PPAR(sic)2, aldose reductase, and TCF7L2 gene polymorphisms: relation to diabetes mellitus

被引:1
作者
Shawki, Hadeel Ahmed [1 ,2 ]
Abo-hashem, Ekbal M. [3 ]
Youssef, Magdy M. [1 ]
Shahin, Maha [2 ]
Elzehery, Rasha [3 ]
机构
[1] Mansoura Univ, Biochem Div, Chem Dept, Fac Sci, Mansoura, Egypt
[2] Mansoura Univ, Mansoura Ophthalm Ctr, Mansoura, Egypt
[3] Mansoura Univ, Dept Clin Pathol, Fac Med, Mansoura, Egypt
基金
英国科研创新办公室;
关键词
PPAR(sic)2; Aldose reductase; TCF7L2; Gene polymorphism; T1DM; T2DM; ACTIVATED RECEPTOR-GAMMA; PRO12ALA POLYMORPHISM; C161T POLYMORPHISMS; ASSOCIATION; PPARG; SUSCEPTIBILITY; POPULATION; VARIANTS; DISEASE; C-106T;
D O I
10.1007/s40200-021-00963-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose Diabetes mellitus (DM) is a growing global health concern. Genetic factors play a pivotal role in the development of diabetes. Therefore, the present work aimed to study the relation between peroxisome proliferator-activate receptors (PPAR(sic)2) (rs3856806), aldose reductase (AR) (rs759853), transcription factor 7 like 2 (TCF7L2) (rs7903146) gene polymorphism with diabetes in the Egyptian population. Methods The study included 260 diabetics and 120 healthy subjects. Genotyping was done using polymerase chain reaction-restriction fragment length polymorphism. Results Regression analysis revealed that PPAR(sic)2 TT, TCF7L2 TT were suggested to be independent risk predictors for T1DM and TCF7L2 TC, CC genotype were suggested to be independent protective factors against T1DM development. On the other hand, PPAR(sic)2 TT, AR TT genotypes were suggested to be independent risk predictors for T2DM susceptibility, and PPAR(sic)2 CT genotypes were suggested to be independent protective factors against T2DM development. Conclusion The present study revealed that PPAR(sic)2 (rs3856806), TCF7L2 (rs7903146) and AR (rs759853) gene polymorphism may play an important role in the susceptibility of diabetes. Therefore, these polymorphisms may have a prognostic value for diabetes in the Egyptian population. Further work is required to confirm the role of these polymorphisms in diabetes.
引用
收藏
页码:241 / 250
页数:10
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