Perm State Medical University, Perm, Perm Region, Russia.
Einstein (Sao Paulo). 2021 Sep 27;19:eAO6256. doi: 10.31744/einstein_journal/2021AO6256. eCollection 2021.
To assess the quantitative serum levels of tropomyosin receptor kinase receptor B, and to estimate its association with serum concentration of brain-derived neurotrophic factor and obesity in patients with painful and painless forms of diabetic polyneuropathy.
We examined 70 patients with diabetic polyneuropathy with confirming peripheral nerve dysfunction by electroneuromyography and measuring of serum levels tropomyosin receptor kinase receptor B and brain-derived neurotrophic factor by enzyme immunoassay. Diabetic polyneuropathy was diagnosed using the modified Toronto Consensus (2011) criteria, while neuropathic pain was assessed using an 11-point Numerical Pain Rating Scale. The patients were divided into two groups according to presence or absence of neuropathic pain. Control Group consisted of 14 healthy persons.
The serum levels of tropomyosin receptor kinase receptor B and brain-derived neurotrophic factor in patients with diabetic polyneuropathy are significantly higher than healthy controls (p=0.000). Hyperexpression of brain-derived neurotrophic factor in serum was associated with painful form of diabetic polyneuropathy (R=0.392, p=0.012) and obesity (R=0.412, p=0.001). On the contrary high concentration of tropomyosin receptor kinase receptor B in serum associated with painless diabetic polyneuropathy by Pain DETECT (R=-0.354, p=0.015), low body weight (R=-0.354, p=0.015) and severe demyelization of nerve fibers (R=-0.574, p=0.001), indicated "non-working" receptor detected in serum.
Tropomyosin receptor kinase receptor B signaling is involved in the modulation of neuropathic pain and obesity in diabetic polyneuropathy.
评估原肌球蛋白受体激酶受体 B 的血清定量水平，并评估其与痛性和无痛性糖尿病多发性神经病患者血清脑源性神经营养因子浓度的相关性。
我们通过电神经肌电图检查和酶联免疫吸附试验测量血清原肌球蛋白受体激酶受体 B 和脑源性神经营养因子的浓度，检查了 70 例经证实存在周围神经功能障碍的糖尿病多发性神经病患者。糖尿病多发性神经病的诊断采用改良的多伦多共识（2011 年）标准，神经病理性疼痛采用 11 分数字疼痛评分量表进行评估。根据是否存在神经病理性疼痛，将患者分为两组。对照组由 14 名健康人组成。
糖尿病多发性神经病患者的血清原肌球蛋白受体激酶受体 B 和脑源性神经营养因子水平明显高于健康对照组（p=0.000）。血清脑源性神经营养因子的高表达与痛性糖尿病多发性神经病（R=0.392，p=0.012）和肥胖（R=0.412，p=0.001）有关。相反，血清中高浓度的原肌球蛋白受体激酶受体 B 与无痛性糖尿病多发性神经病的 Pain DETECT 呈负相关（R=-0.354，p=0.015），与体重低（R=-0.354，p=0.015）和神经纤维严重脱髓鞘（R=-0.574，p=0.001）有关，表明血清中检测到“非工作”受体。
原肌球蛋白受体激酶受体 B 信号转导参与了糖尿病多发性神经病中神经病理性疼痛和肥胖的调节。
