Women with polycystic ovary syndrome (PCOS) often develop type 2 diabetes mellitus (T2DM). To determine the magnitude of risk of developing T2DM among women with PCOS, development of T2DM was prospectively assessed among women who had T2DM (n = 97) and controls (n = 95) using Kaplan-Meier survival analysis and Cox proportional hazards modeling. The women with T2DM had higher baseline weight (body mass index, P < 0.01) and lower insulin sensitivity (homeostasis assessment model of insulin resistance, P < 0.01). The 8-year incidence rate among cases and controls was 13.4% and 5.8%, respectively (relative risk = 2.3). Obese cases had a fivefold risk of T2DM developing (P < 0.01) compared with age-adjusted obese controls, indicating significant interaction between PCOS and obesity to effect T2DM risk.
This is a preview of subscription content, access via your institution.
Buy single article
Instant access to the full article PDF.
Tax calculation will be finalised during checkout.
References and Recommended Reading
Yen SS: Chronic anovulation caused by peripheral endocrine disorders. In Reproductive Endocrinology: Physiology, Pathophysiology and Clinical Management, edn 2. Edited by Yen S, Jaffe R. Philadelphia: W.B. Saunders Co.; 1986:576–630.
Ehrmann DA: Polycystic ovary syndrome. N Engl J Med 2005, 352:1223–1236.
Azziz R, Woods KS, Reyna R, et al.: The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab 2004, 89:2745–2749.
Legro RS, Bentley-Lewis R, Driscoll D, et al.: Insulin resistance in the sisters of women with polycystic ovary syndrome: association with hyperandrogenemia rather than menstrual irregularity. J Clin Endocrinol Metab 2002, 87:2128–2133.
Kiddy DS, Hamilton-Fairley D, Bush A, et al.: Improvement in endocrine and ovarian function during dietary treatment of obese women with polycystic ovary syndrome. Clin Endocrinol 1992, 36:105–111.
Dunaif A, Scott D, Finegood D, et al.: The insulin sensitizing agent troglitazone improves metabolic and reproductive abnormalities in PCOS. J Clin Endocrinol Metab 1996, 81:3299–3306.
Dunaif A: Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis. Endocr Rev 1997, 18:774–800.
Talbott E, Guzick D, Clerici A, et al.: Coronary heart disease risk factors in women with polycystic ovary syndrome. Arterioscler Thromb Vasc Biol 1995, 15:821–826.
Nordt TK, Sawa H, Fujii S, et al.: Induction of plasminogen activator inhibitor type-1 (PAI-1) by proinsulin and insulin in vivo. Circulation 1995, 91:764–770.
Talbott E, Clerici A, Berga SL, et al.: Adverse lipid and coronary heart disease risk profiles in young women with polycystic ovary syndrome: results of a case-control study. J Clin Epidemiol 1998, 51:415–422.
Talbott EO, Guzick DS, Sutton-Tyrrell K, 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.
Dunaif A, Graf M, Mandeli J, et al.: Characterization of groups of hyperandrogenic women with acanthosis nigricans, impaired glucose tolerance, and/or hyperinsulinemia. J Clin Endocrinol Metab 1987, 65:499–507.
Dunaif A, Finegood DT: Beta-cell dysfunction independent of obesity and glucose intolerance in the polycystic ovary syndrome. J Clin Endocrinol Metab 1996, 81:942–947.
Legro RS, Kunselman AR, Dodson WC, et al.: Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovar y syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab 1999, 84:165–169.
Weerakiet S, Srisombut C, Bunnag P, et al.: Prevalence of t ype 2 diabetes mellitus and impaired glucose tolerance in Asian women with polyc ystic ovar y syndrome. Int J Gynaecol Obstet 2001, 75:177–184.
Talbott EO, Zborowski JV, Boudreaux MY: Do women with polycystic ovary syndrome have an increased risk of cardiovascular disease? A review of the evidence. Minerva Ginecol 2004, 56:27–39. This review of cardiovascular risk in women with PCOS significantly contributed to the literature through comprehensive review of clinical and subclinical factors through which PCOS may affect cardiovascular profiles of affected women. The longitudinal data used in compiling this review are unique in that there was longer duration of follow-up than normally available in other PCOS cohorts and in the older subset of women used in assessing risk.
Ehrmann DA, Barnes RB, Rosenfield RL, et al.: Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome. Diabetes Care 1999, 22:141–146.
Norman RJ, Masters L, Milner CR, et al.: Relative risk of conversion from normoglycaemia to impaired glucose tolerance or non-insulin dependent diabetes mellitus in polycystic ovarian syndrome. Hum Reprod 2001, 16:1995–1998. Norman et al. did the only other pure incidence assessment of T2DM among women with PCOS. Their contribution showed the early impact of PCOS on development and T2DM through use of a relatively young population and their results highlighted how early differentiation between PCOS and non-PCOS affected groups can be seen.
Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus [no authors listed]. Diabetes Care 1997, 20:1183–1197.
Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group: Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 2004, 81:19–25.
Warnick GR, Albers JJ: A comprehensive evaluation of heparin-manganese precipitation procedure for estimating high density lipoprotein cholesterol. J Lipid Res 1978, 19:65–76.
Bucolo G, David H: Quantitative determination of serum triglycerides by the use of enzymes. Clin Chem 1973, 19:476–482.
Fried LP, Borhani NO, Enright P, et al.: The Cardiovascular Health Study: design and rationale. Ann Epidemiol 1991, 1:263–276.
Bondar RJ, Mead DC: Evaluation of glucose-6-phosphate dehydrogenase from Leuconostoc mesenteroides in the hexokinase method for determining glucose in serum. Clin Chem 1974, 20:586–590.
Matthews DR, Hosker JP, Rudenski AS, et al.: Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985, 28:412–419.
Bonora E, Targher G, Alberiche M, et al.: Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity: studies in subjects with various degrees of glucose tolerance and insulin sensitivity. Diabetes Care 2000, 23:57–63.
Hanson RL, Pratley RE, Bogardus C, et al.: Evaluation of simple indices of insulin sensitivity and insulin secretion for use in epidemiologic studies. Am J Epidemiol 2000, 151:190–198.
Howard G, Bergman R, Wagenknecht LE, et al.: Ability of alternative indices of insulin sensitivity to predict cardiovascular risk: comparison with the "minimal model." Insulin Resistance Atherosclerosis Study (IRAS) Investigators. Ann Epidemiol 1998, 8:358–369.
Hauner H: Managing type 2 diabetes mellitus in patients with obesity. Treat Endocrinol 2004, 3:223–232.
Ovalle F, Azziz R: Insulin resistance, polycystic ovary syndrome, and type 2 diabetes mellitus. Fertil Steril 2002, 77:1095–1105.
Harris MI, Flegal KM, Cowie CC, et al.: Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988–1994. Diabetes Care 1998, 21:518–524.
Nelson VL, Qin KN, Rosen.eld RL, et al.: The biochemical basis for increased testosterone production in theca cells propagated from patients with polycystic ovary syndrome. J Clin Endocrinol Metab 2001, 86:5925–5933.
Nelson VL, Legro RS, Strauss JF 3rd, McAllister JM: Augmented androgen production is a stable steroidogenic phenotype of propagated theca cells from polycystic ovaries. Mol Endocrinol 1999, 13:946–957.
Wickenheisser JK, Nelson-DeGrave VL, Quinn PG, McAllister JM: Increased cytochrome P450 17alpha-hydroxylase promoter function in theca cells isolated from patients with polycystic ovary syndrome involves nuclear factor-1. Mol Endocrinol 2004, 18:588–605.
Wickenheisser JK, Nelson-Degrave VL, McAllister JM: Dysregulation of cytochrome P450 17alpha-hydroxylase messenger ribonucleic acid stability in theca cells isolated from women with polycystic ovary syndrome. J Clin Endocrinol Metab 2005, 90:1720–1727.
Burghen GA, Givens JR, Kitabchi AE: Correlation of hyperandrogenism with hyperinsulinism in polycystic ovarian disease. J Clin Endocrinol Metab 1980, 50:113–116.
Dunaif A, Segal KR, Futterweit W, et al.: Profound peripheral insulin resistance, independent of obesity, in polycystic ovary syndrome. Diabetes 1989, 38:1165–1174.
Chang RJ, Nakamura RM, Judd HL, et al.: Insulin resistance in nonobese patients with polycystic ovarian disease. J Clin Endocrinol Metab 1983, 57:356–359.
dos Reis RM, Foss MC, de Moura MD, et al.: Insulin secretion in obese and non-obese women with polycystic ovary syndrome and its relationship with hyperandrogenism. Gynecol Endocrinol 1995, 9:45–50.
Shoupe D, Kumar DD, Lobo RA: Insulin resistance in polycystic ovary syndrome. Am J Obstet Gynecol 1983, 147:588–592.
About this article
Cite this article
Boudreaux, M.Y., Talbott, E.O., Kip, K.E. et al. Risk of T2DM and impaired fasting glucose among pcos subjects: Results of an 8-year follow-up. Curr Diab Rep 6, 77–83 (2006). https://doi.org/10.1007/s11892-006-0056-1
- Body Mass Index
- Impaired Glucose Tolerance
- Polycystic Ovary Syndrome
- Impair Fasting Glucose
- Arterioscler Thromb Vasc Biol