ArticlePloS one2021
Potential role of the ABCG2-Q141K polymorphism in type 2 diabetes.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 12 citations in OpenAlex.
- ABCG2 transporter: Structural and functional associations with gout (Review).International journal of molecular medicine · 2026Review
- rs2231142 (421 C>A, Q141K) Is More Functionally Influential than rs2231137 (34 G>A, V12M) on Anticancer Drug Resistance Mediated by theInternational journal of molecular sciences · 2025Article
- Genetic Variants of the Human Thiamine Transporter (International journal of molecular sciences · 2025Article
- Association of theHeliyon · 2024Article
- Associations of serum uric acid with cardiovascular disease risk factors: a retrospective cohort study in southeastern China.BMJ open · 2023Article
- Cannabis Pharmacogenomics: A Path to Personalized Medicine.Current issues in molecular biology · 2023Review
- Genetic Modulation of the GLUT1 Transporter Expression-Potential Relevance in Complex Diseases.Biology · 2022Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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Abstract
Type 2 diabetes mellitus (T2DM) is a complex metabolic disease and variations in multispecific membrane transporter functions may affect T2DM development, complications or treatment. In this work we have analyzed the potential effects of a major polymorphism, the Q141K variant of the ABCG2 transporter in T2DM. The ABCG2 protein is a multispecific xeno- and endobiotic transporter, affecting drug metabolism and playing a key role in uric acid extrusion. The ABCG2-Q141K variant, with reduced expression level and function, is present in 15-35% of individuals, depending on the genetic background of the population, and has been shown to significantly affect gout development. Several other diseases, including hypertension, chronic renal failure, and T2DM have also been reported to be associated with high serum uric acid levels, suggesting that ABCG2 may also play a role in these conditions. In this work we have compared relatively small cohorts (n = 203) of T2DM patients (n = 99) and healthy (n = 104) individuals regarding the major laboratory indicators of T2DM and determined the presence of the SNP rs2231142 (C421A), resulting the ABCG2-Q141K protein variant. We found significantly higher blood glucose and HbA1c levels in the T2DM patients carrying the ABCG2-Q141K variant. These findings may emphasize the potential metabolic role of ABCG2 in T2DM and indicate that further research should explore how prevention and treatment of this disease may be affected by the frequent polymorphism of ABCG2.
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