David Olufemi Adebo1 
, Mathew Folaranmi Olaniyan2 , Gabriel Olufemi Daramola3 , Christian Onosetale Ugege2 , Odekunle Bola Odegbemi * 4
, Mathew Folaranmi Olaniyan2 , Gabriel Olufemi Daramola3 , Christian Onosetale Ugege2 , Odekunle Bola Odegbemi * 4
1- Medical Laboratory Science Department, Edo State University, Uzairue, Edo State, Nigeria ; Chemical Pathology Department, Ekiti State University Teaching Hospital, Ado-Ekiti, Ekiti State, Nigeria
2- Medical Laboratory Science Department, Edo State University, Uzairue, Edo State, Nigeria
3- Medical Microbiology and Parasitology Department, Ekiti State University Teaching Hospital, Ado-Ekiti, Ekiti State, Nigeria ; Medical Laboratory Science Department, College of Medicine, Ekiti State University, Ado-Ekiti, Ekiti State, Nigeria
4- Medical Laboratory Science Department, Edo State University, Uzairue, Edo State, Nigeria;Medical Laboratory Science Department, Nigerian Navy Hospital, Warri, Delta State, Nigeria ,odegbemi21.odekunle@edouniversity.edu.ng
2- Medical Laboratory Science Department, Edo State University, Uzairue, Edo State, Nigeria
3- Medical Microbiology and Parasitology Department, Ekiti State University Teaching Hospital, Ado-Ekiti, Ekiti State, Nigeria ; Medical Laboratory Science Department, College of Medicine, Ekiti State University, Ado-Ekiti, Ekiti State, Nigeria
4- Medical Laboratory Science Department, Edo State University, Uzairue, Edo State, Nigeria;Medical Laboratory Science Department, Nigerian Navy Hospital, Warri, Delta State, Nigeria ,
Abstract: (56 Views)
Background: This study investigated the role of PPARG genetic variants in type 2 diabetes mellitus complications among individuals in Ekiti State, Nigeria. The focus was on understanding how these genetic variants may influence biochemical markers and, consequently, the risk of complications.
Methods: We recruited 74 diabetic patients and 20 controls from a university teaching hospital. Ten milliliters of whole blood samples were collected by venipuncture and divided into two 5-milliliter aliquots. One aliquot was placed in an EDTA bottle, and the other in a fluoride oxalate bottle, before centrifugation to obtain plasma. PPARG genotyping and biochemical marker analyses, including Cystatin C, ALT, CK-MB, and IL-10, were performed.
Results: Significant differences in PPARG genotype distribution were observed, with the GG genotype being more common in diabetic individuals. Diabetic subjects showed elevated Cystatin C, ALT, and CK-MB levels, along with reduced IL-10, particularly among females. PPARG genotypes were associated with several biochemical markers, notably Cystatin C (p = 0.002), ALT (p = 0.030), and FBS (p = 0.017).
Conclusion: These findings highlight a complex relationship between PPARG genotypes and the pathophysiology of diabetes in the Nigerian population, emphasizing the potential for personalized medicine approaches in type 2 diabetes mellitus management.
Methods: We recruited 74 diabetic patients and 20 controls from a university teaching hospital. Ten milliliters of whole blood samples were collected by venipuncture and divided into two 5-milliliter aliquots. One aliquot was placed in an EDTA bottle, and the other in a fluoride oxalate bottle, before centrifugation to obtain plasma. PPARG genotyping and biochemical marker analyses, including Cystatin C, ALT, CK-MB, and IL-10, were performed.
Results: Significant differences in PPARG genotype distribution were observed, with the GG genotype being more common in diabetic individuals. Diabetic subjects showed elevated Cystatin C, ALT, and CK-MB levels, along with reduced IL-10, particularly among females. PPARG genotypes were associated with several biochemical markers, notably Cystatin C (p = 0.002), ALT (p = 0.030), and FBS (p = 0.017).
Conclusion: These findings highlight a complex relationship between PPARG genotypes and the pathophysiology of diabetes in the Nigerian population, emphasizing the potential for personalized medicine approaches in type 2 diabetes mellitus management.
Article Type: Research |
Subject:
Biochemistry
References
1. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2014;37(Supplement 1):S81-90. [View at Publisher] [DOI] [PMID] [Google Scholar]
2. World Health Organization. Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: report of a WHO/IDF consultation. 2006. [View at Publisher] [Google Scholar]
3. International Diabetes Federation. IDF Diabetes Atlas, 9th Ed. Brussels, Belgium:International Diabetes Federation;2019. [View at Publisher] [Google Scholar]
4. Shaw JE, Sicree RA, Zimmet PZ. Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes Res Clin Pract. 2010;87(1):4-14. [View at Publisher] [DOI] [PMID] [Google Scholar]
5. Nathan DM. Long-term complications of diabetes mellitus. N Engl J Med. 1993;328(23):1676-85. [View at Publisher] [DOI] [PMID] [Google Scholar]
6. Fowler MJ. Microvascular and macrovascular complications of diabetes. Clin Diabetes. 2008;26(2):77-82. [View at Publisher] [DOI] [Google Scholar]
7. Uloko AE, Musa BM, Ramalan MA, Gezawa ID, Puepet FH, Uloko AT, et al. Prevalence and risk factors for diabetes mellitus in Nigeria: a systematic review and meta-analysis. Diabetes Ther. 2018;9(3):1307-16. [View at Publisher] [DOI] [PMID] [Google Scholar]
8. Ogbera AO, Ekpebegh C. Diabetes mellitus in Nigeria: The past, present and future. World J Diabetes. 2014;5(6):905-11. [View at Publisher] [DOI] [PMID] [Google Scholar]
9. Lima JEBF, Moreira NCS, Sakamoto-Hojo ET. Mechanisms underlying the pathophysiology of type 2 diabetes: From risk factors to oxidative stress, metabolic dysfunction, and hyperglycemia. Mutat Res Genet Toxicol Environ Mutagen. 2022;874-875:503437. [View at Publisher] [DOI] [PMID] [Google Scholar]
10. Barroso I, Gurnell M, Crowley VE, Agostini M, Schwabe JW, Soos MA, et al. Dominant negative mutations in human PPARγ associated with severe insulin resistance, diabetes mellitus and hypertension. Nature. 1999;402(6764):880-3. [View at Publisher] [DOI] [PMID] [Google Scholar]
11. American Diabetes Association. Classification and diagnosis of diabetes: Standards of Medical Care in Diabetes-2021. Diabetes Care. 2021;44(Suppl 1):S15-33. [View at Publisher] [DOI] [PMID] [Google Scholar]
12. Saeedi P, Petersohn I, Salpea P, Malanda B, Karuranga S, Unwin N, et al. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Res Clin Pract. 2019;157:107843. [View at Publisher] [DOI] [PMID] [Google Scholar]
13. Stumvoll M, Häring H. The peroxisome proliferator-activated receptor-gamma2 Pro12 Ala polymorphism. Diabetes. 2002;51(8):2341-7. [View at Publisher] [DOI] [PMID] [Google Scholar]
14. Gouda HN, Sagoo GS, Harding AH, Yates J, Sandhu MS, Higgins JP. The association between the peroxisome proliferator-activated receptor-gamma2 (PPARG2) Pro12Ala gene variant and type 2 diabetes mellitus: A HuGE review and meta-analysis. Am J Epidemiol. 2010;171(6):645-55. [View at Publisher] [DOI] [Google Scholar]
15. McCarthy MI. Genomics, type 2 diabetes, and obesity. N Engl J Med. 2010;363(24):2339-50. [View at Publisher] [DOI] [PMID] [Google Scholar]
16. Langenberg C, Lotta LA. Genomic insights into the causes of type 2 diabetes. Lancet. 2018;391(10138):2463-74. [View at Publisher] [DOI] [PMID] [Google Scholar]
17. Shlipak MG, Matsushita K, Ärnlöv J, Inker LA, Katz R, Polkinghorne KR, et al. Cystatin C versus creatinine in determining risk based on kidney function. N Engl J Med. 2013;369(10):932-43. [View at Publisher] [DOI] [PMID] [Google Scholar]
18. Targher G, Bertolini L, Poli F, Rodella S, Scala L, Tessari R, et al. Nonalcoholic fatty liver disease and risk of future cardiovascular events among type 2 diabetic patients. Diabetes. 2005;54(12):3541-6. [View at Publisher] [DOI] [PMID] [Google Scholar]
19. Selvin E, Marinopoulos S, Berkenblit G, Rami T, Brancati FL, Powe NR, et al. Meta-analysis: Glycosylated hemoglobin and cardiovascular disease in diabetes mellitus. Ann Intern Med. 2004;141(6):421-31. [View at Publisher] [DOI] [PMID] [Google Scholar]
20. Esposito K, Nappo F, Marfella R, Giugliano G, Giugliano F, Ciotola M, et al. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: Role of oxidative stress. Circulation. 2002;106(16):2067-72. [View at Publisher] [DOI] [PMID] [Google Scholar]
21. Sarafidis PA, Stafylas PC, Georgianos PI, Avramides A, Lasaridis AN. Effect of thiazolidinediones on albuminuria and proteinuria in patients with type 2 diabetes: A meta-analysis. Am J Kidney Dis. 2010;55(5):835-47. [View at Publisher] [DOI] [PMID] [Google Scholar]
22. Gavrilova O, Haluzik M, Matsusue K, Cutson JJ, Johnson L, Dietz KR, et al. Liver peroxisome proliferator-activated receptor gamma contributes to hepatic steatosis, triglyceride clearance, and regulation of body fat mass. J Biol Chem. 2003;278(36):34268-76. [View at Publisher] [DOI] [PMID] [Google Scholar]
23. Ricote M, Huang JT, Welch JS, Schmedtje JF Jr, Liebman MN, Collins T, Glass CK. The peroxisome proliferator-activated receptor-gamma is a negative regulator of macrophage activation. Nature. 1998;391(6662):79-82. [View at Publisher] [DOI] [PMID] [Google Scholar]
24. Altshuler D, Hirschhorn JN, Klannemark M, Lindgren CM, Vohl MC, Nemesh J, et al. The common PPARgamma Pro12Ala polymorphism is associated with decreased risk of type 2 diabetes. Nat Genet. 2000;26(1):76-80. [View at Publisher] [DOI] [PMID] [Google Scholar]
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0).