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Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy
OBJECTIVE: 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. METHODS: We examined 70 pati...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Instituto Israelita de Ensino e Pesquisa Albert Einstein
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8448548/ https://www.ncbi.nlm.nih.gov/pubmed/34586159 http://dx.doi.org/10.31744/einstein_journal/2021AO6256 |
Sumario: | OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: Tropomyosin receptor kinase receptor B signaling is involved in the modulation of neuropathic pain and obesity in diabetic polyneuropathy. |
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