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Role of obesity and adiposity in polycystic ovary syndrome

Abstract

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age. Obesity may have a marked impact on both the development and progression of the syndrome. A high proportion of women with PCOS are obese. Regardless of the degree of obesity, women with PCOS are more likely to have central (abdominal) distribution of body fat, which is associated with insulin resistance and hyperandrogenaemia. PCOS is not only a reproductive disorder, but is also associated with significant increase in metabolic aberrations and cardiovascular risk factors. It has been shown that weight loss improves the metabolic and reproductive abnormalities that characterise the syndrome.

Definition and diagnostic criteria

The polycystic ovary syndrome (PCOS) is a heterogeneous condition of unknown aetiology characterised by hyperandrogenic chronic anovulation. The syndrome was first described in 1935. Diagnostic criteria for the syndrome were defined at an NIH/NICHHD conference in 1990. These criteria are the presence of both hyperandrogenism (clinical and/or biochemical) and chronic anovulation and, importantly, the exclusion of other androgen excess disorders. PCOS can, therefore, be considered a diagnosis of exclusion.

In 2003, another expert conference, held in Rotterdam, included polycystic ovary morphology by ultrasound in the diagnostic criteria. Under the Rotterdam criteria, PCOS is diagnosed in the presence of at least two of the following three features: hyperandrogenism, chronic anovulation and/or polycystic ovaries.1 It is important to note that the ultrasound appearance of polycystic ovaries is not by itself diagnostic of the syndrome, as it does not confirm the function of the ovarian tissue. However, in a contemporary report, the Androgen Excess Society suggested that PCOS should be first considered as a disorder of androgen excess or hyperandrogenism. The absence of clinical or biochemical hyperandrogenism in the untreated state makes a diagnosis of PCOS less certain, regardless of the presence of ovulatory or menstrual dysfunction or the ultrasonographic appearance of polycystic ovaries.2

Epidemiology: prevalence and clinical features

The worldwide prevalence of PCOS is 6.5–6.8%, as defined by the NIH criteria.3, 4, 5

The clinical features of the syndrome may change throughout the life cycle from adolescence to post-menopause. In adolescents, oligomenorrhoea, hirsutism and obesity are among the more common clinical problems. For reproductive age women, anovulatory infertility is a leading complaint. For the mature woman, obesity, dyslipidaemia, impaired glucose tolerance (IGT) and diabetes are common problems related to PCOS.

An overview of the pathophysiology and molecular defects in PCOS

PCOS is associated with defects in insulin action and secretion with profound insulin resistance (IR)6, 7, 8, 9 and pancreatic β-cell dysfunction.10 The current concept of insulin signalling defects in PCOS points to the element of tissue specificity, accommodating research data of a 30% decrease in insulin receptor autophosphorylation in adipocytes,11 increased serine phosphorylation in the fibroblasts of 50% of PCOS patients,12 and lower insulin receptor substrate 1 associated with phosphoinositide-3 kinase (IRS-1-associated PI3K) activity in muscle cells.12

Extending the complexity and multiplicity of insulin actions at the ovarian level, IR and its attendant hyperinsulinaemia have been suggested to play a key role in the aetiology of PCOS. Interestingly, several studies have shown a potent synergistic effect of insulin on steroidogenesis in ovarian compartments, in spite of peripheral IR.11

Ovarian as well as adrenal steroidogenic abnormalities, which cause hyperandrogenaemia, have been demonstrated in women with PCOS. An intrinsic ovarian defect, possibly of genetic origin, may be present.13 In support of this hypothesis, theca cells from PCOS patients uniformly show increased activities and expression of certain steroidogenic enzymes.10

Additional manifestations in PCOS, other than insulin resistance and present in about 50–70%6 include a clustering of metabolic syndrome features: obesity, dyslipidaemia, hypertension and IGT.10 Young women with PCOS have higher risks for IGT and type 2 diabetes14, 15, 16 and also demonstrate increased cardiovascular risk factors.17, 18

Effect of obesity on pathophysiology of PCOS

Obesity may play a pathogenic role in the development of PCOS in susceptible individuals, as well as exacerbating the clinical and metabolic features of the syndrome. Obesity is present in 30–75% of women with the syndrome19 and has a negative impact. Women who are obese more often have severe hyperandrogenism (hirsutism, menstrual abnormalities and anovulation) than normal weight women with PCOS.

The distribution of body fat also has an important impact on the pathophysiology of PCOS. Studies have shown that 50–60% of women with PCOS have an abdominal distribution of body fat (central obesity), regardless of their body mass index (BMI).20, 21 Kirchengast et al.21 reported that lean women with PCOS had a significantly higher amount of body fat and lower amount of lean body mass than healthy women matched for age, weight and BMI. In the same study, a gynoid fat distribution was seen in all lean controls but in only 30% of lean PCOS patients.

In women with PCOS, intravisceral adipocytes behave in an abnormal way in terms of their effects on the metabolic and hormonal profile. This abnormal adipocyte behaviour is associated with defective insulin activity, leading to impaired glucose tolerance, hyperinsulinaemia and insulin resistance. The adipocytes also have an effect on steroid metabolism, and specifically on androgen metabolism.

There is a complex inter-relationship between obesity, insulin resistance and endocrine abnormalities in PCOS, the nature of which is still largely unresolved. Hyperinsulinaemia is likely to be a major mechanism underlying the pathological processes whereby obesity amplifies the clinical features of the syndrome since insulin in addition to the metabolic impact, stimulates ovarian androgen production, regulates androgen metabolism and influences follicular development.

There is no defect in the process by which insulin binds to its receptor in women with PCOS. Instead, visceral adipocytes are believed to express defects in insulin intracellular signalling. These intracellular defects in insulin activity are illustrated in Figure 1.6 This figure represents an adipocyte showing (at the top) insulin linked to its cell surface receptor (α- and β-subunits). The β-subunits of the insulin receptor increase serine phosphorylation, which inhibits the intracellular transmission of the insulin message in the adipocytes, and decreases tyrosine phosphorylation. This defect is, in turn, translated into decreased activity of the PI3K (phosphoinositide-3 kinase) enzyme, which is the key enzyme for recruitment of GLUT-4 (glucose transporter-4). GLUT-4 is responsible for the insulin-dependent glucose uptake by the cells, so the reduction in its activity can therefore result in decreased cellular glucose uptake with an increased risk of glucose intolerance and type 2 diabetes.

Figure 1
figure1

Molecular defect of insulin activity in adipose tissue in women with PCOS. The illustration shows how defects in insulin intracellular signalling can result in hyperinsulinaemia and insulin resistance (adapted from Diamanti-Kandarakis et al.6). GLUT-4, glucose transporter-4; PI3 kinase, phosphoinositide-3 kinase; IRS, insulin-receptor substrate, GSK-3, glycogen synthase kinase-3; PKA/HSL, protein kinase A/hormone sensitive lipase; PKB, protein kinase B.

The visceral adipocytes also show increased sensitivity to lipolysis, which is in keeping with the insulin resistance. The mechanism is believed to reflect the fact that the complex formed by protein kinase A and hormone-sensitive lipase is overactivated in women with PCOS.22

The role of adipocytes on steroid hormonal metabolism in PCOS is also important. As shown in Figure 2, adipocytes from centrally located adipose tissue can convert Δ-4 androstenedione to testosterone, a strong androgen, via 17-β hydroxydehydrogenase enzyme. Androgens lead to increased central adiposity. In turn, visceral adipocytes are able to convert inactive cortisone to metabolically active cortisol, which therefore enhances insulin resistance. The increased cortisol and testosterone then by a feedback mechanism lead to an increase in the degree of central obesity.23 The adipocytes in PCOS therefore appear to over convert weak androgens to strong androgens.

Figure 2
figure2

Adipose tissue and steroid hormone metabolism in PCOS (adapted from Ahima et al.23). 17ß-HS oxidoreductase, 17 ß-hydroxysteroid oxidoreductase; 11-ß HSD-1, 11 ß-hydroxysteroid dehydrogenase-1.

These mechanisms explain how obesity increases insulin resistance and hyperinsulinaemia in women with PCOS. This insulin resistance and hyperinsulinaemia is present in up to 65% of obese women with PCOS and around 20% of lean women with PCOS24 and is interlinked with hyperandrogenism and anovulation. It is well known that hyperinsulinaemia has adverse effects on metabolic parameters. In PCOS, it has an additional detrimental effect on ovulation because insulin stimulates the production of androgens in the intra-ovarian tissue in these individuals.

Human ovaries have insulin receptors and the hormone acts in two key enzyme processes in steroidogenesis: in the ovarian theca cells insulin activates the side chain cleavage enzyme and the complex of 17-hydroxylase and 17,20-lyase, key enzymes of androgen production.19

These concepts are summarised in Figure 3, which illustrates how as the degree of overall and in particular central obesity increases, androgen production increases and fertility decreases. At the same time, increased lipolysis from adipocytes also contributes to potentiate the degree of insulin resistance, which further enhances the reproductive as well as the adverse metabolic impact and the cardiovascular risks in women with PCOS.

Figure 3
figure3

Effects of obesity and adiposity in PCOS. FFA, free fatty acid; SHBG, sex hormone binding globulin.

Systemic sequelae

It is clear from the above that PCOS must be considered to be more than just a disorder of reproduction. It is also an important metabolic disorder and has systemic sequelae that can contribute to long-term morbidity. PCOS significantly increases the level of metabolic and cardiovascular risk factors. The Kaiser Permanente Northern California PCOS study included 11 035 women with PCOS, with a mean age of 30.7 years. Compared with age-matched controls, women with PCOS were found to have a significantly higher prevalence of several known cardiovascular risk factors, including hypertension, diabetes mellitus, dysfibrinolysis, elevated atherogenic molecules, dyslipidaemia and elevated triglyceride levels.25, 26

In adolescent and young adult women, PCOS is also a leading risk factor for type 2 diabetes. Studies have shown that women with PCOS have an increased prevalence of IGT and of type 2 diabetes compared with control groups.26, 27 Legro et al.26 reported that the incidence of PCOS was associated with a significantly increased risk for IGT and type 2 diabetes at all bodyweights and at a young age. However, the risk is further increased in obese PCOS women. Figure 4 shows how the prevalence of IGT and type 2 diabetes increases with increasing BMI in this patient population.

Figure 4
figure4

Prevalence of glucose intolerance by body mass index in a US population of women with PCOS (adapted from Legro et al.26).

Inflammation is thought to play an important role in the progression and development of complications of atherosclerosis and there is evidence of low-grade chronic inflammation in women with PCOS, as indicated by elevated levels of the metabolic risk factors shown in Table 1.

Table 1 PCOS metabolic abnormalities indicating increased cardiovascular risk

The clinical significance of the early markers of chronic inflammation in young women with PCOS remains to be assessed.

Management of PCOS

Management of patients with PCOS involves first lifestyle modification and specifically weight reduction, which aims to control the metabolic aberrations and reduce the cardiovascular risk factors.

Pasquali and Gambineri41 have reported that moderate weight loss can improve risk factors in PCOS women. In their study, women were treated for 1 year with a hypocaloric diet. After only a modest weight loss (BMI was reduced from 38 to 34 kg/m2), women were found to have significantly decreased degrees of hirsutism, improvement in their menses, a decrease in testosterone levels and insulinaemia, improvement in insulin sensitivity indices and an increase in HDL-cholesterol. With moderate improvement in their bodyweight these women, therefore, showed improvement in all parameters of the syndrome.

Pharmacological therapy has also been investigated to improve cardiovascular risk factors in women with PCOS. We have assessed the impact of the insulin sensitiser metformin on flow-mediated dilatation, a measure of early endothelial dysfunction and, hence, an early cardiovascular risk factor. Women with PCOS, despite their young age, had decreased flow-mediated dilatation compared with a control group. After treatment with metformin, there was improvement in endothelial function.36

Treatment with metformin has also been shown to have a statistically significant beneficial effect on inflammatory markers. Six months' treatment was associated with a reduction in plasma levels of the cellular adhesion molecule sVCAM-1 and the independent cardiovascular risk factor, C-reactive protein.40

The effect of weight loss induced by sibutramine has also recently been investigated. In an open label, randomised study, the effect of sibutramine plus diet was compared with diet alone on BMI and triglycerides in obese women with PCOS. After 6 months of combined treatment (sibutramine and diet), BMI and triglyceride levels were reduced significantly compared with the diet-only group (author's unpublished data).

Summary

PCOS is the most common endocrinopathy of women in reproductive age, affecting around 6.7%. In addition to the well known reproductive abnormalities characterising the syndrome, metabolic and cardiovascular risk factors are significantly increased in PCOS. Increased obesity and abdominal adiposity further aggravate the clinical, hormonal and metabolic parameters in PCOS and, if treated, can reverse most of these abnormalities to a clinically significant degree.

Conflict of interest

The author has lectured at Abbott-sponsored symposia.

References

  1. 1

    Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fert Steril 2004; 81: 19–25.

    Google Scholar 

  2. 2

    Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W et al. Criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an androgen excess society guideline. J Clin Endocrinol Metab 2006; 91: 4237–4245.

    CAS  Article  Google Scholar 

  3. 3

    Diamanti-Kandarakis E, Kouli CR, Bergiele AT, Filandra FA, Tsianateli TC, Spina GG et al. A survey of the polycystic ovary syndrome in the Greek island of Lesbos: hormonal and metabolic profile. J Clin Endocrinol Metab 1999; 84: 4006–4011.

    CAS  Article  Google Scholar 

  4. 4

    Asuncion M, Calvo RM, San Millan JL, Sancho J, Avila S, Escobar-Morreale HF . A prospective study of the prevalence of the polycystic ovary syndrome in unselected caucasian women from Spain. J Clin Endocrinol Metab 2000; 85: 2434–2438.

    CAS  PubMed  Google Scholar 

  5. 5

    Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO . The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab 2004; 89: 2745–2749.

    CAS  Article  Google Scholar 

  6. 6

    Diamanti-Kandarakis E, Papavassiliou AG . Molecular mechanisms of insulin resistance in polycystic ovary syndrome. Trends Mol Med 2006; 12: 324–332.

    CAS  Article  Google Scholar 

  7. 7

    Diamanti-Kandarakis E, Piperi C . Genetics of polycystic ovary syndrome: searching for the way out of the labyrinth. Hum Reprod Update 2005; 11: 631–643.

    CAS  Article  Google Scholar 

  8. 8

    Diamanti-Kandarakis E, Piperi C, Spina J, Argyrakopoulou G, Papanastasiou L, Bergiele A et al. Polycystic ovary syndrome: the influence of environmental and genetic factors. Hormones (Athens) 2006; 5: 17–34.

    Article  Google Scholar 

  9. 9

    Mlinar B, Marc J, Janez A, Pfeifer M . Molecular mechanisms of insulin resistance and associated diseases. Clin Chim Acta 2007; 375: 20–35.

    CAS  Article  Google Scholar 

  10. 10

    Ehrmann DA, Kasza K, Azziz R, Legro RS, Ghazzi MN, PCOS/Troglitazone Study Group. Effects of race and family history of type 2 diabetes on metabolic status of women with polycystic ovary syndrome. J Clin Endocrinol Metab 2005; 90: 66–71.

    CAS  Article  Google Scholar 

  11. 11

    Dunaif A, Xia J, Book CB, Schenker E, Tang Z . Excessive insulin receptor serine phosphorylation in cultured fibroblasts and in skeletal muscle. A potential mechanism for insulin resistance in the polycystic ovary syndrome. J Clin Invest 1995; 96: 801–810.

    CAS  Article  Google Scholar 

  12. 12

    Dunaif A, Wu X, Lee A, Diamanti-Kandarakis E . Defects in insulin receptor signaling in vivo in the polycystic ovary syndrome (PCOS). Am J Physiol Endocrinol Metab 2001; 281: E392–E399.

    CAS  Article  Google Scholar 

  13. 13

    Strauss JF . Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome. Ann N Y Acad Sci 2003; 997: 42–48.

    Article  Google Scholar 

  14. 14

    Cussons AJ, Stuckey BG, Watts GF . Cardiovascular disease in the polycystic ovary syndrome: new insights and perspectives. Atherosclerosis 2006; 185: 227–239.

    CAS  Article  Google Scholar 

  15. 15

    Dahlgren E, Janson PO, Johansson S, Lapidus L, Oden A . Polycystic ovary syndrome and risk for myocardial infarction. Evaluated from a risk factor model based on a prospective population study of women. Acta Obstet Gynecol Scand 1992; 71: 599–604.

    CAS  Article  Google Scholar 

  16. 16

    Talbott EO, Guzick DS, Sutton-Tyrrell K, McHugh-Pemu KP, Zborowski JV, Remsberg KE et al. Evidence for association between polycystic ovary syndrome and premature carotid atherosclerosis in middle-aged women. Arterioscler Thromb Vasc Biol 2000; 20: 2414–2421.

    CAS  Article  Google Scholar 

  17. 17

    Diamanti-Kandarakis E . Insulin resistance in PCOS. Endocrine 2006; 30: 13–17.

    CAS  Article  Google Scholar 

  18. 18

    Diamanti-Kandarakis E, Alexandraki K, Protogerou A, Piperi C, Papamichael C, Aessopos A et al. Metformin administration improves endothelial function in women with polycystic ovary syndrome. Eur J Endocrinol 2005; 152: 749–756.

    CAS  Article  Google Scholar 

  19. 19

    Ehrmann DA . Polycystic ovary syndrome. N Engl J Med 2005; 352: 1223–1236.

    CAS  Article  Google Scholar 

  20. 20

    Horejsi R, Moller R, Rackl S, Giuliani A, Freytag U, Crailsheim K et al. Android subcutaneous adipose tissue topography in lean and obese women suffering from PCOS: comparison with type 2 diabetic women. Am J Phys Anthropol 2004; 124: 275–281.

    CAS  Article  Google Scholar 

  21. 21

    Kirchengast S, Huber J . Body composition characteristics and body fat distribution in lean women with polycystic ovary syndrome. Hum Reprod 2001; 16: 1255–1260.

    CAS  Article  Google Scholar 

  22. 22

    Ek I, Arner P, Rydén M, Holm C, Thörne A, Hoffstedt J et al. A unique defect in the regulation of visceral fat cell lipolysis in the polycystic ovary syndrome as an early link to insulin resistance. Diabetes 2002; 51: 484–492.

    CAS  Article  Google Scholar 

  23. 23

    Ahima RS, Flier JS . Adipose tissue as an endocrine organ. Trends Endocrinol Metab 2000; 11: 327–332.

    CAS  Article  Google Scholar 

  24. 24

    Dale PO, Tanbo T, Vaaler S, Abyholm T . Body weight, hyperinsulinemia, and gonadotropin levels in the polycystic ovarian syndrome: evidence of two distinct populations. Fertil Steril 1992; 58: 487–491.

    CAS  Article  Google Scholar 

  25. 25

    Lo JC, Feigenbaum SL, Yang J, Pressman AR, Selby JV, Go AS . Epidemiology and adverse cardiovascular risk profile of diagnosed polycystic ovary syndrome. J Clin Endocrinol Metab 2006; 91: 1357–1363.

    CAS  Article  Google Scholar 

  26. 26

    Legro RS, Kunselman AR, Dodson WC, Dunaif A . Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab 1999; 84: 165–169.

    CAS  PubMed  Google Scholar 

  27. 27

    Palmert MR, Gordon CM, Kartashov AI, Legro RS, Emans SJ, Dunaif A . Screening for abnormal glucose tolerance in adolescents with polycystic ovary syndrome. J Clin Endocrinol Metab 2002; 87: 1017–1023.

    CAS  Article  Google Scholar 

  28. 28

    Rajkhowa M, Neary RH, Kumpatla P, Game FL, Jones PW, Obhrai MS et al. Altered composition of high density lipoproteins in women with the polycystic ovary syndrome. J Clin Endocrinol Metab 1997; 82: 3389–3394.

    CAS  PubMed  Google Scholar 

  29. 29

    Orio F, Palomba S, Spinelli L, Cascella T, Tauchmanova L, Zullo F et al. The cardiovascular risk of young women with polycystic ovary syndrome: an observational, analytical, prospective case–control study. J Clin Endocrinol Metab 2004; 86: 3696–3701.

    Article  Google Scholar 

  30. 30

    Taponen S, Martikainen H, Jarvelin MR, Sovio U, Laitinen J, Pouta A, et al., Northern Finland Birth Cohort 1966 Study. Metabolic cardiovascular disease risk factors in women with self-reported symptoms of oligomenorrhea and/or hirsutism: northern Finland birth cohort 1966 study. J Clin Endocrinol Metab 2004; 89: 2114–2118.

    CAS  Article  Google Scholar 

  31. 31

    Boulman N, Levy Y, Leiba R, Shachar S, Linn R, Zinder O et al. Increased C-reactive protein levels in the polycystic ovary syndrome: a marker of cardiovascular disease. J Clin Endocrinol Metab 2004; 89: 2160–2165.

    CAS  Article  Google Scholar 

  32. 32

    Diamanti-Kandarakis E, Paterakis T, Alexandraki K, Piperi C, Aessopos A, Katsikis I et al. Indices of low-grade chronic inflammation in polycystic ovary syndrome and the beneficial effect of metformin. Hum Reprod 2006; 21: 1426–1431.

    CAS  Article  Google Scholar 

  33. 33

    Diamanti-Kandarakis E, Piperi C, Kalofoutis A, Creatsas G . Increased levels of serum advanced glycation end-products in women with polycystic ovary syndrome. Clin Endocrinol (Oxf) 2005; 62: 37–43.

    CAS  Article  Google Scholar 

  34. 34

    Orio Jr F, Palomba S, Cascella T, Di Biase S, Manguso F, Tauchmanova L et al. The increase of leukocytes as a new putative marker of low-grade chronic inflammation and early cardiovascular risk in polycystic ovary syndrome. J Clin Endocrinol Metab 2005; 90: 2–5.

    CAS  Article  Google Scholar 

  35. 35

    Paradisi G, Steinberg HO, Hempfling A, Cronin J, Hook G, Shepard MK et al. Polycystic ovary syndrome is associated with endothelial dysfunction. Circulation 2001; 103: 1410–1415.

    CAS  Article  Google Scholar 

  36. 36

    Diamanti-Kandarakis E, Alexandraki K, Protogerou A, Piperi C, Papamichael C, Aessopos A et al. Metformin administration improves endothelial function in women with polycystic ovary syndrome. Eur J Endocrinol 2005; 152: 749–756.

    CAS  Article  Google Scholar 

  37. 37

    Apridonidze T, Essah PA, Iuorno MJ, Nestler JE . Prevalence and characteristics of the metabolic syndrome in women with polycystic ovary syndrome. J Clin Endocrinol Metab 2005; 90: 1929–1935.

    CAS  Article  Google Scholar 

  38. 38

    Diamanti-Kandarakis E, Palioniko G, Alexandraki K, Bergiele A, Koutsouba T, Bartzis M . The prevalence of 4G5G polymorphism of plasminogen activator inhibitor-1 (PAI-1) gene in polycystic ovarian syndrome and its association with plasma PAI-1 levels. Eur J Endocrinol 2004; 150: 793–798.

    CAS  Article  Google Scholar 

  39. 39

    Diamanti-Kandarakis E, Spina G, Kouli C, Migdalis I . Increased endothelin-1 levels in women with polycystic ovary syndrome and the beneficial effect of metformin therapy. J Clin Endocrinol Metab 2001; 86: 4666–4673.

    CAS  Article  Google Scholar 

  40. 40

    Yildiz BO, Haznedaroglu IC, Kirazli S, Bayraktar M . Global fibrinolytic capacity is decreased in polycystic ovary syndrome, suggesting a prothrombotic state. J Clin Endocrinol Metab 2002; 87: 3871–3875.

    CAS  Article  Google Scholar 

  41. 41

    Pasquali R, Gambineri A . Role of changes in dietary habits in polycystic ovary syndrome. Reprod Biomed Online 2004; 8: 431–439.

    Article  Google Scholar 

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Diamanti-Kandarakis, E. Role of obesity and adiposity in polycystic ovary syndrome. Int J Obes 31, S8–S13 (2007). https://doi.org/10.1038/sj.ijo.0803730

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Keywords

  • polycystic ovary syndrome
  • visceral adipocyte
  • insulin resistance
  • hyperinsulinaemia

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