Association of XbaI &amp;lt;i&amp;gt;GLUT&amp;lt;/i&amp;gt;1 Polymorphism with Susceptibility to Type 2 Diabetes Mellitus and Diabetic Nephropathy

Ramadan, Ragaa Abdelkader; Zaki, Ahmad Mohamed; Magour, Gehan Mahmoud; Zaki, Moyassar Ahmad; Madkour, M. A.

doi:10.4236/ajmb.2016.62008

Cited by 2 publications

(4 citation statements)

References 23 publications

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“…FBG did not differ between the GLUT1 rs841853 genotypes as previously reported [ 24 ]. The dominant model showed no significant association between rs841853-CA + AA genotype and FBG in our study.…”

Section: Discussionsupporting

confidence: 86%

“…Previous literature contains contradictory findings regarding rs841853 and diabetes. For instance, rs841853 was not significantly associated with diabetes in several studies [ 24 , 66 – 68 ]. Contrarily, the variant was confirmed as a diabetes-related SNP in Japanese [ 33 , 69 ], Tunisian [ 34 ], and Bangladeshi [ 35 ] women.…”

Section: Discussionmentioning

confidence: 99%

“…Glucose transporter 1 (or GLUT1), also called the solute carrier family 2, facilitated glucose transporter member 1 (SLC2A1) and thioredoxin-interacting protein (TXNIP) located on chromosome 1 are notable candidate genes for T2D diabetes [ 16 – 24 ]. GLUT1 is a well-characterized solute transporter that mainly regulates the cellular uptake of glucose in humans [ 13 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

“…Association studies and meta-analyses identified GLUT1 rs841853 single nucleotide polymorphism (SNP), also known as GLUT1 XbaI polymorphism as one of the genetic variants associated with diabetes and diabetic nephropathy, a diabetes-related complication [ 24 – 35 ].…”

Section: Introductionmentioning

confidence: 99%

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Interaction between a diabetes-related methylation site (TXNIP cg19693031) and variant (GLUT1 rs841853) on fasting blood glucose levels among non-diabetics

Tsai

Shen

et al. 2022

J Transl Med

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Background Type 2 diabetes mellitus (T2DM) is caused by a combination of environmental, genetic, and epigenetic factors including, fasting blood glucose (FBG), genetic variant rs841853, and cg19693031 methylation. We evaluated the interaction between rs841853 and cg19693031 on the FBG levels of non-diabetic Taiwanese adults. Methods We used Taiwan Biobank (TWB) data collected between 2008 and 2016. The TWB data source contains information on basic demographics, personal lifestyles, medical history, methylation, and genotype. The study participants included 1300 people with DNA methylation data. The association of cg19693031 methylation (stratified into quartiles) with rs841853 and FBG was determined using multiple linear regression analysis. The beta-coefficients (β) and p-values were estimated. Results The mean ± standard deviation (SD) of FBG in rs841853-CC individuals (92.07 ± 7.78) did not differ significantly from that in the CA + AA individuals (91.62 ± 7.14). However, the cg19693031 methylation levels were significantly different in the two groups (0.7716 ± 0.05 in CC individuals and 0.7631 ± 0.05 in CA + AA individuals (p = 0.002). The cg19693031 methylation levels according to quartiles were β < 0.738592 (< Q1), 0.738592 ≤ 0.769992 (Q1–Q2), 0.769992 ≤ 0.800918 (Q2–Q3), and β ≥ 0.800918 (≥ Q3). FBG increased with decreasing cg19693031 methylation levels in a dose–response manner (ptrend = 0.005). The β-coefficient was − 0.0236 (p = 0.965) for Q2–Q3, 1.0317 (p = 0.058) for Q1–Q2, and 1.3336 (p = 0.019 for < Q1 compared to the reference quartile (≥ Q3). The genetic variant rs841853 was not significantly associated with FBG. However, its interaction with cg19693031 methylation was significant (p-value = 0.036). Based on stratification by rs841853 genotypes, only the CC group retained the inverse and dose–response association between FBG and cg19693031 methylation. The β (p-value) was 0.8082 (0.255) for Q2–Q3, 1.6930 (0.022) for Q1–Q2, and 2.2190 (0.004) for < Q1 compared to the reference quartile (≥ Q3). The ptrend was 0.002. Conclusion Summarily, methylation at cg19693031 was inversely associated with fasting blood glucose in a dose-dependent manner. The inverse association was more prominent in rs841853-CC individuals, suggesting that rs841853 could modulate the association between cg19693031 methylation and FBG. Our results suggest that genetic variants may be involved in epigenetic mechanisms associated with FBG, a hallmark of diabetes. Therefore, integrating genetic and epigenetic data may provide more insight into the early-onset of diabetes.

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Section: Discussionsupporting

confidence: 86%