In this paper we investigated lipid and metabolite changes in diabetic neuropathy, using untargeted lipidomics and metabolomics analyses of the spinal cords from streptozotocin-treated diabetic rats.170 metabolites and 45 lipids were dysregulated in the painful diabetic neuropathy (PDN) phase. Pathway enrichment analysis revealed perturbations in starch and sucrose, tryptophan, pyrimidine, cysteine and methionine, thiamine, tyrosine, and nucleotides. The disturbance of tyrosine, tryptophan, methionine, triacylglycerol, and phosphatidylethanolamine metabolism indicated that pathological mechanisms in the PDN involved energy metabolism, oxidative stress, and neural reparative regeneration. These revelations offered potential biomarkers for PDN and enriched the comprehension of the complex molecular mechanisms characterizing PDN, establishing a solid foundation for subsequent inquiries into neural convalescence and recovery after PDN.
Keyphrases
- diabetic rats
- oxidative stress
- spinal cord
- wound healing
- mass spectrometry
- type diabetes
- single cell
- stem cells
- dna damage
- spinal cord injury
- ischemia reperfusion injury
- fatty acid
- amino acid
- metabolic syndrome
- liquid chromatography
- high resolution
- newly diagnosed
- fluorescent probe
- gas chromatography mass spectrometry
- atomic force microscopy
- simultaneous determination