| In recent years,the number of patients with Diabetic peripheral neuropathy(DPN)is increasing year by year.Limb sensory disorders or spontaneous pain will seriously affect patients’ physical and mental health and bring economic burden to individuals and the society.At present,the pathogenesis of DPN is not clear.In this study,the differentially expressed gene Ugcg of sciatic nerve of DPN and normal mice was screened by bioinformatics method,and the changes of serum of Ugcg in DPN patients were detected,and the correlation between Ugcg and DPN and it effects on painful diabetic neuropathy was explored.Objective:1.Bioinformatics method was used to analyze the differentially expressed genes of sciatic nerve between DPN and normal mice to find a new target for DPN pathogenesis;2.Logistic regression was used to verify the role of this target in DPN and its correlation with painful diabetic neuropathy in clinical setting.Methods:1.Select data set “GSE146733” for analysis.R software was used to analyze the GO and KEGG pathways in this dataset,and the protein-protein interaction analysis was constructed by gene involved in the pathways with significant differences in expression to obtain the hub protein,namely Ugcg.2.A retrospective observational study was conducted in 62 patients with non-painful diabetic neuropathy(NP group),23 patients with painful diabetic neuropathy(P group),and 60 diabetes mellitus patients without peripheral neuropathy(DM group)admitted to the Department of Endocrinology,Affiliated People’s Hospital of Jiangsu University from June 2022 to December 2022.3.Data were collected:(1)general data(age,etc.),(2)serological data(fasting C-peptide,etc.),(3)electrophysiological data(sensory nerve conduction velocity and amplitude of right median nerve,etc),(4)patients’ serum of Ugcg was measured by Elisa.4.With DPN as the outcome,DM as the control,Logistic regression was used to explore the correlation between Ugcg and DPN.With painful diabetic neuropathy as the outcome,nonpainful dibetic neuropathy as the control,Logistic regression was used to explore the correlation between Ugcg and.Main outcomes:1.There were 2095 differentially expressed genes,of which 917 were up-regulated and1178 were down-regulated.2.There were significant differences in the "myelin synthesis" and other pathways(P<0.05).Heatmap showed "Ugcg" was downregulated.Protein-protein interaction analysis shows "Ugcg" as the most crucial hub protein.3.The serum of Ugcg in NP group was lower than that in DM group(P<0.01).There were significant differences in age,weight,BMI and drinking history between NP group and DM group(P<0.05).Patients in NP group had a lower fasting C-peptide level(P<0.001).Lower triglyceride level(P<0.001);Higher high-density protein level(P=0.001);There were no significant differences in Hb A1 c and fasting blood glucose between the two groups(P>0.05).The nerve conduction velocity and amplitude in NP group were significantly lower than those in DM group(P<0.001).The decrease of Ugcg expression was positively correlated with the decrease of nerve conduction function.Multivariate Logistic regression showed that Ugcg(OR:0.979,95%CI: 0.963-0.994,P=0.007)was an independent risk factor for DPN.When serum of Ugcg was less than 107 ng/L in T2 DM patients,the risk of neuropathy was increased(OR:2.96,95%CI: 1.41-6.19,P<0.001).4.The serum of Ugcg in P group was higher than that in NP group(P<0.001).Logistic regression showed that the increase of serum of Ugcg was correlated with the occurrence of pain(OR: 1.032,95%CI: 1.015-1.049,P<0.001).Conclusion:Downregulation of Ugcg expression plays an important role in the pathogenesis of DPN.The increased expression of Ugcg in DPN patients may be related to the occurrence of pain. |