Comparison of metabolic abnormalities in patients with new-diagnostic polycystic ovary syndrome and with new-diagnostic Type 2 diabetes mellitus


Background: Metabolic abnormalities have been widely studied in women with polycystic ovary syndrome (PCOS) and in patients with Type 2 diabetes mellitus (T2DM). However, there are few studies on the comparison of the metabolic disturbances between the two diseases although they have partly common pathogenesis. This study compares the metabolic parameters of PCOS and T2DM, and evaluates the association between metabolic parameters and gonadotropic hormones. Methods: Fifity newly diagnosed PCOS women and 56 newly diagnosed Type 2 diabetes women were enrolled in the study. The metabolic parameters including body mass index, waist to hip ratio, blood pressure, total cholesterol, triglycerides, high-density and low-density lipoprotein cholesterol, fasting and postprandial plasma glucose, fasting and postprandial plasma insulin, HOMA-IR index and uric acid, along with the gonadal and gonadotropic hormones were analyzed between the two groups. The lutein hormone (LH) responses to the GnRH stimulating test were compared between different glucose tolerance groups in PCOS women. The peak values of LH in the GnRH test are studied with metabolic parameters using Pearson correlation analysis. Results: PCOS patients have higher body weight index, waist to hip ratio, fasting and postprandial insulin, HOMA-IR and uric acid than T2DM patients. There are no significant differences in lipid metabolism excluding the age influence. On the other hand, T2DM patients have significantly higher systolic blood pressure and plasma glucose than those in PCOS patients. But there is less clinical significance in the level of plasma glucose. After GnRH injection in PCOS women, there are significant differences in LH reaction between the three groups with different glucose tolerance. Conclusion: Women with PCOS have more severe metabolic disturbance than women with T2DM except for systolic blood pressure. Insulin resistance affects the function of thalamus-pituitary-gonad axis.

Share and Cite:

Fang, F. , Gu, M. , Chen, L. , Li, N. , Ding, X. and Peng, Y. (2014) Comparison of metabolic abnormalities in patients with new-diagnostic polycystic ovary syndrome and with new-diagnostic Type 2 diabetes mellitus. Journal of Diabetes Mellitus, 4, 54-58. doi: 10.4236/jdm.2014.41010.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] Salley, K.E., Wickham, E.P., Cheang, K.I., Essah, P.A., Karjane, N.W. and Nestler, J.E. (2007) Glucose intolerance in polycystic ovary syndrome—A position statement of the Androgen Excess Society. The Journal of Clinical Endocrinology and Metabolism, 92, 4546-4556.
[2] Moran, L.J., Misso, M.L., Wild, R.A., Norman, R.J. (2010) Impaired glucose tolerance, Type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: A systematic review and meta-analysis. Hum Reprod Update, 16, 347-363.
[3] Wild, R.A., Carmina, E., Diamanti-Kandarakis, E., Dokras, A., Escobar-Morreale, H.F., Futterweit, W., Lobo, R., Norman, R.J., Talbott, E. and Dumesic, D.A. (2010) Assessment of cardiovascular risk and prevention of cardiovascular disease in women with the polycystic ovary syndrome: A consensus statement by the Androgen Excess and Polycystic Ovary Syndrome (AE-PCOS) Society. The Journal of Clinical Endocrinology and Metabolism, 95, 2038-2049.
[4] Levy, J.C., Matthews, D.R. and Hermans, M.P. (1998) Correct homeostasis model assessment (HOMA) evaluation uses the computer program[J]. Diabetes Care, 21, 2191-2192. diacare.21.12.2191
[5] Burghen, G.A., Givens, J.R. and Kitabchi, A.E. (1980) Correlation of hyperandrogenism with hyperinsulinism in polycystic ovarian disease. The Journal of Clinical Endocrinology and Metabolism, 50,113-116.
[6] Dunaif, A. and Thomas, A. (2001) Current Concepts in the polycystic ovary syndrome. Annual Review of Medicine, 52, 401-404.
[7] Lin, T.C., Yen, J.M., Gong, K.B., et al. (2006) Abnormal glucose tolerance and insulin resistance in polycystic ovary syndrome amongst the Taiwanese populationnot correlated with insulin receptor substrate-1 Gly972Arg/ Ala513Pro polymorphism. BMC Medical Genetics, 7, 36-38.
[8] Fruzzetti, F., Perini, D., Lazzarini, V., et al. (2009) Hyperandrogenemia influences the prevalence of the metabolic syndrome abnormalities in adolescents with the polycystic ovary syndrome. Gynecological Endocrinology, 25, 335-343.
[9] Ghazeeri, G., Kutteh, W.H., Bryer-Ash, M., et al. (2003) Effect of rosiglitazone on spontaneous and clomiphene citrate-induced ovulation in women with polycystic ovary syndrome. Fertility and Sterility, 79, 562-566.

Copyright © 2022 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.