Endocrinol Diabetes Metab. 2021 May 24;4(3):e00267. doi: 10.1002/edm2.267. eCollection 2021 Jul.
The relationships of sex hormone-binding globulin, total testosterone, androstenedione and free testosterone with metabolic and reproductive features of polycystic ovary syndrome.
Endocrinology, diabetes & metabolism
Pomme I H G Simons, Olivier Valkenburg, Judith A P Bons, Coen D A Stehouwer, Martijn C G J Brouwers
Affiliations
Affiliations
- Division of Endocrinology and Metabolic Diseases Department of Internal Medicine Maastricht University Medical Centre Maastricht The Netherlands.
- Laboratory for Metabolism and Vascular Medicine Maastricht University Maastricht The Netherlands.
- CARIM School for Cardiovascular Diseases Maastricht University Maastricht The Netherlands.
- Department of Reproductive Medicine Maastricht University Medical Centre Maastricht The Netherlands.
- Central Diagnostic Laboratory Maastricht University Medical Centre Maastricht The Netherlands.
- Division of General Internal Medicine Department of Internal Medicine Maastricht University Medical Centre Maastricht The Netherlands.
PMID: 34277990
PMCID: PMC8279613 DOI: 10.1002/edm2.267
Abstract
OBJECTIVE: A recent Mendelian randomization study has suggested a causal role for sex hormone-binding globulin (SHBG), total testosterone and free testosterone in the pathogenesis of polycystic ovary syndrome (PCOS). The aim of this study was to assess the relationships of SHBG, androstenedione, total and free testosterone with the individual metabolic and reproductive features of PCOS.
DESIGN: Cross-sectional data in PCOS patients (n=96) prospectively collected in a secondary/tertiary clinic for menstrual cycle disorders.
METHODS: Multivariable regression analyses were conducted to study the associations between SHBG, androstenedione, total and free testosterone with metabolic (BMI, waist circumference, systolic and diastolic blood pressure, total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides and homeostatic model assessment for insulin resistance [HOMA2-IR]) and reproductive features (menstrual cycle length, antral follicle count, anti-Müllerian hormone, luteinizing hormone, follicle-stimulating hormone and Ferriman-Gallwey score) of PCOS.
RESULTS: Serum SHBG and free testosterone, but not total testosterone or androstenedione, were significantly associated with BMI, waist circumference, serum triglycerides, HDL cholesterol, LDL cholesterol and HOMA2-IR. The strength of the associations with serum lipids was reduced after adjustment for BMI, but not for HOMA2-IR. Total testosterone was significantly associated with antral follicle count. SHBG, total testosterone and androstenedione were significantly associated with serum AMH. Only the strength of the association for SHBG was reduced after adjustment for BMI.
CONCLUSIONS: Serum SHBG is associated with primarily metabolic features, whereas total testosterone and androstenedione are associated with reproductive features of PCOS. These results suggest a differential underlying pathophysiology for the metabolic and reproductive features of PCOS.
© 2021 The Authors. Endocrinology, Diabetes & Metabolism published by John Wiley & Sons Ltd.
Keywords: androgens; metabolic syndrome; polycystic ovary syndrome; sex hormone‐binding globulin
Conflict of interest statement
The authors declare that there is no conflict of interest.
References
- Trends Endocrinol Metab. 2008 Nov;19(9):340-7 - PubMed
- J Clin Endocrinol Metab. 2020 Jun 1;105(6): - PubMed
- Obstet Gynecol Surv. 2002 Nov;57(11):755-67 - PubMed
- Mol Metab. 2020 May;35:100937 - PubMed
- Fertil Steril. 2004 Jan;81(1):19-25 - PubMed
- Nat Med. 2020 Feb;26(2):252-258 - PubMed
- Clin Chem Lab Med. 2005;43(6):613-6 - PubMed
- J Clin Endocrinol Metab. 2006 Apr;91(4):1345-50 - PubMed
- J Clin Invest. 2007 Dec;117(12):3979-87 - PubMed
- Eur J Endocrinol. 2011 Feb;164(2):197-203 - PubMed
- Int J Environ Res Public Health. 2018 Nov 20;15(11): - PubMed
- PLoS Med. 2020 Jun 23;17(6):e1003132 - PubMed
- Hum Reprod. 2018 Sep 1;33(9):1602-1618 - PubMed
- Am J Clin Nutr. 2003 Jan;77(1):43-50 - PubMed
- J Clin Endocrinol Metab. 2005 Jul;90(7):4112-4 - PubMed
- Clin Endocrinol (Oxf). 2017 Sep;87(3):217-230 - PubMed
- Int J Endocrinol. 2018 Sep 10;2018:7956951 - PubMed
- J Clin Endocrinol Metab. 2004 Feb;89(2):453-62 - PubMed
- Mol Hum Reprod. 2013 Dec;19(12):828-37 - PubMed
- Hum Reprod. 2016 Dec;31(12):2796-2802 - PubMed
- J Endocrinol Invest. 2013 Dec;36(11):1004-10 - PubMed
- Trends Endocrinol Metab. 2002 Aug;13(6):251-7 - PubMed
- Fertil Steril. 2013 Aug;100(2):585-92.e1 - PubMed
- Nat Rev Dis Primers. 2016 Aug 11;2:16057 - PubMed
- Int J Epidemiol. 2015 Apr;44(2):623-37 - PubMed
- J Endocrinol Invest. 1998 Oct;21(9):602-11 - PubMed
- Clin Chem. 1972 Jun;18(6):499-502 - PubMed
- J Clin Invest. 2020 Mar 2;130(3):1453-1460 - PubMed
- Clin Chim Acta. 2019 Dec;499:142-148 - PubMed
- Eur J Endocrinol. 2007 Oct;157(4):499-507 - PubMed
- Clin Endocrinol (Oxf). 2021 Jul;95(1):101-106 - PubMed
- Hum Reprod. 2005 Oct;20(10):2893-8 - PubMed
- Fertil Steril. 2011 Sep;96(3):792-6 - PubMed
- Trends Endocrinol Metab. 2018 Dec;29(12):841-852 - PubMed
- Andrology. 2013 Jan;1(1):17-23 - PubMed
- Syst Biol Reprod Med. 2018 Feb;64(1):12-24 - PubMed
- N Engl J Med. 2009 Sep 17;361(12):1152-63 - PubMed
- J Clin Endocrinol Metab. 1998 Jun;83(6):2001-5 - PubMed
- Hum Mol Genet. 2010 Feb 1;19(3):535-44 - PubMed
- J Nutr Biochem. 2020 Nov;85:108480 - PubMed
- Endocrine. 2014 Nov;47(2):631-8 - PubMed
- Circulation. 2005 Oct 25;112(17):2735-52 - PubMed
Publication Types