Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 1.736
5-Year Impact Factor – 2.135
Index Copernicus  – 168.52
MEiN – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

Download original text (EN)

Advances in Clinical and Experimental Medicine

2020, vol. 29, nr 10, October, p. 1181–1186

doi: 10.17219/acem/126291

Publication type: original article

Language: English

License: Creative Commons Attribution 3.0 Unported (CC BY 3.0)

Download citation:

  • BIBTEX (JabRef, Mendeley)
  • RIS (Papers, Reference Manager, RefWorks, Zotero)

Gender differences in variables associated with dipeptidyl peptidase 4 genetic polymorphisms in coronary artery disease

Shih-Min Chiang1,B,C,E, Kwo-Chang Ueng2,3,A,B,E,F, Yi-Sun Yang2,3,A,D,F

1 Institute of Medicine, Chung-Shan Medical University, Taichung, Taiwan

2 School of Medicine, Chung-Shan Medical University, Taichung, Taiwan

3 Department of Internal Medicine, Chung-Shan Medical University Hospital, Taichung, Taiwan

Abstract

Background. In recent years, considerable effort has been devoted to identifying genes that contribute to the risk of coronary artery disease (CAD). Genetic factors can be used to identify individuals who have additional genetic risks. Genetic variations might contribute to cardiovascular disease differentially in men and women. Dipeptidyl peptidase-4 (DPP-4) may be involved in the development of atherosclerotic diseases.
Objectives. To examine the associations between genetic variations of DPP-4 in men and women with CAD.
Material and Methods. In this case-control study, blood samples of patients with angiographically documented CAD and of those without CAD were collected. We focused on the DPP-4 gene (rs7608798 and rs3788979 polymorphisms) to assess the association of single nucleotide polymorphisms (SNPs) and the risk of CAD.
Results. We identified 1 SNP (rs3788979) that was significantly related to angiographic CAD in women (odds ratio (OR) = 2.437; p = 0.019). Moreover, the SNP (rs7608798) seemed to have a protective effect (OR = 0.291; p = 0.032). We did not find an association between CAD risk factors and DPP-4 polymorphisms. Our study is the first to demonstrate that CAD pathogenesis is influenced by gender differences in polymorphisms in the DPP-4 gene.
Conclusion. This study provides new information on the association of DPP-4 polymorphisms with the risk of CAD in the Taiwanese population, especially in women. Further studies should be performed to verify this association.

Key words

women, coronary artery disease, DPP-4 polymorphisms

References (27)

  1. Joseph P, Leong D, McKee M, et al. Reducing the global burden of cardiovascular disease. Part 1: The epidemiology and risk factors. Circ Res. 2017;121(6):677–694.
  2. Leong DP, Joseph PG, McKee M, et al. Reducing the global burden of cardiovascular disease. Part 2: Prevention and treatment of cardiovascular disease. Circ Res. 2017;121(6):695–710.
  3. Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CLJ. Global and regional burden of disease and risk factors, 2001: Systematic analysis of population health data. Lancet. 2006;367(9524):1747–1757.
  4. Wang B, Fu ZY, Ma YT, et al. Identification of a CYP19 gene single-nucleotide polymorphism associated with a reduced risk of coronary heart disease. Genet Test Mol Biomarkers. 2016;20(1):2–10.
  5. Winkelmann BR, Hager J. Genetic variation in coronary heart disease and myocardial infarction: Methodological overview and clinical evidence. Pharmacogenomics. 2000;1(1):73–94.
  6. Inzucchi SE, McGuire DK. New drugs for the treatment of diabetes. Part II: Incretin-based therapy and beyond. Circulation. 2008;117(4):574–584.
  7. Augustyns K, Bal G, Thonus G, et al. The unique properties of dipeptidyl-peptidase IV (DPP IV/CD26) and the therapeutic potential of DPP IV inhibitors. Curr Med Chem. 1999;6(4):311–327.
  8. Duan L, Rao X, Xia C, et al. The regulatory role of DPP-4 in atherosclerotic disease. Cardiovasc Diabetol. 2017;16:76.
  9. Pala L, Rotella CM. The role of DPP-4 activity in cardiovascular districts: In vivo and in vitro evidence. J Diabetes Res. 2013;2013:590456.
  10. Kazafeos K. Incretin effect: GLP-1, GIP, DPP-4. Diabetes Res Clin Pract. 2011;93(Suppl 1):S32–S36.
  11. White WB, Cannon CP, Heller SR, et al; EXAMINE Investigators. Alogliptin after acute coronary syndrome in patients with type 2 diabetes. N Engl J Med. 2013;369(14):1327–1335.
  12. Scirica BM, Bhatt DL, Braunwald E, et al; SAVOR-TIMI 53 Steering Committee and Investigators; Saxagliptin and cardiovascular outcomes in patients with type 2 diabetes mellitus. N Engl J Med. 2013;369:1317–1326.
  13. Green JB, Bethel MA, Armstrong PW, et al; TECOS Study Group. Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes. N Engl J Med. 2015;373(3):232–242.
  14. Xing X, Han Y, Zhou X, et al. Association between DPP-4 gene polymorphism and serum lipid levels in Chinese type 2 diabetes individuals. Neuropeptides. 2016;60:1–6.
  15. Aghili N, Devaney JM, Alderman LO, Zukowska Z, Epstein SE, Burnett MS. Polymorphisms in dipeptidyl peptidase IV gene are associated with the risk of myocardial infarction in patients with atherosclerosis. Neuropeptides. 2012;46(6):367–371.
  16. Spence JD, Pilote L. Importance of sex and gender in atherosclerosis and cardiovascular disease. Atherosclerosis. 2015;241(1):208–210.
  17. Orth-Gomer K, Deter HC. Sex and gender issues in cardiovascular research. Psychosom Med. 2015;77(9):1067–1068.
  18. Hausenloy DJ, Whittington HJ, Wynne AM, et al. Dipeptidyl peptidase-4 inhibitors and GLP-1 reduce myocardial infarct size in a glucose-dependent manner. Cardiovasc Diabetol. 2013;12:154.
  19. Chinda K, Palee S, Surinkaew S, Phornphutkul M, Chattipakorn S, Chattipakorn N. Cardioprotective effect of dipeptidyl peptidase-4 inhibitor during ischemia-reperfusion injury. Int J Cardiol. 2013;167(2):451–457.
  20. Silva Jr WS, Godoy-Matos AF, Kraemer-Aguiar LG. Dipeptidyl peptidase 4: A new link between diabetes mellitus and atherosclerosis? Biomed Res Int. 2015;2015:816164.
  21. Sato Y, Koshioka S, Kirino Y, et al. Role of dipeptidyl peptidase IV (DPP-4) in the development of dyslipidemia: DPP-4 contributes to the steroid metabolism pathway. Life Sci. 2011;88(1–2):43–49.
  22. Lei Y, Yang G, Hu L, et al; FAHA. Increased dipeptidyl peptidase-4 accelerates diet-related vascular aging and atherosclerosis in ApoE-deficient mice under chronic stress. Int J Cardiol. 2017;243:413–420.
  23. Mulvihill EE, Varin EM, Ussher JR, et al. Inhibition of dipeptidyl peptidase-4 impairs ventricular function and promotes cardiac fibrosis in high fat-fed diabetic mice. Diabetes. 2016;65(3):742–754.
  24. Shah Z, Kampfrath T, Deiuliis JA, et al. Long-term dipeptidyl-peptidase 4 inhibition reduces atherosclerosis and inflammation via effects on monocyte recruitment and chemotaxis. Circulation. 2011;124(21):2338–2349.
  25. Ida S, Murata K, Betou K, et al. Effect of trelagliptin on vascular endothelial functions and serum adiponectin level in patients with type 2 diabetes: A preliminary single-arm prospective pilot study. Cardiovasc Diabetol. 2016;15:153.
  26. Manrique C, Habibi J, Aroor AR, et al. Dipeptidyl peptidase-4 inhibition with linagliptin prevents Western diet-induced vascular abnormalities in female mice. Cardiovasc Diabetol. 2016;15:94.
  27. Aroor AR, Habibi J, Kandikattu HK, et al. Dipeptidyl peptidase-4 (DPP-4) inhibition with linagliptin reduces Western diet-induced myocardial TRAF3IP2 expression, inflammation and fibrosis in female mice. Cardiovasc Diabetol. 2017;16(1):61.
© Wroclaw Medical University