“…Currently, the following metabolic and vascular factors underlie the development of DPN: activation under conditions of hypoxia in diabetes alternative, polyol, glucose oxidation pathway with the formation of sorbitol and fructose, reduced levels of myo-inositol and increased activity of protein kinase C, which leads to disruption membrane Na + /K + -ATPases and accumulation of sodium inside the cell, which causes an increase in intracellular osmolarity; violation of the synthesis of fatty acids contributes to inhibition of prostaglandin production by endothelium and impaired endoneural blood flow, which leads to the development of ischemia, hypoxia and damage to the membrane structures of the nerve, microvascular and hemorhe-ological disorders; oxidative stress; deficiency of neurotrophic factors (nerve growth factor (NGF), insulin-like growth factor, neurospecific enolase (NSE), etc.) and disruption of axonal transport; accumulation of the end products of excess glycation in nerve and/or vascular wall proteins; immunological processes with an increase in systemic inflammation and the formation of autoantibodies [1][2][3].…”