Investigating the relation between transforming growth factor-β1 bioavailability with vitamin D and calcium in PCOS patients
DOI:
https://doi.org/10.22317/jcms.v9i6.1466Keywords:
Calcium, Polycystic Ovary Syndrome, Transforming Growth Factor-beta1, Soluble Endoglin, Vitamin DAbstract
Objective: This study seeks to explore the association between TGF-β1 bioavailability and vitamin D/calcium levels in women with
polycystic ovary syndrome (PCOS), aiming to uncover potential links that could contribute to understanding the pathogenesis of PCOS
and its management.
Methods: Case-control study comprises of 60 women with PCOS and 60 healthy control women. Fasting serum TGF-β1, sEND, vitamin D
and calcium were measured. Additionally, Anthropometric parameters: age, body mass index, blood pressure; diabetes parameters: fasting glucose, fasting insulin, homeostatic model assessment of insulin resistance index (HOMA-IR), homeostatic model assessment of beta–cell function (HOMA-B2); Lipid profile: TC, TG, LDL, HDL, VLDL were assessed.
Results: There were significant increasing in serum TGF-β1 and its bioavailability in PCOS compared to control whereas there were
significant decreasing in serum sENG in PCOS compared to control. Additionally, serum vitamin D was lower significantly in PCOS than in
control while serum calcium was higher significantly in PCOS than in control. The correlation did not find between TGF-β1, sENG, TGF-β1/
sENG with vitamin D and calcium and with other metabolic parameters. However, positive correlation was found between calcium and BMI and between TGF-β1 and it bioavailability (TGF-β1/sENG).
Conclusion: Elevated TGF-β1 bioavailability results from increase serum TGF-β1 combine with decrease serum sENG, suggesting a potential role of TGF-β1 bioavailability in arresting follicular development in PCOS patients. Moreover, significant decrease in vitamin D and significant increase of calcium in PCOS patients, indicating that vitamin D and calcium may be involve in PCOS pathogenesis.
References
Al-Tu’ma F J, Farhan N H and Al-Safi W G (2015) Association between fat mass and obesity gene (re9939609) polymorphism with PCOS women in Iraqi poipulation. Int. J. Pharm.Pharm. Res. 5(1), 62–72.
Norman RJ, Dewailly D, Legro RS and Hickey TEl (2007) Polycystic ovary syndrome. Lancet370(9588),685-97.
Carmina, E, Oberfield SE, and Lobo RA (2010) The diagnosis of polycystic ovary syndrome in adolescents. Am J Obstet Gynecol 203(3), 201.e1-5.
Al-Tu’ma F J, Farhan N H and Al-Safi W G (2017) Polymorphism of tumor necrosis factor-alpha 308 G/A gene in Iraqi patients with polycystic ovarian syndrome. Iraq Med J. 1( 2),45–49.
Corduk N, Abban G, Yildirim B and Sarioglu-Buke A (2012) The effect of vitamin D on expression of TGF β1 in ovary. Exp Clin Endocrinol Diabetes 120(8), 490-3.
Eldar-Geva T, Spitz IM, Groome NJ, Margalioth EJ and Homburg R (2001) Follistatin and activin A serum concentrations in obese and non-obese patients with polycystic ovary syndrome. Human Reproduction 16(12), 2552-2556.
Welt CK, Taylor AE, Fox J, Messerlain GM, Adams JM and Schneyer AL (2005) Follicular Arrest in Polycystic Ovary Syndrome Is Associated with Deficient Inhibin A and B Biosynthesis. The Journal of Clinical Endocrinology & Metabolism 90(10), 5582-5587.
Fleming R, Harborne L, MacLaughlin DT et al (2005) Metformin reduces serum mullerian-inhibiting substance levels in women with polycystic ovary syndrome after protracted treatment. Fertil Steril 83(1), 130-6.
Jordan CD, Dohling SD Charbonneau NL and Sakai LY (2010) Fibrillins in adult human ovary and polycystic ovary syndrome: is fibrillin-3 affected in PCOS? J Histochem Cytochem 58(10), 903-15.
Ewens KG, Stewart DR and Ankener W (2010) Family-based analysis of candidate genes for polycystic ovary syndrome. J Clin Endocrinol Metab 95(5), 2306-15.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2023 Journal of Contemporary Medical Sciences
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
