Glycated hemoglobin has shown disagreements with other glycemic indices; termed the glycation gap. The glycation gap can be influenced by nonglycemic factors, such as protein deglycation, through the fructosamine-3-kinase (FN3K) enzyme. This cross-sectional study aimed to examine whether single nucleotide polymorphisms (SNPs) in the FN3K gene can explain the glycation gap. Among the 826 participants, 79.8% were female, 22.3% presented with diabetes, and the median age was 53 years. The results suggest that genetic polymorphisms in the FN3K gene may influence the glycation gap in individuals with diabetes. With the SNP rs1056534 analysis, the CC genotype was associated with a negative glycation gap (all P < 0.02), whereas the GG genotype was associated with a positive glycation gap (all P < 0.03) in the adjusted models. Similarly, with the SNP rs2256339, the TT genotype was associated with a negative glycation gap (P < 0.08), whereas the TA genotype was associated with a positive glycation gap (all P < 0.05) in the adjusted models. The studied genotypes are associated with protein glycation, contributing to differences in measures of glycemic control. Future studies are needed to explore the clinical implications of these findings.
- Discrepancies between glycated hemoglobin (HbA1c) and other measures of glycemia have been reported, and these may be due to nonglycemic factors.
- We assessed the association between FN3K gene variants and the discrepancy between HbA1c and fructosamines as indicated by the glycation gap.
- Our results showed significant associations between the FN3K SNP genotypes and the glycation gap in individuals with diabetes mellitus.
- Polymorphisms in the FN3K gene are associated with the glycation gap, suggesting a potential genetic contribution to the discrepancy in glycemic control measures.
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