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Review

Cortisol and the polycystic ovary syndrome

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Pages 555-566 | Published online: 10 Jan 2014

References

  • The Rotterdam ESHRE/ASRM-Sponsored PCOS consensus workshop group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum. Reprod. 19, 41–47 (2004).
  • Azziz R, Carmina E, Dewailly D et al.; Androgen Excess Society. Positions statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. J. Clin. Endocrinol. Metab. 91(11), 4237–4245 (2006).
  • Nestler JE. Metformin for the treatment of the polycystic ovary syndrome. N. Engl. J. Med. 358(1), 47–54 (2008).
  • Ehrmann DA. Polycystic ovary syndrome. N. Engl. J. Med. 352(12), 1223–1236 (2005).
  • Pasquali R. Obesity and androgens: facts and perspectives. Fertil. Steril. 85(5), 1319–1340 (2006).
  • Morales AJ, Laughlin GA, Bützow T, Maheshwari H, Baumann G, Yen SS. Insulin, somatotropic, and luteinizing hormone axes in lean and obese women with polycystic ovary syndrome: common and distinct features. J. Clin. Endocrinol. Metab. 81(8), 2854–2864 (1996).
  • Rosenfield RL. Ovarian and adrenal function in polycystic ovary syndrome. Endocrinol. Metab. Clin. North Am. 28(2), 265–293 (1999).
  • Yildiz BO, Azziz R. The adrenal and polycystic ovary syndrome. Rev. Endocr. Metab. Disord. 8(4), 331–342 (2007).
  • Yildiz BO, Woods KS, Stanczyk F, Bartolucci A, Azziz R. Stability of adrenocortical steroidogenesis over time in healthy women and women with polycystic ovary syndrome. J. Clin. Endocrinol. Metab. 89(11), 5558–5562 (2004).
  • Lightman SL. The neuroendocrinology of stress: a never ending story. J. Neuroendocrinol. 20(6), 880–884 (2008).
  • Herman JP, Figueiredo H, Mueller NK et al. Central mechanisms of stress integration: hierarchical circuitry controlling hypothalamo–pituitary–adrenocortical responsiveness. Front. Neuroendocrinol. 24(3), 151–180 (2003).
  • Viau V. Functional cross-talk between the hypothalamic–pituitary–gonadal and – drenal axes. J. Neuroendocrinol. 14(6), 506–513 (2002).
  • Williamson M, Bingham B, Viau V. Central organization of androgen-sensitive pathways to the hypothalamic–pituitary–adrenal axis: implications for individual differences in responses to homeostatic threat and predisposition to disease. Prog. Neuropsychopharmacol. Biol. Psychiatry 29(8), 1239–1248 (2005).
  • Lanzone A, Petraglia F, Fulghesu AM, Ciampelli M, Caruso A, Mancuso S. Corticotropin-releasing hormone induces an exaggerated response of adrenocorticotropic hormone and cortisol in polycystic ovary syndrome. Fertil. Steril. 63(6), 1195–1199 (1995).
  • Lanzone A, Fulghesu AM, Guido M, Cucinelli F, Caruso A, Mancuso S. Somatostatin treatment reduces the exaggerated response of adrenocorticotropin hormone and cortisol to corticotropin-releasing hormone in polycystic ovary syndrome. Fertil. Steril. 67(1), 34–39 (1997).
  • Azziz R, Black V, Hines GA, Fox LM, Boots LR. Adrenal androgen excess in the polycystic ovary syndrome: sensitivity and responsivity of the hypothalamic–pituitary–adrenal axis. J. Clin. Endocrinol. Metab. 83(7), 2317–2323 (1998).
  • Wu XK, Zhou SY, Sallinen K, Pöllänen P, Erkkola R. Ovarian-adrenal cross-talk in polycystic ovary syndrome: evidence from wedge resection. Eur. J. Endocrinol. 143(3), 383–388 (2000).
  • Kondoh Y, Uemura T, Ishikawa M, Yokoi N, Hirahara F. Classification of polycystic ovary syndrome into three types according to response to human corticotropin-releasing hormone. Fertil. Steril. 72(1), 15–20 (1999).
  • Fulghesu AM, Ciampelli M, Guido M et al. Role of opioid tone in the pathophysiology of hyperinsulinemia and insulin resistance in polycystic ovarian disease. Metab. Clin. Exp. 47(2), 158–162 (1998).
  • Lanzone A, Guido M, Ciampelli M et al. Evidence of a disturbance of the hypothalamic–pituitary–adrenal axis in polycystic ovary syndrome: effect of naloxone. Clin. Endocrinol. 45(1), 73–77 (1996).
  • Gennarelli G, Holte J, Stridsberg M et al. Response of the pituitary–adrenal axis to hypoglycemic stress in women with the polycystic ovary syndrome. J. Clin. Endocrinol. Metab. 84(1), 76–81 (1999).
  • Gurusinghe D, Gill S, Almario RU et al. In polycystic ovary syndrome, adrenal steroids are regulated differently in the morning versus in response to nutrient intake. Fertil. Steril. 93(4), 1192–1199 (2010).
  • Veldhuis JD, Roelfsema F, Iranmanesh A, Carroll BJ, Keenan DM, Pincus SM. Basal, pulsatile, entropic (patterned), and spiky (staccato-like) properties of ACTH secretion: impact of age, gender, and body mass index. J. Clin. Endocrinol. Metab. 94(10), 4045–4052 (2009).
  • Pasquali R, Vicennati V, Gambineri A, Pagotto U. Sex-dependent role of glucocorticoids and androgens in the pathophysiology of human obesity. Int. J. Obes. 32(12), 1764–1779 (2008).
  • Chalew S, Nagel H, Shore S. The hypothalamic–pituitary–adrenal axis in obesity. Obes. Res. 3(4), 371–382 (1995).
  • Pasquali R, Biscotti D, Spinucci G et al. Pulsatile secretion of ACTH and cortisol in premenopausal women: effect of obesity and body fat distribution. Clin. Endocrinol. 48(5), 603–612 (1998).
  • Pasquali R, Cantobelli S, Casimirri F et al. The hypothalamic–pituitary–adrenal axis in obese women with different patterns of body fat distribution. J. Clin. Endocrinol. Metab. 77(2), 341–346 (1993).
  • Duclos M, Corcuff JB, Etcheverry N, Rashedi M, Tabarin A, Roger P. Abdominal obesity increases overnight cortisol excretion. J. Endocrinol. Invest. 22(6), 465–471 (1999).
  • Epel EE, Moyer AE, Martin CD et al. Stress-induced cortisol, mood, and fat distribution in men. Obes. Res. 7(1), 9–15 (1999).
  • Pasquali R, Vicennati V, Cacciari M, Pagotto U. The hypothalamic–pituitary–adrenal axis activity in obesity and the metabolic syndrome. Ann. NY Acad. Sci. 1083, 111–128 (2006).
  • Vicennati V, Pasquali R. Abnormalities of the hypothalamic–pituitary–adrenal axis in women with the abdominal obesity and relationship with insulin resistance: evidence for a central and peripheral alteration. J. Clin. Endocrinol. Metab. 24, 416–422 (2000).
  • Bertagna X, Coste J, Raux-Demay MC, Letrait M, Strauch G. The combined corticotropin-releasing hormone/lysine vasopressin test discloses a corticotroph phenotype. J. Clin. Endocrinol. Metab. 79(2), 390–394 (1994).
  • Mårin P, Darin N, Amemiya T, Andersson B, Jern S, Björntorp P. Cortisol secretion in relation to body fat distribution in obese premenopausal women. Metab. Clin. Exp. 41(8), 882–886 (1992).
  • Ljung T, Andersson B, Bengtsson BA, Björntorp P, Mårin P. Inhibition of cortisol secretion by dexamethasone in relation to body fat distribution: a dose-response study. Obes. Res. 4(3), 277–282 (1996).
  • Pasquali R, Ambrosi B, Armanini D et al.; Study Group on Obesity of the Italian Society of Endocrinology. Cortisol and ACTH response to oral dexamethasone in obesity and effects of sex, body fat distribution, and dexamethasone concentrations: a dose-response study. J. Clin. Endocrinol. Metab. 87(1), 166–175 (2002).
  • Roelfsema F, Kok P, Pereira AM, Pijl H. Cortisol production rate is similarly elevated in obese women with or without the polycystic ovary syndrome. J. Clin. Endocrinol. Metab. 95(7), 3318–3324 (2010).
  • Dunkelman SS, Fairhurst B, Plager J, Waterhouse C. Cortisol metabolism in obesity. J. Clin. Endocrinol. Metab. 24, 832–841 (1964).
  • Strain GW, Zumoff B, Strain JJ, Levin J, Fukushima DK. Cortisol production in obesity. Metab. Clin. Exp. 29(10), 980–985 (1980).
  • Stewart PM, Boulton A, Kumar S, Clark PM, Shackleton CH. Cortisol metabolism in human obesity: impaired cortisone→cortisol conversion in subjects with central adiposity. J. Clin. Endocrinol. Metab. 84(3), 1022–1027 (1999).
  • Andrew R, Phillips DI, Walker BR. Obesity and gender influence cortisol secretion and metabolism in man. J. Clin. Endocrinol. Metab. 83(5), 1806–1809 (1998).
  • Purnell JQ, Kahn SE, Samuels MH, Brandon D, Loriaux DL, Brunzell JD. Enhanced cortisol production rates, free cortisol, and 11b-HSD-1 expression correlate with visceral fat and insulin resistance in men: effect of weight loss. Am. J. Physiol. Endocrinol. Metab. 296(2), E351–E357 (2009).
  • Roelfsema F, Kok P, Frolich M, Pereira AM, Pijl H. Disordered and increased adrenocorticotropin secretion with diminished adrenocorticotropin potency in obese in premenopausal women. J. Clin. Endocrinol. Metab. 94(8), 2991–2997 (2009).
  • Pasquali R, Casimirri F, De Iasio R et al. Insulin regulates testosterone and sex hormone-binding globulin concentrations in adult normal weight and obese men. J. Clin. Endocrinol. Metab. 80(2), 654–658 (1995).
  • Poretsky L, Piper B. Insulin resistance, hypersecretion of LH, and a dual-defect hypothesis for the pathogenesis of polycystic ovary syndrome. Obstet. Gynecol. 84(4), 613–621 (1994).
  • Dunaif A, Graf M. Insulin administration alters gonadal steroid metabolism independent of changes in gonadotropin secretion in insulin-resistant women with the polycystic ovary syndrome. J. Clin. Invest. 83(1), 23–29 (1989).
  • Nestler JE, Clore JN, Strauss JF 3rd, Blackard WG. The effects of hyperinsulinemia on serum testosterone, progesterone, dehydroepiandrosterone sulfate, and cortisol levels in normal women and in a woman with hyperandrogenism, insulin resistance, and acanthosis nigricans. J. Clin. Endocrinol. Metab. 64(1), 180–184 (1987).
  • Stuart CA, Prince MJ, Peters EJ, Meyer WJ 3rd. Hyperinsulinemia and hyperandrogenemia: in vivo androgen response to insulin infusion. Obstet. Gynecol. 69(6), 921–925 (1987).
  • Lawson MA, Jain S, Sun S, Patel K, Malcolm PJ, Chang RJ. Evidence for insulin suppression of baseline luteinizing hormone in women with polycystic ovarian syndrome and normal women. J. Clin. Endocrinol. Metab. 93(6), 2089–2096 (2008).
  • Poretsky L, Cataldo NA, Rosenwaks Z, Giudice LC. The insulin-related ovarian regulatory system in health and disease. Endocr. Rev. 20(4), 535–582 (1999).
  • Tosi F, Negri C, Perrone F et al. Hyperinsulinemia amplifies GnRH agonist stimulated ovarian steroid secretion in women with polycystic ovary syndrome. J. Clin. Endocrinol. Metab. 97(5), 1712–1719 (2012).
  • Hines GA, Smith ER, Azziz R. Influence of insulin and testosterone on adrenocortical steroidogenesis in vitro: preliminary studies. Fertil. Steril. 76(4), 730–735 (2001).
  • Cara JF, Rosenfield RL. Insulin-like growth factor I and insulin potentiate luteinizing hormone-induced androgen synthesis by rat ovarian thecal-interstitial cells. Endocrinology 123(2), 733–739 (1988).
  • Rosenfield RL, Barnes RB, Cara JF, Lucky AW. Dysregulation of cytochrome P450c 17 α as the cause of polycystic ovarian syndrome. Fertil. Steril. 53(5), 785–791 (1990).
  • Moghetti P, Castello R, Negri C et al. Insulin infusion amplifies 17 α-hydroxycorticosteroid intermediates response to adrenocorticotropin in hyperandrogenic women: apparent relative impairment of 17,20-lyase activity. J. Clin. Endocrinol. Metab. 81(3), 881–886 (1996).
  • Tosi F, Negri C, Brun E et al. Insulin enhances ACTH-stimulated androgen and glucocorticoid metabolism in hyperandrogenic women. Eur. J. Endocrinol. 164(2), 197–203 (2011).
  • Romualdi D, Giuliani M, Draisci G et al. Pioglitazone reduces the adrenal androgen response to corticotropin-releasing factor without changes in ACTH release in hyperinsulinemic women with polycystic ovary syndrome. Fertil. Steril. 88(1), 131–138 (2007).
  • Glintborg D, Hermann AP, Hagen C et al. A randomized placebo-controlled study on the effects of pioglitazone on cortisol metabolism in polycystic ovary syndrome. Fertil. Steril. 91(3), 842–850 (2009).
  • Vrbíková J, Hill M, Stárka L et al. The effects of long-term metformin treatment on adrenal and ovarian steroidogenesis in women with polycystic ovary syndrome. Eur. J. Endocrinol. 144(6), 619–628 (2001).
  • Unlühizarci K, Kelestimur F, Sahin Y, Bayram F. The treatment of insulin resistance does not improve adrenal cytochrome P450c17α enzyme dysregulation in polycystic ovary syndrome. Eur. J. Endocrinol. 140(1), 56–61 (1999).
  • Benson S, Arck PC, Tan S et al. Disturbed stress responses in women with polycystic ovary syndrome. Psychoneuroendocrinology 34(5), 727–735 (2009).
  • Hill AJ, Williams J. Psychological health in a non-clinical sample of obese women. Int. J. Obes. Relat. Metab. Disord. 22(6), 578–583 (1998).
  • Johnson F, Wardle J. Dietary restraint, body dissatisfaction, and psychological distress: a prospective analysis. J. Abnorm. Psychol. 114(1), 119–125 (2005).
  • Vicennati V, Pasqui F, Cavazza C, Pagotto U, Pasquali R. Stress-related development of obesity and cortisol in women. Obesity (Silver Spring). 17(9), 1678–1683 (2009).
  • Vicennati V, Pasqui F, Cavazza C et al. Cortisol, energy intake, and food frequency in overweight/obese women. Nutrition 27(6), 677–680 (2011).
  • Dallman MF, la Fleur SE, Pecoraro NC, Gomez F, Houshyar H, Akana SF. Minireview: glucocorticoids – food intake, abdominal obesity, and wealthy nations in 2004. Endocrinology 145(6), 2633–2638 (2004).
  • Leal AM, Moreira AC. Food and the circadian activity of the hypothalamic–pituitary–adrenal axis. Braz. J. Med. Biol. Res. 30(12), 1391–1405 (1997).
  • Ishizuka B, Quigley ME, Yen SS. Pituitary hormone release in response to food ingestion: evidence for neuroendocrine signals from gut to brain. J. Clin. Endocrinol. Metab. 57(6), 1111–1116 (1983).
  • Follenius M, Brandenberger G, Hietter B. Diurnal cortisol peaks and their relationships to meals. J. Clin. Endocrinol. Metab. 55(4), 757–761 (1982).
  • Slag MF, Ahmad M, Gannon MC, Nuttall FQ. Meal stimulation of cortisol secretion: a protein induced effect. Metab. Clin. Exp. 30(11), 1104–1108 (1981).
  • Gibson EL, Checkley S, Papadopoulos A, Poon L, Daley S, Wardle J. Increased salivary cortisol reliably induced by a protein-rich midday meal. Psychosom. Med. 61(2), 214–224 (1999).
  • Korbonits M, Trainer PJ, Little JA et al. Leptin levels do not change acutely with food administration in normal or obese subjects, but are negatively correlated with pituitary–adrenal activity. Clin. Endocrinol. 46(6), 751–757 (1997).
  • Vicennati V, Ceroni L, Gagliardi L, Gambineri A, Pasquali R. Comment: response of the hypothalamic-pituitary-adrenocortical axis to high-protein/fat and high-carbohydrate meals in women with different obesity phenotypes. J. Clin. Endocrinol. Metab. 87(8), 3984–3988 (2002).
  • de Niet JE, de Koning CM, Pastoor H et al. Psychological well-being and sexarche in women with polycystic ovary syndrome. Hum. Reprod. 25(6), 1497–1503 (2010).
  • Sundararaman PG, Shweta, Sridhar GR. Psychosocial aspects of women with polycystic ovary syndrome from south India. J. Assoc. Physicians India 56, 945–948 (2008).
  • Eggers S, Kirchengast S. The polycystic ovary syndrome – a medical condition but also an important psychosocial problem. Coll. Antropol. 25(2), 673–685 (2001).
  • Barry JA, Hardiman PJ, Saxby BK, Kuczmierczyk A. Testosterone and mood dysfunction in women with polycystic ovarian syndrome compared to subfertile controls. J. Psychosom. Obstet. Gynaecol. 32(2), 104–111 (2011).
  • Brady C, Mousa SS, Mousa SA. Polycystic ovary syndrome and its impact on women’s quality of life: more than just an endocrine disorder. Drug. Healthc. Patient Saf. 1, 9–15 (2009).
  • Lim SS, Norman RJ, Clifton PM, Noakes M. Hyperandrogenemia, psychological distress, and food cravings in young women. Physiol. Behav. 98(3), 276–280 (2009).
  • Dallman MF. Stress-induced obesity and the emotional nervous system. Trends Endocrinol. Metab. 21(3), 159–165 (2010).
  • Altieri P, Cavazza C, Pasqui F, Morselli AM, Gambineri A, Pasquali R. Dietary habits and their relationship with hormones and metabolism in overweight and obese women with polycystic ovary syndrome. Clin. Endocrinol. doi:10.1111/j.1365-2265.2012.04355.x (2012) (Epub ahead of print).
  • Mormede P, Foury A, Barat P et al. Molecular genetics of hypothalamic–pituitary–adrenal axis activity and function. Ann. NY Acad. Sci. 1220, 127–136 (2011).
  • Goodarzi MO, Dumesic DA, Chazenbalk G, Azziz R. Polycystic ovary syndrome: etiology, pathogenesis and diagnosis. Nat. Rev. Endocrinol. 7(4), 219–231 (2011).
  • Goodarzi MO, Guo X, Yildiz BO, Stanczyk FZ, Azziz R. Correlation of adrenocorticotropin steroid levels between women with polycystic ovary syndrome and their sisters. Am. J. Obstet. Gynecol. 196(4), 398.e1–e5; discussion 398.e5 (2007).
  • Glintborg D, Hermann AP, Brusgaard K, Hangaard J, Hagen C, Andersen M. Significantly higher adrenocorticotropin-stimulated cortisol and 17-hydroxyprogesterone levels in 337 consecutive, premenopausal, caucasian, hirsute patients compared with healthy controls. J. Clin. Endocrinol. Metab. 90(3), 1347–1353 (2005).
  • Valkenburg O, Uitterlinden AG, Themmen AP et al. Genetic polymorphisms of the glucocorticoid receptor may affect the phenotype of women with anovulatory polycystic ovary syndrome. Hum. Reprod. 26(10), 2902–2911 (2011).
  • Gagliardi L, Ho JT, Torpy DJ. Corticosteroid-binding globulin: the clinical significance of altered levels and heritable mutations. Mol. Cell. Endocrinol. 316(1), 24–34 (2010).
  • Seckl JR, Walker BR. Minireview: 11b-hydroxysteroid dehydrogenase type 1- a tissue-specific amplifier of glucocorticoid action. Endocrinology 142(4), 1371–1376 (2001).
  • Stewart PM, Krozowski ZS. 11 b-Hydroxysteroid dehydrogenase. Vitam. Horm. 57, 249–324 (1999).
  • Andrew R, Smith K, Jones GC, Walker BR. Distinguishing the activities of 11b-hydroxysteroid dehydrogenases in vivo using isotopically labeled cortisol. J. Clin. Endocrinol. Metab. 87(1), 277–285 (2002).
  • Basu R, Singh RJ, Basu A et al. Splanchnic cortisol production occurs in humans: evidence for conversion of cortisone to cortisol via the 11-b hydroxysteroid dehydrogenase (11b-hsd) type 1 pathway. Diabetes 53(8), 2051–2059 (2004).
  • Monder C, White PC. 11 b-hydroxysteroid dehydrogenase. Vitam. Horm. 47, 187–271 (1993).
  • Masuzaki H, Paterson J, Shinyama H et al. A transgenic model of visceral obesity and the metabolic syndrome. Science 294(5549), 2166–2170 (2001).
  • Morton NM, Holmes MC, Fiévet C et al. Improved lipid and lipoprotein profile, hepatic insulin sensitivity, and glucose tolerance in 11b-hydroxysteroid dehydrogenase type 1 null mice. J. Biol. Chem. 276(44), 41293–41300 (2001).
  • Rebuffé-Scrive M. Neuroregulation of adipose tissue: molecular and hormonal mechanisms. Int. J. Obes. 15(Suppl. 2), 83–86 (1991).
  • Paterson JM, Morton NM, Fievet C et al. Metabolic syndrome without obesity: hepatic overexpression of 11b-hydroxysteroid dehydrogenase type 1 in transgenic mice. Proc. Natl Acad. Sci. USA 101(18), 7088–7093 (2004).
  • Hermanowski-Vosatka A, Balkovec JM, Cheng K et al. 11b-HSD1 inhibition ameliorates metabolic syndrome and prevents progression of atherosclerosis in mice. J. Exp. Med. 202(4), 517–527 (2005).
  • Sandeep TC, Andrew R, Homer NZ, Andrews RC, Smith K, Walker BR. Increased in vivo regeneration of cortisol in adipose tissue in human obesity and effects of the 11b-hydroxysteroid dehydrogenase type 1 inhibitor carbenoxolone. Diabetes 54(3), 872–879 (2005).
  • Basu R, Singh RJ, Basu A et al. Obesity and Type 2 diabetes do not alter splanchnic cortisol production in humans. J. Clin. Endocrinol. Metab. 90(7), 3919–3926 (2005).
  • Wake DJ, Rask E, Livingstone DE, Söderberg S, Olsson T, Walker BR. Local and systemic impact of transcriptional up-regulation of 11b-hydroxysteroid dehydrogenase Type 1 in adipose tissue in human obesity. J. Clin. Endocrinol. Metab. 88(8), 3983–3988 (2003).
  • Gambineri A, Repaci A, Patton L et al. Prominent role of low HDL-cholesterol in explaining the high prevalence of the metabolic syndrome in polycystic ovary syndrome. Nutr. Metab. Cardiovasc. Dis. 19(11), 797–804 (2009).
  • Rodin A, Thakkar H, Taylor N, Clayton R. Hyperandrogenism in polycystic ovary syndrome. Evidence of dysregulation of 11 b-hydroxysteroid dehydrogenase. N. Engl. J. Med. 330(7), 460–465 (1994).
  • Tsilchorozidou T, Honour JW, Conway GS. Altered cortisol metabolism in polycystic ovary syndrome: insulin enhances 5α-reduction but not the elevated adrenal steroid production rates. J. Clin. Endocrinol. Metab. 88(12), 5907–5913 (2003).
  • Gambineri A, Forlani G, Munarini A et al. Increased clearance of cortisol by 5b-reductase in a subgroup of women with adrenal hyperandrogenism in polycystic ovary syndrome. J. Endocrinol. Invest. 32(3), 210–218 (2009).
  • Stewart PM, Shackleton CH, Beastall GH, Edwards CR. 5 α-reductase activity in polycystic ovary syndrome. Lancet 335(8687), 431–433 (1990).
  • Chin D, Shackleton C, Prasad VK et al. Increased 5α-reductase and normal 11b-hydroxysteroid dehydrogenase metabolism of C19 and C21 steroids in a young population with polycystic ovarian syndrome. J. Pediatr. Endocrinol. Metab. 13(3), 253–259 (2000).
  • Gambineri A, Tomassoni F, Munarini A et al. A combination of polymorphisms in HSD11B1 associates with in vivo 11{b}-HSD1 activity and metabolic syndrome in women with and without polycystic ovary syndrome. Eur. J. Endocrinol. 165(2), 283–292 (2011).
  • Svendsen PF, Madsbad S, Nilas L, Paulsen SK, Pedersen SB. Expression of 11b-hydroxysteroid dehydrogenase 1 and 2 in subcutaneous adipose tissue of lean and obese women with and without polycystic ovary syndrome. Int. J. Obes. 33(11), 1249–1256 (2009).
  • Tomlinson JW, Walker EA, Bujalska IJ et al. 11b-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response. Endocr. Rev. 25(5), 831–866 (2004).
  • Wake DJ, Homer NZ, Andrew R, Walker BR. Acute in vivo regulation of 11b-hydroxysteroid dehydrogenase type 1 activity by insulin and intralipid infusions in humans. J. Clin. Endocrinol. Metab. 91(11), 4682–4688 (2006).
  • Draper N, Echwald SM, Lavery GG et al. Association studies between microsatellite markers within the gene encoding human 11b-hydroxysteroid dehydrogenase type 1 and body mass index, waist to hip ratio, and glucocorticoid metabolism. J. Clin. Endocrinol. Metab. 87(11), 4984–4990 (2002).
  • Nair S, Lee YH, Lindsay RS et al. 11b-Hydroxysteroid dehydrogenase type 1: genetic polymorphisms are associated with Type 2 diabetes in Pima Indians independently of obesity and expression in adipocyte and muscle. Diabetologia 47(6), 1088–1095 (2004).
  • Franks PW, Knowler WC, Nair S et al. Interaction between an 11bHSD1 gene variant and birth era modifies the risk of hypertension in Pima Indians. Hypertension 44(5), 681–688 (2004).
  • Draper N, Walker EA, Bujalska IJ et al. Mutations in the genes encoding 11b-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase deficiency. Nat. Genet. 34(4), 434–439 (2003).
  • Gambineri A, Vicennati V, Genghini S et al. Genetic variation in 11b-hydroxysteroid dehydrogenase type 1 predicts adrenal hyperandrogenism among lean women with polycystic ovary syndrome. J. Clin. Endocrinol. Metab. 91(6), 2295–2302 (2006).

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