Endocrine Abstracts

Progression of the diabetic peripheral neuropathy (DPN) demonstrated differences in the individual considered the contribution of genetic predisposition. We aim to study the relationship between the −866G/A polymorphism in the promoter region of the uncoupling protein 2 (UCP2) which enhances transcriptional activity and A allele frequency with nerve conduction velocities (NCV) and clinical factors. We compared 370 type 2 diabetic patients with healthy control. Subjective neuropatic symptoms, neurologic examination and electrophysiologic measurements were evaluated. Diabetic patients were divided into two groups Group 1: (G/G) and Group 2: (G/A+A/A) according to genotype. Clinical features and NCV were compared and also independent risk factors of the DPN were defined. The comparison of two independent group was performed with Mann–Whitney U-test or Fisher’s Exact test. Relationship between NCV with UCP2 genotype and cinical factors assessed through multiple regression analysis (MRA) and ANOVA. Pearson correlation was performed for correlation analysis. DPN was present in 46.2% of the cases. DPN was significantly correlated with HbA1c, duration of DM, age at DM onset, retinopathy and nephropathy. The proportions of the individuals carrying genotype (-866G/A and A/A) and A allele frequency were significantly higher in the diabetic patients with DPN than that in the controls respectively (P<0.009, P<0.004). Group 2 had an early age at DM onset (P<0.0001) and high proportion of retinopathy (P=0.03). NCV was significantly lower in Group 2 than that in Group 1. MRA showed that UCP2 genotype and HbA1c were related with the impairment of NCV independently of other clinical factors. HbA1C, and retinopathy. In conclusion, higher A allele frequency with DPN and early age at DM onset in the Turkish diabetic population might partly indicate the genetic predisposition. Higher UCP2 activity related to A allele which was independent risk factor in the impairment of NCV may contribute to reduce NCV via decreased ATP production in mitochondria. On the other hand, increased UCP2 in the DPN may be a marker of an inadequate antioxidant effect of the UCP2 in the chronic oxidative stress. Investigation of the genetic tendency for DPN may guide to define the risk factors and also in the new insights for the treatment.