FGF2 is a neurotrophic factor that can act as a key regulatory molecule of neuroprotection, neurogenesis, and angiogenesis in various injuries. To explore the genetic background of the FGF2 gene on DPN development, this study analyzed the correlation between SNPs in the 3'UTR of the FGF2 gene and their interaction with environmental factors in DPN patients of Han Chinese nationality. Sanger sequencing was used to analyze the FGF2 genotypes at the rs1048201, rs3804158, rs41348645, rs6854081, rs3747676, rs7683093, rs1476215, and rs1476217 loci in 150 DPN patients, 150 NDPN patients, and 150 healthy control patients. Plasma FGF2 levels were measured in all subjects by using ELISAs. Subjects carrying the T allele at the rs1048201 locus in the FGF2 gene had a significantly lower risk of developing DPN compared with subjects carrying the C allele (OR = 0.43, 95% CI = 0.33–0.56, p < 0.01). Subjects with the G genotype at the rs6854081 locus had an exceptionally higher risk of developing DPN than subjects with the T allele (OR = 1.66, 95% CI = 1.39–1.89, p < 0.01). Individuals harboring the G allele at the rs7683093 locus had a markedly higher risk of DPN than patients with the C allele (OR = 1.63, 95% CI = 1.36–1.87, p < 0.01). Finally, individuals having the A genotype at the rs1476215 locus had a significantly higher risk of DPN than individuals carrying the T allele (OR = 1.82, 95% CI = 1.53–2.02, p < 0.01). There was an interaction between age and alcohol consumption and the SNP rs7683093. SNPs at rs1048201, rs6854081, rs7683093, and rs1476215 in the FGF2 3’UTR were strongly associated with plasma levels of FGF2 (p < 0.05). SNPs at the rs1048201, rs6854081, rs7683093, and rs1476215 loci in the FGF2 gene were significantly associated with the risk of DPN. A possible mechanism is that these SNPs affect the expression level of FGF2 by interrupting the binding of microRNAs to target sites in the 3'UTR.

FGF2 是一种神经营养因子，可作为各种损伤中神经保护、神经发生和血管生成的关键调节分子。为探讨FGF2基因对DPN发育的遗传背景，本研究分析了汉族DPN患者FGF2基因3'UTR中SNPs与环境因素相互作用的相关性。Sanger测序用于分析rs1048201、rs3804158、rs41348645、rs6854081、rs3747676、rs7683093、rs1476215和rs14505PN健康患者1、ND1005和rs715005个健康对照患者1、14505PN105名患者中的FGF2基因型。通过使用 ELISA 在所有受试者中测量血浆 FGF2 水平。在FGF2的 rs1048201 基因座处携带 T 等位基因的受试者与携带 C 等位基因的受试者相比，基因发生 DPN 的风险显着降低（OR = 0.43，95% CI = 0.33–0.56，p  < 0.01）。rs6854081 基因座具有 G 基因型的受试者发生 DPN 的风险比具有 T 等位基因的受试者高得多（OR = 1.66，95% CI = 1.39–1.89，p  < 0.01）。在 rs7683093 位点携带 G 等位基因的个体患 DPN 的风险明显高于 C 等位基因患者（OR = 1.63，95% CI = 1.36–1.87，p  < 0.01）。最后，在 rs1476215 基因座具有 A 基因型的个体比携带 T 等位基因的个体具有显着更高的 DPN 风险（OR = 1.82，95% CI = 1.53–2.02，p < 0.01)。年龄和饮酒量与 SNP rs7683093 之间存在交互作用。FGF2 3'UTR 中rs1048201、rs6854081、rs7683093 和 rs1476215 的 SNP 与FGF2 的血浆水平密切相关 ( p  < 0.05)。FGF2基因中rs1048201、rs6854081、rs7683093 和 rs1476215 位点的 SNP与 DPN 风险显着相关。一种可能的机制是这些 SNP 通过中断 microRNA 与 3'UTR 中的靶位点的结合来影响 FGF2 的表达水平。