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PubMed1996

Beta-cell dysfunction independent of obesity and glucose intolerance in the polycystic ovary syndrome.

Several distinct groups of subjects at high risk to develop noninsulin-dependent diabetes mallitus (NIDDM) have been found to have insulin secretory defects when beta-cell function is assessed in the context of peripheral insulin sensitivity. We investigated this with a modified frequently sampled iv glucose tolerance test to determine acute insulin responses to glucose (AIRg) as well as insulin action by minimal model analysis in 28 women with polycystic ovary syndrome (PCOS; 15 obese and 13 nonobese) and 29 age- and weight-matched normal women (14 obese and 15 nonobese). No subject, PCOS or control, had fasting hyperglycemia, but seven PCOS women (six obese and one nonobese) had impaired glucose tolerance or NIDDM. The PCOS women had significantly decreased insulin sensitivity compared to the normal women (P < or = 0.001), and the obese women were less sensitive than the nonobese women (P < or = 0.001). The empiric measure of insulin release, AIRg, was significantly increased by obesity (P < or = 0.01), but not by PCOS. However, the disposition index (insulin sensitivity x AIRg) was significantly decreased by both PCOS (< or = 0.005) and obesity (< or = 0.005), suggesting that AIRg was inadequate for the degree of insulin resistance. When the PCOS women with impaired glucose tolerance or NIDDM were removed from the analysis, all of the reported PCOS-related changes in insulin action and secretion remained significant. We conclude that both obese and nonobese PCOS women have beta-cell dysfunction as well as insulin resistance. However, this was not associated with glucose intolerance in the majority of PCOS women.

Adult↗

PubMed1997

Determinants of abnormal gonadotropin secretion in clinically defined women with polycystic ovary syndrome.

UNLABELLED: Polycystic ovary syndrome (PCOS) is a heterogeneous disorder of reproductive age women characterized in its broadest definition by the presence of oligoamenorrhea and hyperandrogenism and the absence of other disorders. Defects of gonadotropin secretion, including an elevated LH level, elevated LH to FSH ratio, and an increased frequency and amplitude of LH pulsations have been described, but the prevalence of these defects in a large, unbiased population of PCOS patients has not been determined. Sixty-one women with PCOS defined by oligomenorrhea and hyperandrogenism and 24 normal women in the early follicular phase had LH samples obtained every 10 min for 8-12 h. Pool LH levels from the frequent sampling studies were within the normal range in the 9 PCOS patients (14.8%) who were studied within 21 days after a documented spontaneous ovulation. Excluding these post-ovulatory patients, 75.0% of the PCOS patients had an elevated pool LH level (above the 95th percentile of the normal controls), and 94% had an elevated LH to FSH ratio. In the anovulatory PCOS patients, pool LH correlated positively with 17-OH progesterone (R = 0.30, P = 0.03), but not with estradiol, estrone, testosterone, androstenedione, or DHEA-S. Pool LH and LH to FSH ratio correlated positively with LH pulse frequency (R = 0.40, P = 0.004 for pool LH, and R = 0.39; P = 0.005 for LH/FSH). There was also a strong negative correlation between pool LH and body mass index (BMI) (R = -0.59, P < 10(-5)). The relationship between BMI and LH secretion in the PCOS patients appeared to be strongest with body fatness, as pool LH was correlated inversely with percent body fat, whether measured by skinfolds (R = -0.61, P < 10(-5)), bioimpedance (R = -0.55, P < 10(-4)), or dual energy x-ray absorptiometry (DEXA) (R = -0.70, P = 0.001; n = 18 for DEXA only). By DEXA, the only body region that was highly correlated with pool LH was the trunk (R = -0.71, P = 0.001). The relationship between body fatness and LH secretion occurred via a decrease in LH pulse amplitude (R = -0.63, P < 10(-5) for BMI; R = -0.58, P < 10(-4) for bioimpedance; and R = -0.64, P = 0.004 for whole body DEXA), with no significant change in pulse frequency with increasing obesity (R = -0.17, P = 0.23 for BMI). IN CONCLUSION: 1) the prevalence of gonadotropin abnormalities is very high in women with PCOS selected on purely clinical grounds, but is modified by recent spontaneous ovulation; 2) the positive relationship between LH pulse frequency and both pool LH and LH to FSH ratio supports the hypothesis that a rapid frequency of GnRH secretion may play a key etiologic role in the gonadotropin defect in PCOS patients; 3) pool LH and LH pulse amplitude are inversely related to body mass index and percent body fat in a continuous fashion; and 4) the occurrence of a continuous spectrum of gonadotropin abnormalities varying with body fat suggests that nonobese and obese patients with PCOS do not represent distinct pathophysiologic subsets of this disorder.

Adolescent↗

PubMed1998

Mid-follicular phase pulses of inhibin B are absent in polycystic ovarian syndrome and are initiated by successful laparoscopic ovarian diathermy: a possible mechanism regulating emergence of the dominant follicle.

The hypothalamic pulse generator of GnRH is recognized to be central to ovulatory function as evidenced by the anovulation of women with hypogonadotrophic hypogonadism due to Kallmann's syndrome or severe anorexia nervosa. LH is released from the anterior pituitary in pulses, the frequency of which is closely entrained with those of GnRH. In contrast, secretion of FSH is influenced by a number of regulatory molecules, including GnRH, estradiol, inhibin, and activin. The close temporal relationship between changes in levels of inhibin B and FSH in the mid-follicular phase suggests that the release of inhibin B by the preovulatory follicle critically regulates pituitary FSH secretion. Polycystic ovarian syndrome (PCOS) is one of the most common endocrine disorders affecting ovulation, and abnormal ovarian morphology as detected by ultrasonography remains the most sensitive diagnostic marker for this disorder. The etiology of PCOS is unclear, but its effective treatment by both anti-estrogens and by exogenous FSH suggests that a primary disorder of FSH regulation may be central. To investigate the possible role of inhibin B in the pathology of PCOS, serum inhibin B levels were measured in 10 women with PCOS on cycle day 5 of a spontaneous or progestrogen-provoked bleed and compared with levels on cycle day 5 of 10 women with regular ovulatory cycles. The mean serum inhibin B levels in the PCOS patients were significantly higher at 248 (+/- 43.4) pg/mL compared with normal controls, 126 (+/- 18.6) pg/mL (P < 0.01). Ten women with clomiphene resistant PCOS and 5 normal controls consented to undergo serial blood sampling on cycle day 5. Time Series Analysis using a Fourier Transformation to analyze the power spectrum of the data revealed that in normal women there is a distinct periodicity in inhibin B levels with a clear peak detectable every 60-70 min (P < 0.05), whereas in women with ovulatory dysfunction due to PCOS, no such pattern of regular pulsatility was seen. Four women with PCOS whose anovulation was successfully treated with laparoscopic ovarian diathermy (LOD) underwent repeat venous sampling following LOD. Their serum inhibin B levels fell to the upper limit of the normal range (160 +/- 38.5) pg/mL, and pulsatility was initiated. It is possible that inhibin B pulses are being generated directly by the ovary in response to pulses of GnRH in the peripheral circulation, or indirectly in response to FSH pulses arising in the pituitary. The function of inhibin B pulses in the mid-follicular phase of the normal cycle remains to be elucidated, but the absence of the normal pulsatile pattern in women with PCOS, in conjunction with high basal levels of inhibin B arising from the multiple small follicles characteristic of the PCOS ovary, appears to reinforce the development of a large cohort of small, developmentally arrested, and ultimately atretic follicles in these patients. Initiation of normal inhibin B pulsatility by LOD in patients with polycystic ovaries appears to correlate with the post-operative onset of ovular cycles.

Diathermy↗

PubMed1999

Response of the pituitary-adrenal axis to hypoglycemic stress in women with the polycystic ovary syndrome.

The role of the adrenals in the polycystic ovary syndrome (PCOS) is debated. Both single steroid-converting enzyme abnormalities and increased adrenal activity have received support. The conventional Synacthen test using pharmacological doses of ACTH results in unphysiological levels of ACTH. Therefore, we used insulin-induced hypoglycemia (0.15 IU/kg BW) to asses the responses of ACTH, cortisol, pregnenolone, 17-hydroxypregnenolone, dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and androstenedione in 18 women with PCOS and in 17 normal women of similar age and body mass index. The blood glucose concentration at 30 min was 2 mmol/L or less in all women, i.e. well below the threshold of the hormonal counterregulatory response. The women with PCOS showed a lower ACTH response, expressed as the maximum increment above basal [mean (95% confidence interval): PCOS, 11.1 (6.9-15.3); controls, 19.9 (13.8-26) pmol/L; P < 0.05], but a quantitatively comparable [PCOS, 207.2 (148.5-266.5); controls, 167.1 (100.6-233.2) nmol/L; P = NS] and more prompt cortisol response than the controls (by chi2 test, P < 0.05), resulting in a higher molar ratio between the maximum increments of cortisol and ACTH [PCOS, 13.9 (8.7-19); controls, 8.8 (5.7-12); P < 0.05]. The women with PCOS did, however, show a more rapid decline in cortisol levels than the controls (P < 0.05 at 120 and 180 min). The responses of the androgens and intermediate adrenal steroids were similar in women with PCOS and controls. The findings suggest an adaptation to increased adrenal reactivity to endogenous ACTH in women with PCOS. Exposure to hypoglycemia as a model of stress was not followed by hypersecretion of adrenal androgens and revealed no signs of steroid enzyme disturbances in women with PCOS.

Adrenocorticotropic Hormone↗

PubMed2000

Differential activity of the cytochrome P450 17alpha-hydroxylase and steroidogenic acute regulatory protein gene promoters in normal and polycystic ovary syndrome theca cells.

17alpha-Hydroxylase (CYP17) expression in propagated theca cells isolated from the ovaries of women with polycystic ovary syndrome (PCOS) is persistently elevated, compared with theca cells isolated from normal ovaries. To investigate the mechanism for increased CYP17 messenger RNA accumulation in PCOS theca cells, we examined CYP17 and steroidogenic acute regulatory protein (StAR) promoter activities in normal and PCOS theca cells. Conditions were established to transiently transfect human theca cells with reporter gene constructs containing 5' truncations of the human CYP17 and StAR promoters. Cotransfection of a steroidogenic factor-1 expression plasmid was found to be required for detection of basal and forskolin-stimulated CYP17 promoter activity but not for StAR promoter activity. However, cotransfection with a steroidogenic factor-1 expression plasmid augmented both basal and forskolin-stimulated StAR promoter activity. CYP17 reporter activity was compared in theca cells isolated from normal and PCOS patients. Basal and forskolin-stimulated CYP17 promoter activity was 4-fold greater in PCOS cells than in theca cells isolated from normal ovaries. In contrast, StAR promoter activity, and the activity of a reporter construct containing three copies of a cAMP response element (3xCRE), were similar in normal and PCOS theca cells. The results of these studies document: 1) that basal and cAMP-dependent CYP17 gene transcription is increased in PCOS theca cells; 2) that there is differential regulation of promoters of genes required for steroidogenesis in PCOS theca cells; and 3) that passaged normal and PCOS theca cells provide a model system for studying tissue-specific regulation of genes encoding steroidogenic enzymes and identifying the molecular mechanisms involved in increased androgen production in PCOS.

Cells, Cultured↗

PubMed2003

Increased cytochrome P450 17alpha-hydroxylase promoter function in theca cells isolated from patients with polycystic ovary syndrome involves nuclear factor-1.

Cytochrome P450 17alpha-hydroxylase (CYP17) gene expression and androgen biosynthesis are persistently elevated in theca cells isolated from ovaries of women with polycystic ovary syndrome (PCOS). We previously reported that -235 to -109 bp of the CYP17 promoter confers increased CYP17 promoter function in PCOS theca cells. In this report, additional deletion and mutational analyses of the CYP17 promoter were performed to identify the sequences that contribute to increased CYP17 promoter function in PCOS theca cells. Results of these analyses established that augmented promoter function in PCOS theca cells results from preferentially increased basal regulation conferred by sequences between -188 and -147 bp of the CYP17 promoter. Scanning mutant analysis demonstrated that mutations within a 16-bp sequence, spanning -174 to -158 bp of the promoter, ablated increased basal CYP17 promoter function in PCOS theca cells. EMSA analysis demonstrated that the NF-1 family member, NF-1C, bound this sequence. Cotransfection of several NF-1C isoforms expressed in normal and PCOS cells repressed CYP17 promoter function. NF-1C protein and DNA binding were reduced in PCOS theca cell nuclear extracts, as compared with normal. Another NF-1C site between -102 and -90 bp of the promoter was also identified. However, mutation of this site had no effect on differential promoter function in PCOS theca cells. These studies demonstrate that 1) augmented CYP17 promoter function in PCOS theca cells results from increased basal regulation, and 2) diminished NF-1C-dependent repression may be one mechanism underlying increased basal CYP17 promoter activity and altered gene expression in PCOS theca cells.

Adult↗

PubMedDate not supplied

Overweight status of adolescent girls with polycystic ovary syndrome: body mass index as mediator of quality of life.

PURPOSE: Adolescent girls with polycystic ovary syndrome (PCOS) have significant disruption in health-related quality of life (HRQL) compared to their healthy peers, but it is unclear which aspects of the disorder have the greatest impact on these quality-of-life changes. Studies of adult women have indicated that weight status has a significant impact on subjective symptomatology; however, a similar effect of weight status on HRQL in adolescents with PCOS has not been established. This study evaluated the effect of body mass index (BMI) on quality-of-life disturbances in adolescent girls with PCOS. METHODS: Data were derived from the Adolescent PCOS Quality of Life Study, a cross-sectional study of healthy (n = 186) and PCOS-affected adolescent girls (n = 97). The study was conducted at an urban, hospital-based adolescent medicine clinical practice. Medical staff obtained anthropomorphic measurements. Participants in both groups completed the Child Health Questionnaire-Version CF-87 as a measure of HRQL. BMI was tested as a mediator of HRQL using bivariate analyses and multivariate linear regression models. RESULTS: The average BMI was 31.7 kg/m(2) (standard deviation [SD] = 8.4) for adolescents with PCOS and 23.5 kg/m(2) (SD = 4.2) for healthy adolescents. BMI was associated with PCOS status and HRQL. Girls with PCOS scored lower on the general health perceptions scale, physical functioning scale, family activities scale, and the general behavior scale and higher on the change in health in the last year subscale. When BMI was added to the multivariate linear regression models, coefficients were reduced on average by 3 points and became nonsignificant, indicating that the HRQL differences are mediated by the higher BMI. CONCLUSION: This study demonstrates that BMI is a primary mediator in the relationship between PCOS and the HRQL reductions experienced by girls with the disorder. Clinical interventions that effectively address weight issues in adolescents with PCOS may improve overall HRQL and other obesity-related clinical outcomes.

Adolescent↗

PubMed2004

Effect of adiponectin gene polymorphisms on circulating adiponectin and insulin resistance indexes in women with polycystic ovary syndrome.

BACKGROUND: We examined the possible association of adiponectin gene polymorphisms with polycystic ovary syndrome (PCOS) and their influence on serum adiponectin and insulin resistance indexes in Greek women with PCOS. METHODS: We genotyped samples from 100 women with PCOS characterized with respect to body mass index (BMI), glucose and insulin concentrations during an oral glucose tolerance test (OGTT), lipid profile, and serum adiponectin concentrations and from 140 healthy controls for the 45T>G and 276G>T polymorphisms in the adiponectin gene. RESULTS: The distributions of genotypes and alleles of both polymorphisms were no different in women with PCOS and controls, indicating that the individual polymorphisms are not associated with increased risk for PCOS. However, the two polymorphisms were found to be associated with insulin resistance indexes among women with PCOS and to influence adiponectin production. In particular, carriers of the TG genotype at position +45 had greater hyperinsulinemia, as estimated by the area under the curve for insulin (AUC(insulin)) during the OGTT, than those with the TT genotype (P <0.05), and this was independent of age and BMI. In addition, women with PCOS with the GG or GT genotypes at position +276 had a higher BMI (P = 0.01) and greater AUC(insulin) (P = 0.01) than carriers of the TT genotype. The latter genotype was found less frequently among overweight/obese women with PCOS than in normal-weight individuals (P = 0.002). In addition, the presence of the GG or GT genotype was associated with lower serum adiponectin than the TT genotype, independent of age, BMI, and insulin concentrations (P = 0.03). Serum adiponectin was negatively correlated with serum triglycerides and insulin resistance indexes and positively with HDL-cholesterol. CONCLUSIONS: Adiponectin gene polymorphisms at positions +45 and +276 are not associated with PCOS. However, these genomic variants may influence production of adiponectin and the metabolic variables related to insulin resistance/metabolic syndrome in patients with PCOS.

Adiponectin↗

PubMedDate not supplied

Early microvascular and macrovascular dysfunction is not accompanied by structural arterial injury in polycystic ovary syndrome.

OBJECTIVE: During the last decade cardiovascular risk factors and endothelial dysfunction have been shown to be present early in life in women with Polycystic Ovary Syndrome (PCOS). The aim of the present study was a global assessment of abnormalities in the arterial bed of young women with PCOS by non-invasive, reproducible methods. DESIGN: 27 women with PCOS and 27 control women of comparable age, body mass index and waist-to-hip ratio were studied. Macrovascular function was assessed by flow-mediated dilatation (FMD) on the brachial artery. Nitrate-induced dilatation (NID) was performed to exclude a vascular smooth muscle cells injury. Microvascular function was assessed by venous occlusion plethysmography studying forearm blood flow. Arterial structure was evaluated by ultrasonographic assessment of intima-media thickness (IMT) of the carotid artery. RESULTS: FMD values were lower in women with PCOS compared to controls (PCOS: 3.84+/-0.74% vs. controls: 9.83+/-0.97%, P<0.001), but no difference was observed in NID (PCOS: 16.59+/-1.84% vs. controls: 16.64+/-2.05%, P=0.98) values. The time required for reactive hyperemia to reach peak value, a plethysmography parameter, was longer in PCOS women (PCOS: 20.63+/-4.67 sec vs. controls: 10.38+/-5.11 sec, P=0.02). No difference was observed in the combined IMT among the studied groups (PCOS: 0.49+/-0.01 mm v.s. controls: 0.51+/-0.02 mm, P=0.19). CONCLUSIONS: Using non invasive methodologies endothelial dysfunction in the macrocirculation and early impairment in the microcirculation were demonstrated in young women with PCOS who had normal profile of glycemia, lipidemia and blood pressure, and no evidence of structural arterial impairment.

Adult↗

PubMed2002

A comparison between the effects of low dose (1 microg) and standard dose (250 microg) ACTH stimulation tests on adrenal P450c17alpha enzyme activity in women with polycystic ovary syndrome.

OBJECTIVE: Numerous studies have found elevated androgen production by the adrenal glands in patients with polycystic ovary syndrome (PCOS). However, the role and the mechanisms responsible for the adrenal androgen excess in women with PCOS are not well understood. DESIGN: Our aim was to compare 17-hydroxyprogesterone (17-OHP), androstenedione, dehydroepiandrosterone sulfate (DHEAS) and cortisol responses to a low dose (1 microg) ACTH stimulation test (LDT) with the responses to a standard dose (250 microg) ACTH stimulation test (SDT) in patients with PCOS. METHODS: Fifty women with PCOS (mean age 25.4+/-0.7 years) and 20 healthy women (mean age 27.3+/-2.2 years) were included in the study. The patients and controls underwent ACTH stimulation tests with 1 microg and 250 microg synthetic ACTH in the follicular phase of their cycles. Venous blood was drawn at 0, 30 and 60 min for determination of serum cortisol, 17-OHP, androstenedione and DHEAS levels. RESULTS: In PCOS subjects, peak and area under the curve (AUC) 17-OHP (9.3+/-0.3 nmol/l, 378.4+/-61 nmol/lx60 min), androstenedione (15.6+/-0.6 nmol/l, 806.4+/-52 nmol/lx60 min) and DHEAS (7.5+/-0.4 micromol/l, 385.6+/-25.5 micromol/lx60 min) responses to SDT were significantly higher than the levels in healthy women (respectively 5.7+/-0.3 nmol/l and 249.4+/-52.2 nmol/lx60 min for 17-OHP; 9.1+/-0.3 nmol/l and 413.7+/-31.6 nmol/lx60 min for androstenedione; 4.3+/-0.4 micromol/l and 224.9+/-24.5 micromol/lx60 min for DHEAS) (P<0.05). Peak and AUC cortisol responses to SDT were similar in PCOS and control subjects. Peak and AUC cortisol and 17-OHP responses to LDT in women with PCOS were similar to the values obtained in healthy women. Peak androstenedione (12.5+/-0.6 nmol/l) and peak (6.5+/-0.5 nmol/l) and AUC (336.3+/-22.4 micromol/lx60 min) DHEAS responses to LDT were significantly higher in women with PCOS. CONCLUSIONS: These results show that LDT is capable of revealing the adrenal hyperactivity in women with PCOS. Adrenal P450c17alpha enzyme dysregulation in PCOS is revealed by ACTH stimulation at a pharmacological dose (250 microg) but not by a physiological dose (1 microg). LDT is able to demonstrate adrenal hyperactivity characterized by an increase in DHEAS levels.

17-alpha-Hydroxyprogesterone↗

PubMed2004

Effects of metformin treatment on luteal phase progesterone concentration in polycystic ovary syndrome.

The causes of luteal phase progesterone deficiency in polycystic ovary syndrome (PCOS) are not known. To determine the possible involvement of hyperinsulinemia in luteal phase progesterone deficiency in women with PCOS, we examined the relationship between progesterone, luteinizing hormone (LH) and insulin during the luteal phase and studied the effect of metformin on luteal progesterone levels in PCOS. Patients with PCOS (19 women aged 18-35 years) were treated with metformin (500 mg three times daily) for 4 weeks prior to the test cycle and throughout the study period, and submitted to ovulation induction with clomiphene citrate. Blood samples were collected from control (N = 5, same age range as PCOS women) and PCOS women during the late follicular (one sample) and luteal (3 samples) phases and LH, insulin and progesterone concentrations were determined. Results were analyzed by one-way analysis of variance (ANOVA), Duncan's test and Karl Pearson's coefficient of correlation (r). The endocrine study showed low progesterone level (4.9 ng/ml) during luteal phase in the PCOS women as compared with control (21.6 ng/ml). A significant negative correlation was observed between insulin and progesterone (r = -0.60; P < 0.01) and between progesterone and LH (r = -0.56; P < 0.05) concentrations, and a positive correlation (r = 0.83; P < 0.001) was observed between LH and insulin. The study further demonstrated a significant enhancement in luteal progesterone concentration (16.97 ng/ml) in PCOS women treated with metformin. The results suggest that hyperinsulinemia/insulin resistance may be responsible for low progesterone levels during the luteal phase in PCOS. The luteal progesterone level may be enhanced in PCOS by decreasing insulin secretion with metformin.

Adolescent↗

PubMed2006

Diagnosis and management of polycystic ovary syndrome: a practical guide.

Polycystic ovary syndrome (PCOS) is a syndrome, which can be defined as a group of recognisable patterns of symptoms or abnormalities that indicate a particular medical situation. The current definition of PCOS requires the presence of two of the following three conditions: (i) oligo- and/or anovulation; (ii) clinical and/or biochemical signs of hyperandrogenism; and (iii) polycystic ovaries--and the exclusion of other aetiologies. It is generally accepted that the prevalence of PCOS is approximately 5-10%, and that of polycystic ovaries alone is 21-23%. Other features of PCOS are obesity, insulin resistance, impaired glucose tolerance and type 2 diabetes mellitus, dyslipidaemia, cardiovascular disease, obstructive sleep apnoea and infertility. An approach to a patient with possible PCOS should be directed towards making a diagnosis and screening for associated endocrine abnormalities. Therapeutic interventions are directed towards addressing the needs of the patient at present and towards preventing long-term complications of the syndrome. Body mass index, which is a primary mediator in the relationship between PCOS and health-related quality of life in obese PCOS adolescents, may play a similar role in other PCOS patients. Any intervention directed at reducing central obesity will not only improve quality of life but also correct hyperinsulinism and improve fertility and lipid and androgen profiles. It is also the only currently available intervention that can have a lifelong impact on reducing possible long-term complications of the syndrome. Lifestyle modification is the cardinal intervention. Pharmacological treatments are available for specific indications. Infertility can be treated with clomifene (clomiphene citrate), metformin, gonadotropins or surgery to the ovaries. Cyproterone (alone or in combination with ethinylestradiol) and spironolactone are the main drugs used in the treatment of hirsutism. Other drugs that can be considered include flutamide, ketoconazole and finasteride. Women with PCOS require ongoing surveillance to detect impaired glucose tolerance, hyperlipidaemia, endometrial hyperplasia and consequent complications. Obese women, in particular, require regular glucose tolerance testing because of the potential for rapid progression from normal to impaired glucose tolerance and diabetes. The focus of this article is the epidemiology, diagnosis and management of this common endocrine disorder. Diagnostic and co-morbid features are discussed separately to facilitate understanding of PCOS. Symptom-directed strategies, as well as short- and long-term goals of treatment, are outlined.

Female↗

PubMed2002

A unique defect in the regulation of visceral fat cell lipolysis in the polycystic ovary syndrome as an early link to insulin resistance.

The etiology of polycystic ovary syndrome (PCOS) is unknown. However, PCOS has a strong resemblance to the insulin resistance (metabolic) syndrome, where an increased rate of visceral fat cell lipolysis is believed to play a pathophysiological role. We hypothesized that primary defects in visceral lipolysis might also exist in PCOS. Ten young, nonobese, and otherwise healthy PCOS women were compared with 13 matched control women. In vitro lipolysis regulation and stoichiometric properties of the final step in lipolysis activation, namely the protein kinase A (PKA)-hormone sensitive lipase (HSL) complex, were investigated in isolated visceral (i.e., omental) fat cells. Body fat distribution and circulating levels of insulin, glucose, and lipids were normal in PCOS women. However, in vivo insulin sensitivity was slightly decreased (P = 0.03). Catecholamine-induced adipocyte lipolysis was markedly (i.e., about twofold) increased in PCOS women due to changes at the postreceptor level, although there was no change in the antilipolytic properties of visceral fat cells. Western blot analyses of visceral adipose tissue showed twofold increased levels of the catalytic and the regulatory Ialpha components of PKA. In contrast, the regulatory RIIbeta component of PKA was almost 50% decreased in visceral adipose tissue in PCOS women. Recent studies on genetically modified mice have shown that a similar transition in the regulatory PKA units induces an increased lipolytic response to catecholamines. Further analysis showed that the level of HSL-short, an enzymatically inactive splice form of HSL, was decreased in PCOS (P < 0.01). The altered lipolysis in PCOS is different from that observed in visceral fat cells in the insulin resistance syndrome that occurs at the level of adrenergic receptors. We concluded that increased catecholamine-induced lipolysis in visceral fat cells may be due to unique alterations in the stoichiometric properties of the adipose PKA-HSL holoenzymes. This could be an early and possibly primary lipolysis defect in PCOS.

Adipocytes↗

PubMed2000

[Obesity, arterial hypertension, metabolic disorders, and polycystic ovary syndrome].

OBJECTIVE: To determine the prevalence of central and general obesity, arterial hypertension, and alterations in cholesterol, triglycerids, glycaemia and uric acid levels in patients with PCOS and to compare them with women who do not present this syndrome. To establish the possible association of this with the PCOS. MATERIALS AND METHODS: This is a transversal analytic study. It includes fifty-five cases of PCOS and fifty-five healthy controls from gynecologic and familiar medicine consultation during the period from May 2nd to November 30th, 1999. It excludes patients with the Cushing disease, congenital suprarenal hyperplasia, pregnant women or women under hormonal treatments until three months prior the beginning of the study. The diagnostic of PCOS was established when the patient presents three of the following characteristics: menstrual disturbances, hirsutism, a LH/FSH relation > or = than 1.5 and ultrasound with polycystic ovaries. Their weight and height was taken in order to calculate the body mass index (BMI) and the waist/hip index (WHI) Blood samples in fasting where obtained to determine the FSH, LH, cholesterol, triglycerids, glycaemia and uric acid levels. Descriptive statistics where applied as well as the SPSS software along with the Saphiro-Francia test, the Mann Whitney test and logistic regression. RESULTS: The age of the patients with PCOS varied between 18 and 39 years old, average 26.6 years old and that of the controls from 19 to 39 years old, average 28.2 years old, (p = 0.165). The prevalence of general obesity (BMI > or = 30) was of 50.9% in the group of PCOS and of 18.2% in the group of controls. The systolic hypertension (BP > or = 140 mm Hg) was of 9% against 7.3%. A diastolic hypertension (BP > or = 90 mm Hg) of 25.5% against 7.3%. A hypercholesterolemia (> or = 220 mg/dL) of 30.9% against 10.9%. A hypertriglyceridemia (> or = 160 mg/dL) of 30.9% against 16.4%. A hyperglycaemia(> or = 115 mg/dL) of 5.5% against 3.6% and a hyperuricemia(> or = 6.5 mg/L) of 23.6% against 3.6%. The OR calculated through cross products showed that patients with PCOS have the possibility of presenting obesity, hypercholesterolemia, hypertriglyceridemia, hyperuricemia and diastolic hypertension, 4.6, 3.7, 2.3, 8.2 and 4.4 times more than the controls. The comparison of the average of the variables of both groups showed significant differences (p < 0.5) for the BMI, WHI, systolic BP, cholesterol and uric acid. The multiple logistic regression showed a consistent association between PCOS and hyperuricemia (MR = 5.23, = 1.4-26.26), obesity (MR = 3.26, CI = 1.33-8.01) and hypercholesterolemia (RM = 3.04, CI = 1.02-9.08). CONCLUSIONS: The study showed a higher prevalence of obesity, hypercholesterolemia, hypertriglyceridemia, hyperuricemia and diastolic hypertension in patients with PCOS than in the controls. No such thing for hyperglycaemia and systolic hypertension. Nevertheless, there are significant differences between both groups related to the BMI, WHI, systolic hypertension, hypercholesterolemia and hyperuricemia. A consistent association among the PCOS and hypercholesterolemia, obesity and hyperuricemia was found.

Adolescent↗

PubMed2001

[Prevalence of metabolic disorders among family members of patients with polycystic ovary syndrome].

BACKGROUND: About 60% of patients with polycystic ovary syndrome (PCOS) have insulin resistance, predisposing them to the premature coronary disease and type 2-diabetes mellitus. However, the history of metabolic disorders in family members of patients with PCOS has been seldom documented in the literature. AIM: To evaluate the family profile of metabolic disorders of PCOS patients and to determine their relative risk of developing one of them in comparison to a control group. PATIENTS AND METHODS: Sixty PCOS patients were evaluated. The control group were 60 normal women. The data were obtained from the clinical history and personal interview with the patients, the controls and their relatives (brothers, parents and grandparents). The metabolic disorders considered were: dyslipidemia, obesity, hypertension and diabetes. RESULTS: The ages were similar between groups (PCOS: 24.0 +/- 6.3; control group: 24.8 +/- 6.2 years). The prevalence of metabolic disorders was 62% in the relatives of the PCOS patients and 27.8% in the relatives of the control group (p < 0.005). The probability to develop a metabolic disorder within the family was 2.7 (2.2-3.3) fold higher in the PCOS group compared to the control group. The risk of developing hypertension, dyslipidemia, obesity and diabetes was 2.1 (1.5-2.9); 1.8 (1.5-2.7); 3.6 (2.6-4.9) and 2.7 (1.8-3.9), respectively, in the PCOS group compared to the control group. CONCLUSIONS: The probability of finding a metabolic disorder in the families of PCOS patients, is 2.7 fold higher than in the control group families. The metabolic disorders are more frequent in parents and grandparents of the PCOS patients than in those of normal women.

Adult↗

PubMed2005

[Tyrosine phosphorylation and protein expression of insulin receptor substrate-2 in the adipose tissue from patients with polycystic ovary syndrome].

OBJECTIVE: To explore molecular mechanisms of insulin resistance of polycystic ovary syndrome (PCOS) by determining the tyrosine phosphorylation and protein expression of insulin receptor substrate-2 (IRS-2) in adipose tissue from patients with PCOS. METHODS: Serum and subcutaneous adipose tissue samples from patients with PCOS with insulin resistance (n = 19), PCOS without insulin resistance (n = 17) and controls (n = 20) were collected. The expression of IRS-2 in adipose tissue was assessed by Western blot. Immunohistochemistry was used to detect the distribution of IRS-2 in adipose tissues of all patients. The tyrosine phosphorylation of IRS-2 was measured by immunoprecipitation and enhanced chemiluminescent immunoblotting technique. RESULTS: (1) There was no significant difference of the protein expression of IRS-2 in PCOS with insulin resistance 1.15 +/- 0.26 compared to those in PCOS without insulin resistance 1.13 +/- 0.26 and control group 1.00 +/- 0.25 (P > 0.05); (2) The tyrosine phosphorylation of IRS-2 was significantly decreased in PCOS with insulin resistance 0.77 +/- 0.16 compared to that of PCOS without insulin resistance 0.91 +/- 0.25 and control groups 1.00 +/- 0.12 (P < 0.05). There was no significant difference between PCOS without insulin resistance and control groups (P > 0.05). CONCLUSIONS: The decrease of tyrosine phosphorylation of IRS-2 in PCOS patients, which induces impairment of the insulin signal pathway, may be one of the mechanisms leading to insulin resistance.

Adipose Tissue↗

PubMed2006

Metabolic syndrome in polycystic ovary syndrome.

Because insulin resistance and visceral obesity are important features of polycystic ovary syndrome (PCOS), metabolic syndrome is much more common in women with PCOS than in the general female population of similar age. It has been reported that in the USA almost 50% of women with PCOS present the metabolic syndrome. In Italy, where women with PCOS have a lower mean body weight and less frequently increased serum triglycerides than US PCOS, metabolic syndrome is less common but still 4 times more frequent in PCOS patients than in the general female population of similar age. Patients with mild PCOS phenotype (ovulatory PCOS) have a lower prevalence of metabolic syndrome but, in these patients too, metabolic syndrome is 2 times more frequent than in the normal population. These data suggest that PCOS is the most common cause of increased cardiovascular risk in young adult women. All obese and overweight women with PCOS should be screened for metabolic syndrome and, when the syndrome is not found, the screening should be repeated every 2 or 3 years. Treatment consists in lifestyle intervention. Pharmacological therapies should be used only when lifestyle fails to normalize cardiovascular risk factors.

Adolescent↗

PubMed2006

Pregnancy outcomes after laparoscopic ovarian drilling in women with polycystic ovarian syndrome.

OBJECTIVE: To study whether there is an increased risk of glucose intolerance and hypertensive complications during pregnancy in women with polycystic ovarian syndrome (PCOS) who conceived after laparoscopic ovarian drilling and to investigate if there is an adverse pregnancy outcome. METHODS: This prospective study took place at Salmaniya Medical Complex in Bahrain, between June 1996 and June 2003. We compared the pregnancy and neonatal outcomes of 134 patients with PCOS who were treated with laparoscopic ovarian drilling with 479 pregnant women without PCOS (controls). We used the multiple logistic regression analysis to assess the risk of PCOS on impaired glucose tolerance (IGT), gestational diabetes mellitus (GDM), hypertensive disorders in pregnancy (HDP) and premature delivery. RESULTS: Subjects with PCOS had a significantly greater prepregnancy body mass index, prevalence of obesity and nulliparity as compared with controls. The incidence of IGT (p=0.007), GDM (p=0.01) and HDP (p=0.001) were significantly higher in pregnant PCOS compared with the control group. There were no significant differences in the neonatal outcomes and prevalence of premature delivery between the 2 study groups. When non-obese PCOS patients were compared with non-obese controls, the incidence of GDM (p=0.04) and HDP (p=0.004) were still significantly higher in the former. The prevalence of pregnancy complications were not significantly different when obese PCOS were compared with obese control patients. The PCOS was demonstrated as a risk factor for IGT (p=0.05), GDM (p=0.03) and HDP (p=0.03), but not for premature delivery. CONCLUSION: Women with PCOS who conceived after the drilling were at higher risk of IGT, GDM and HDP, and this risk seemed to be independent of maternal obesity.

Adult↗