The biological actions of brain-derived neurotrophic factor (BDNF) in humans’ painful diabetic peripheral neuropathy (DPN) are relatively poorly understood. Serum levels of high-specific tropomyosin receptor kinase B (TrkB) in human with DPN wasn’t investigated yet. The aim: to study serum levels of BDNF and TrkB in patients with painful DPN. Methods: 60 patients with DPN were examined with clinical examination, measuring of serum levels BDNF and TrkB by enzyme immunoassay and were divided into two groups: the 1st group consists of 28 patients with neuropathic pain, 32 patients with painless form of DPN entered the 2nd group . The peripheral nerve dysfunction was confirmed by electroneuromyography (ENMG) with measuring nerve conduction velocity (NCV) of n.peroneus. Results: In the 2nd group serum content of BDNF (2.38±1.05ng/ml) was significally lower than in the 1st group (3.88±1,12ng/ml, p=0.001), unlike serum level of TrkB (3.14±1.75ng/ml versus 4,874±0,84ng/ml, accordingly, p=0.001). In the 2nd group mean NCV was significantly lower than in the first group (29.85±11.25 m/s versus 38.45±7.9 m/s accordingly, p=0.001). There were revealed correlations between the severity of neuropathic pain by Pain Detect scale and the increase in circulating BDNF level (R=0.392, p=0.03) and the decrease of quantitative content of TrkB in serum. (R=-0.454, p=0.01). There was obtained the inverse dependence between serum TrkB and the NCV (R=-0.531, p<0.05) by ENMG. Conclusions: Neuropathic pain in DPN is characterized by a lower content of TrkB and high expression of BDNF. In contrast the painless form of DPN associated with a higher level of serum TrkB and a more highly demyelinating process according to the ENMG. In this way the study demonstrates BDNF-TrkB signaling is involved in the induction of neuropathic pain in DPN. Peripheral measurements of BDNF and TrkB provides a potential way to both study the pathogenesis of neuropathic pain of DPN as well as act as a biomarker of the disease.
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