Are polymorphisms within the fructosamine-3-kinase gene associated with the discordance between HbA1c and other measures of glycaemia?

Glycated haemoglobin (HbA1c) has shown disagreements with other glycaemic indices; termed the glycation gap. The glycation gap can be influenced by non-glycaemic factors like 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. Amongst the 826 participants, 79.8% were female, 22.3% presented with DM 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 mellitus (DM). With the SNP rs1056534 analysis, the CC genotype was associated with a negative glycation gap (All, p<0.02), whilst the GG genotype was associated with 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 glycaemic control. Future studies are needed to explore the clinical implications of these findings.