte IR specific to PCOS, which may negate the stimulatory impact of hyperinsulinemia on leptin secretion, a proposition requiring further study.
Adipose Tissue↗
Neuropeptide Y, leptin, galanin and insulin in women with polycystic ovary syndrome.
It has been reported that polycystic ovary syndrome (PCOS) is very frequently associated with obesity, insulin resistance and hyperinsulinemia. However, metabolic disorders may lead to suppression of reproductive hormone secretion during undernutrition and in obesity. Some neuropeptides, such as neuropeptide Y (NPY) and galanin, modulate the control of appetite and play an important role in the mechanism of luteinizing hormone-releasing hormone (LHRH) secretion. NPY and galanin regulate appetite via both central and peripheral mechanisms. The interaction between central and peripheral signals for the control of food intake is due to leptin. Leptin can modulate the activity of NPY and other peptides in the hypothalamus that are known to affect eating behavior. In order to evaluate the relationship between NPY, galanin and leptin, 28 women with PCOS, 32 obese women (non-PCOS) and 19 lean healthy women (control group) were investigated. Obese women with PCOS were divided into two groups: PCOS (A) overweight (body mass index, BMI 26-30 kg/m2), and PCOS (B) obese (BMI 31-40 kg/m2). Plasma NPY, galanin and leptin concentrations were measured by radioimmunoassay. Plasma leptin levels in obese women with PCOS (groups A and B) were significantly higher than those in the control group (p < 0.05, p < 0.05, respectively). A significant positive correlation between plasma leptin and BMI in women with PCOS was found (r = 0.427, p < 0.01). A positive correlation was demonstrated between leptin and testosterone in PCOS (r = 0.461, p < 0.01). Plasma galanin concentrations in PCOS were higher than in the control group but the differences were not significant. Plasma NPY levels were significantly elevated in both non-obese (normal) and obese women with PCOS (group A) (p < 0.01, p < 0.005, respectively). However, in obese non-PCOS women plasma NPY levels gradually increased with increase in BMI. No significant correlations were found between galanin, NPY and percentage change in response of LH to LHRH, as well as between NPY and insulin, and galanin and testosterone. Plasma insulin concentrations in women with PCOS (group B) were significantly higher than in the control group (p < 0.001). Increased plasma NPY levels are found in both obese and non-obese women with PCOS. The increase in NPY is independent of the increase in BMI. In obese women with PCOS, plasma leptin is increased compared with control lean women. Serum insulin concentration is increased in obese women with PCOS. A positive correlation exists between leptin and BMI as well as between leptin and testosterone in women with PCOS. These results may suggest that the feedback system in the interaction between leptin and NPY is disturbed in PCOS.
Adolescent↗
[Exploration of the classification of polycystic ovarian syndrome].
OBJECTIVE: To investigate the clinical presentation, hormonal profile and metabolic abnormalities in subgroups of women with PCOS and explore a reasonable classification for PCOS. METHODS: A cross-sectional study of 192 women with PCOS (14 - 38 years of age) was performed. The patients were divided into 3 groups of A, B and C according to the revised 2003 consensus on diagnostic criteria and also divided into 2 groups according to body mass index (BMI): group A (n = 110), long term anovulation, clinical and biochemical evidence of high androgen level, ovary enlargement with its size larger than 10 ml or number of small follicles of 2 - 9 mm >or= 12 under ultrasound with exclusion of other diseases caused by high androgen; group B (n = 46), long term anovulation, clinical and biochemical evidence of high androgen level; group C (n = 36), long term anovulation, ovary enlargement with its size larger than 10 ml or number of small follicles of 2 - 9 mm >or= 12 under ultrasound with exclusion of other disease caused by high androgen; obesity PCOS group (OB-PCOS, n = 70), BMI >or= 25 (kg/m(2)); no obesity PCOS group (NOB-PCOS, n = 122), BMI < 25 (kg/m(2)). One hundred and four women with bilateral tubal block factor caused infertility served as control group. Anthropometric measurements, Ferriman Gallwey hirsutism scoring, presence of acne and acanthosis nigricans were noted. Hormonal profile was assessed by measuring follicle-stimulating hormone (FSH), luteinizing hormone (LH), free testosterone (FT), prolactin (PRL), sex hormone binding globulin (SHBG). The metabolic profile was investigated by measurements of oral glucose tolerance test (OGTT), serum lipid levels, including total cholesterol (Chol), triglycerides (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL). Hyperinsulinemia was estimated by measurement of fasting insulin (FINS) and insulin area under the curve (IAUC). The extent of insulin resistance (IR) and hyperandrogenism was estimated by homeostasis model assessment (HOMA) and free androgen index (FAI) respectively. RESULTS: (1) Clinical phenotypes: the presence of obesity was 36.4% (70/192), among which 80.0% (56/70) were central obesity. Higher rates of acanthosis nigricans were observed in OB-PCOS group (35.7%, 25/70) compared with NOB-PCOS group (7.4%, 9/122; P < 0.01). Waist to hip ratio (WHR) was lower in group C than those in groups A and B (P < 0.05). (2) Endocrinology: FAI level was higher in OB-PCOS group than in NOB-PCOS group (P < 0.01), whereas LH/FSH ratio was lower in OB-PCOS group compared with NOB-PCOS group (P < 0.01). FAI level was higher in groups A and B than in group C (P < 0.01). SHBG, LH/FSH ratio did not differ between groups A, B, and C. (3) Metabolism: the prevalence of IR was 43.2% (83/192). A higher prevalence was observed in group OB-PCOS (82.8%, 58/70) compared with group NOB-PCOS (20.5%, 25/122; P < 0.01). FINS, HOMA-IR, glucose area under the curve (GAUC), IAUC and TG were higher in group OB-PCOS than in group NOB-PCOS (P < 0.01), whereas HOMA-IR, lipid profile did not differ between groups A, B, and C. CONCLUSION: The classification according to the revised 2003 consensus on diagnosis reflects the basic characteristics of PCOS; while the classification based on obesity shows the severity of hyperandrogenism and degree of IR, and thus has substantial significance for evaluation of metabolic complications.
Adolescent↗
Comparison of clinical and laboratory characteristics of cases with polycystic ovarian syndrome based on Rotterdam's criteria and women whose only clinical signs are oligo/anovulation or hirsutism.
This study was an attempt to determine whether the hormonal and clinical profiles of polycystic ovarian syndrome (PCOS) or non-PCOS cases whose only admission signs were oligo/anovulation or hirsutism. This retrospective study comprised a total number of 118, age-matched, young Turkish women with initial admission signs and symptoms of menstrual disorders (MD) like oligo/anovulation or hirsutism. Of these, 66 cases were diagnosed as PCOS, based on 2003 Rotterdam criteria [presence of two of first three criteria such as oligo- and/or anovulation, signs of clinical hyperandrogenism (HA-c) and/or biochemical signs of hyperandrogenism (HA-b) and polycystic ovaries on ultrasonography after exclusion of specific identifiable disorders]. Fifty-two women were diagnosed as cases of oligo/anovulation or hirsutism before the era of PCOS Rotterdam's consensus criteria. These two PCOS and non-PCOS cases were evaluated in terms of body mass index (BMI), waist-to-hip ratio, serum FSH, LH, estradiol (E2), dehydroepiandrosterone sulphate (DHEAS), androstendione (A) 17 hydroxyprogesterone (17-HP), fasting insulin, C-peptide levels, sex hormone-binding globulin (SHBG) and finally, ultrasonographic ovarian morphology. PCOS cases with unilateral and bilateral polycystic ovarian morphology on ultrasound scan were analyzed based on Rotterdam criteria. No statistically significant difference was detected among two groups, in terms of BMI, waist-to-hip ratio, serum FSH, LH, E2, fasting insulin, C-peptide levels (P > 0.05). However, blood levels of DHEAS, A and 17-HP were higher, whilst SHBG levels were remarkably lower (P = 0.008) in PCOS cases. Among PCOS group, hormonal and clinical characteristics did not differ, irrespective or uni- or bilaterality of ovarian morphology on ultrasonographic scan. Percentages of cases with androgenic alopecia, oily skin/acnea and increased ovarian volume were higher in PCOS group; whereas Ferriman-Gallwey score >/= 8 were similar between two groups. Total but not free testosterone remained high in PCOS group (P < 0.01). In both PCOS and non-PCOS cases, a linear correlation was apparent between BMI and insulin levels (r (s )= 0.69 and 0.32, P < 0.05, respectively). Among PCOS group, MD + HA-b + HA-c (n = 40) was present in 60.6% of subjects, MD + HA-b (n = 12) in 18.2%, and MD + HA-c (n = 14) in 21.2%. The three phenotypes did not differ in mean BMI, waist-to-hip ratio and biochemical characteristics. To conclude, non-PCOS women with only sign or symptom of oligo/anovulation or hirsutism had a more favorable endocrine milieu. These cases should be followed in vigilance in an aim to confront the development of short- and long-term adverse effects of impending PCOS in the future. Furthermore, different phenotypes of PCOS cases were clinically or biochemically similar in characteristics.
Adult↗
The effect of sequential administration of octreotide alone and octreotide/growth hormone simultaneously on buserelin stimulated ovarian steroid secretion in women with polycystic ovary syndrome.
OBJECTIVE: GH increases oestradiol secretion and promotes oocyte development in women with polycystic ovary syndrome (PCOS). However, there are no data on ovarian androgen production after GH treatment. We have therefore assessed the effect of sequential treatment with a long-acting somatostatin analogue (octreotide) alone and octreotide/GH simultaneously on ovarian steroid levels in PCOS and non-PCOS normal women. PATIENTS: Twenty-six PCOS and 12 non-PCOS women, aged 18-35 years, were studied. Ten of the PCOS and six of the non-PCOS women received sequential treatment with octreotide alone and followed by octreotide + GH together, while another eight PCOS and six non-PCOS women received saline instead of octreotide-octreotide + GH. The remaining eight PCOS women received GH alone. DESIGN: The octreotide-octreotide + GH and saline studies lasted 12 days, the GH alone 7 days. Octreotide (100 micrograms, s.c., t.d.s.) was given from the 2nd to the 10th and octreotide + GH (4 IU, s.c. at 2300h) from the 7th to the 10th day of the study. The GH alone treatment was given from the 2nd to the 5th day. On the 1st day, two tests were performed: (1) an oral glucose tolerance test (OGTT, 75 g, orally) at 0830h and (2) a buserelin (long-acting GnRH agonist) test (100 micrograms, s.c.) at the end of the OGTT. Both tests were repeated on the 6th and 11th days in the octreotide-octreotide + GH or on the 6th day only in the GH alone study. MEASUREMENTS: Blood glucose, insulin (IRI), C-peptide and IGF-I (at time 0 only) were measured before glucose administration and at 30-minute intervals for 3 hours and LH, FSH, delta 4-androstenedione (delta 4A), testosterone (TT), free testosterone (FT) and oestradiol (E2) before buserelin and at 1,2,6,10,14 and 18 hours. RESULTS: Octreotide alone significantly reduced the basal IGF-I stimulated LH and both basal and stimulated IRI, delta 4A, TT, FT and E2 levels in all PCOS women tested. Both octreotide + GH and GH alone increased significantly the basal IGF-I and both basal and stimulated IRI and E2 levels in all PCOS women, while the basal and stimulated LH, delta 4A, TT and FT levels were completely unaffected. In contrast, octreotide-octreotide + GH treatment did not modify either basal or stimulated gonadotrophin or ovarian steroid levels in non-PCOS women. No changes in either basal or stimulated hormone levels were observed in those PCOS women who received saline. Although both basal and stimulated levels of all ovarian androgens were significantly reduced by octreotide-octreotide + GH treatment in PCOS women, they still remained significantly higher than in the non-PCOS women. CONCLUSIONS: The data show that (1) octreotide is a potent inhibitor of ovarian steroid secretion, (2) GH increases oestradiol secretion, possibly by stimulating ovarian aromatase activity, and (3) the combined treatment with octreotide and GH significantly improves ovarlan function in women with PCOS and may thus have important clinical implications for the management of infertile women with this syndrome.
Adolescent↗
Glucose intolerance, insulin resistance and cardiovascular risk factors in first degree relatives of women with polycystic ovary syndrome.
BACKGROUND: The aim of the present study was to evaluate insulin resistance (IR), glucose tolerance status and cardiovascular risk factors in first degree relatives of patients with polycystic ovary syndrome (PCOS). METHODS: A total of 120 family members [Mothers(PCOS) (n = 40), Fathers(PCOS) (n = 38), Sisters(PCOS) (n = 25) and Brothers(PCOS) (n = 17)] of 55 patients with PCOS and 75 unrelated healthy control subjects without a family history of diabetes or PCOS (four age- and weight-matched subgroups, i.e. Control(Mothers), Control(Fathers), Control(Sisters) and Control(Brothers)) were studied. IR was assessed by homeostatic model assessment (HOMA IR), log HOMA, insulin sensivity index (ISI), the quantitative insulin sensitivity check index (QUICKI) and area under the curve for insulin during the oral glucose tolerance test (AUCI, AUCG) in with normal glucose tolerance (NGT) subjects and controls. Serum adiponectin, resistin, homocysteine and lipid levels were measured. RESULTS: The prevalence of any degree of glucose intolerance was 40% in Mothers(PCOS) and 52% in Fathers(PCOS). In total, six (15%) glucose tolerance disorders were identified in the Control(Mothers) and Control(Fathers) in first degree relatives of control subjects. The first degree relatives of PCOS patients had significantly higher serum fasting insulin, HOMA-IR, Log HOMA and AUCI levels in all subgroups than the control subjects. The control subjects had significantly elevated QUCKI, ISI levels and serum adiponectin levels compared to the first degree relatives of PCOS subjects in all subgroups. The serum Hcy and resistin levels increased significantly in both Fathers(PCOS) and Mothers(PCOS) groups but not Brothers(PCOS) and Sister(PCOS). CONCLUSION: The results of the present study support the finding that the first degree relatives of PCOS patients carry an increased risk of cardiovascular disease, as do PCOS patients.
Adiponectin↗
Effect of long-term treatment with metformin added to hypocaloric diet on body composition, fat distribution, and androgen and insulin levels in abdominally obese women with and without the polycystic ovary syndrome.
Abdominal obesity and hyperinsulinemia play a key role in the development of the polycystic ovary syndrome (PCOS). Dietary-induced weight loss and the administration of insulin-lowering drugs, such as metformin, are usually followed by improved hyperandrogenism and related clinical abnormalities. This study was carried out to evaluate the effects of combined hypocaloric diet and metformin on body weight, fat distribution, the glucose-insulin system, and hormones in a group of 20 obese PCOS women [body mass index (BMI) > 28 kg/m2] with the abdominal phenotype (waist to hip ratio >0.80), and an appropriate control group of 20 obese women who were comparable for age and pattern of body fat distribution but without PCOS. At baseline, we measured sex hormone, sex hormone-binding globulin (SHBG), and leptin blood concentrations and performed an oral glucose tolerance test and computerized tomography (CT) at the L4-L5 level, to measure sc adipose tissue area (SAT) and visceral adipose tissue area. All women were then given a low-calorie diet (1,200-1,400 kcal/day) alone for one month, after which anthropometric parameters and CT scan were newly measured. While continuing dietary treatment, PCOS women and obese controls were subsequently placed, in a random order, on metformin (850 mg/os, twice daily) (12 and 8, respectively) or placebo (8 and 12, respectively), according to a double-blind design, for the following 6 months. Blood tests and the CT scan were performed in each woman at the end of the study while they were still on treatment. During the treatment period, 3 women of the control group (all treated with placebo) were excluded because of noncompliance; and 2 PCOS women, both treated with metformin, were also excluded because they became pregnant. Therefore, the women cohort available for final statistical analysis included 18 PCOS (10 treated with metformin and 8 with placebo) and 17 control women (8 treated with metformin and 9 with placebo). The treatment was well tolerated. In the PCOS group, metformin therapy improved hirsutism and menstrual cycles significantly more than placebo. Baseline anthropometric and CT parameters were similar in all groups. Hypocaloric dieting for 1 month similarly reduced BMI values and the waist circumference in both PCOS and control groups, without any significant effect on CT scan parameters. In both PCOS and control women, however, metformin treatment reduced body weight and BMI significantly more than placebo. Changes in the waist-to-hip ratio values were similar in PCOS women and controls, regardless of pharmacological treatment. Metformin treatment significantly decreased SAT values in both PCOS and control groups, although only in the latter group were SAT changes significantly greater than those observed during the placebo treatment. On the contrary, visceral adipose tissue area values significantly decreased during metformin treatment in both PCOS and control groups, but only in the former was the effect of metformin treatment significantly higher than that of placebo. Fasting insulin significantly decreased in both PCOS women and controls, regardless of treatment, whereas glucose-stimulated insulin significantly decreased only in PCOS women and controls treated with metformin. Neither metformin or placebo significantly modified the levels of LH, FSH, dehydroepiandrosterone sulphate, and progesterone in any group, whereas testosterone concentrations decreased only in PCOS women treated with metformin. SHBG concentrations remained unchanged in all PCOS women; whereas in the control group, they significantly increased after both metformin and placebo. Leptin levels decreased only during metformin treatment in both PCOS and control groups. (ABSTRACT TRUNCATED)
Abdomen↗
Insulin, androgens, and obesity in women with and without polycystic ovary syndrome: a heterogeneous group of disorders.
OBJECTIVE: To analyze the correlations among insulin, androgens, body mass index (BMI), and other related metabolic anomalies in women with and without polycystic ovary syndrome (PCOS). DESIGN: Retrospective study of normal and obese women with and without PCOS. SETTING: Gynecologic endocrinology units of Elche, San Juan, and Alicante Hospitals and Hormone Laboratory at Alicante University Hospital ("Miguel Hernández" University). PATIENT(S): A total of 212 women were studied: 137 with PCOS and 75 without PCOS. INTERVENTION(S): BMI, gonadotropins, insulin, androgens (T, androstenedione, DHEAS), 17alpha-hydroxyprogesterone, sex hormone-binding globulin, and triglycerides were studied. Glycemia and insulin response to the tolerance test (GTT) with a 100-g oral glucose load were also assessed in 103 women. RESULT(S): A good correlation between insulin and BMI was found in normal and obese women without hormonal dysfunction and in patients with or without PCOS. Good correlations, although lower, between insulin and T, and BMI, insulin, and T with triglycerides were also found in patients with PCOS. These patients fell into clearly distinct categories: with or without insulin resistance and with or without obesity, but slim women with PCOS had insulin and metabolic variables similar to those without PCOS, and most obese women with PCOS were insulin-resistant and more hyperandrogenic and hypertriglyceridemic. CONCLUSION(S): Insulin, androgens, and BMI are related in women both with PCOS and without PCOS, especially in obese ones. Insulin and metabolic indices are similar in lean women with PCOS and those without PCOS, but obese women with PCOS are more insulin-resistant, hyperandrogenic, and hypertriglyceridemic. Three types of disorders can be distinguished: simple nonhyperandrogenic obesity, typical nonhyperinsulinemic PCOS, and insulin-resistant PCOS.
17-alpha-Hydroxyprogesterone↗
Plasma homocysteine in polycystic ovary syndrome: does it correlate with insulin resistance and ethnicity?
BACKGROUND: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and premature coronary artery disease (CAD). Hyperhomocysteinaemia is a recognized risk factor for atherosclerosis, particularly among migrant South Asians, and has recently been shown to be correlated positively with the degree of insulin resistance/hyperinsulinaemia. OBJECTIVES: To compare total plasma homocysteine (Hcy) in PCOS with controls from ethnic groups at high and low risk of insulin resistance. METHODS: Case control study of three ethnic groups, Sri Lankans (SL), British Asians (BA) and white Europeans (C), with and without PCOS at specialist centres in Sri Lanka and Yorkshire, UK. Fasting total plasma Hcy concentration was analysed by fluorescence polarization immunoassay and examined for any correlation with age, body mass index (BMI), central obesity, fasting insulin and insulin sensitivity [calculated by the Quantitative Insulin Sensitivity Check Index (QUICKI) method], lipids and testosterone in each ethnic group. RESULTS: Eighty SL with PCOS and 45 controls, 47 BA with PCOS and 11 controls, and 40 C with PCOS and 22 controls were studied. Both Asian groups with PCOS were younger than affected Europeans (P = 0.008). Sri Lankans with PCOS had significantly lower BMI values than other affected groups: mean +/- SEM (SL) 26.3 +/- 0.95; (BA) 30.59 +/- 7.54; (C) 32.1 +/- 5.95 kg/m2 (P = 0.006). However, waist : hip ratios (WHR) of Sri Lankans with PCOS were similar to others: mean +/- SEM (SL) 0.97 +/- 0.01 (BA) 1.04 +/- 0.02 (C) 0.92 +/- 0.01, P = 0.33. Mean plasma Hcy was significantly higher in all PCOS groups than in their ethnically matched controls (Student's t-test): (SL) 10.2 +/- 1.9 vs 9.0 +/- 3.8, P = 0.01; (BA) 7.9 +/- 1.9 vs 6.8 +/- 2.5, P < 0.0001; (C) 8.3 +/- 2.3 vs 6.8 +/- 1.5, P = 0.0007 micromol/l. Sri Lankans with PCOS had significantly greater Hcy concentrations than British Asians and Europeans with PCOS [P = 0.001; single-factor analysis of variance (anova)] and also significantly greater fasting insulin concentrations [(SL) 242.9 +/- 38.9; (BA) 89.4 +/- 8.9; (C) 48.6 +/- 4.8 pmol/l (P = 0.0003)] and significantly lower QUICKI [(SL) 0.308 +/- 0.004; (BA) 0.335 +/- 0.005; (C) 0.375 +/- 0.002 (P = 0.0007)]. Fasting plasma Hcy correlated best with fasting insulin (r = 0.56, P = 0.0001) and QUICKI (r =-0.53, P < 0.0001) in Sri Lankans with PCOS. Hcy in PCOS subjects from all three ethnic groups correlated significantly with fasting insulin following adjustment for age, BMI and WHR (r = 0.45, P = 0.0001), but this was not evident in the controls (r =-0.32, P = 0.1). CONCLUSIONS: Elevation of fasting plasma homocysteine in PCOS varies with ethnicity and correlates significantly with fasting insulin. High homocysteine in young Sri Lankans with PCOS has major implications for their long-term risk for atherosclerosis.
Adult↗
[Genetic aspects of polycystic ovary syndrome].
Polycystic ovary syndrome (PCOS) is a common heterogenous endocrine disorder associated with amenorrhoea (or oligomenorrhoea), hyperandrogenism, hirsutism, obesity, insulin resistance, and an approximately 7-fold increased risk of type 2 diabetes mellitus (NIDDM - non-insulin dependent diabetes mellitus). It is a leading cause of female infertility. The prevalence of PCOS among reproductive-age women has been estimated at 4%-12%. Familial aggregation of this syndrome is well established. There are also ethnic and racial variations in the prevalence of the syndrome and its symptoms. Multiple biochemical pathways have been implicated in the pathogenesis of PCOS. Several genes from these pathways have been tested include genes involved in steroid hormone biosynthesis and metabolism (StAR, CYP11, CYP17, CYP19 HSD17B1-3, HSD3B1-2), gonadotropin and gonadal hormones action (ACTR1, ACTR2A-B, FS, INHA, INHBA-B, INHC, SHBG, LHCGR, FSHR, MADH4, AR), obesity and energy regulation (MC4R, OB, OBR, POMC, UCP2-3), insulin secretion and action (IGF1, IGF1R, IGFBPI1-3, INS VNTR, IR, INSL, IRS1-2, PPARG) and many others. Most women with PCOS, both obese and lean, have a degree of insulin resistance. The minisatellite of insulin gene (INS VNTR), especially class III alleles and III/III genotypes might not only determine the predisposition to anovulatory PCOS but also the concomitant risk for development of type 2 diabetes. The function of the insulin receptor (IR) is probably normal in woman with PCOS. However abnormal serine phosphorylation in the receptor may impair signal transduction accounting for a post-binding defect in insulin action. Serine phosphorylation is also involved in the postranslational regulation of 17,20-lyase activity (CYP17). There may be a common aetiology for both insulin resistance and hyperandrogenism. Polymorphic alleles of both IRS-1 and IRS-2 (insulin receptor substrate 1 - 2), alone or in combination, may have a functional impact on the insulin-resistant component of PCOS. There is no evidence to suggest that follistatin gene polymorphisms play a role in the pathogenesis of insulin resistance in PCOS women. PCOS appears to be associated with the absence of the four-repeat-units allele in a polymorphic region of pentanucleotide (TTTTA)n repeats within CYP11A gene, which encodes cytochrome P450scc. It has been hypothesized that up-regulation of this enzyme could lead to increased androgen production. There is no evidence of any association of alleles of CYP19 gene (encoding cytochrome P450arom) with PCOS. Association exists between androgen receptor gene (AR) polymorphisms an androgens action in PCOS. Increased hirustism and decreased CAG repeat length within AR gene has been also demonstrated in women with normal testosterone levels. Expression of estrogen receptor (ERs) as well as 5-alpha-reeducates (SRD5A1-2 genes) activity was analysed in granulosa (GC) and theca cells (TC). The results of this study demonstrate that there are significant alterations in the expression of ERalpha and ERbeta in PCOS that may be related to abnormal follicular development. On the other hand elevated SRD5A activity in polycystic ovaries supported the hypothesis that 5-alpha-reduced androgens may play a role in the pathogenesis of the syndrome. The genetic aetiology of PCOS remains unknown. There are a number of interlinking factors that affects expression of PCOS. Single cause of PCOS is unlikely. Other possible mechanisms in pathogenesis of PCOS are discussed.
Diabetes Mellitus, Type 2↗