Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Einstein (São Paulo) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082021000100234 |
Resumo: | ABSTRACT 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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Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathyDiabetic neuropathiesBrain-derived neurotrophic factorReceptor, trkBObesityABSTRACT 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.Instituto Israelita de Ensino e Pesquisa Albert Einstein2021-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082021000100234einstein (São Paulo) v.19 2021reponame:Einstein (São Paulo)instname:Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)instacron:IIEPAE10.31744/einstein_journal/2021ao6256info:eu-repo/semantics/openAccessFilimonova,TamaraKarakulova,Yuliaeng2021-09-23T00:00:00Zoai:scielo:S1679-45082021000100234Revistahttps://journal.einstein.br/pt-br/ONGhttps://old.scielo.br/oai/scielo-oai.php||revista@einstein.br2317-63851679-4508opendoar:2021-09-23T00:00Einstein (São Paulo) - Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)false |
dc.title.none.fl_str_mv |
Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy |
title |
Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy |
spellingShingle |
Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy Filimonova,Tamara Diabetic neuropathies Brain-derived neurotrophic factor Receptor, trkB Obesity |
title_short |
Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy |
title_full |
Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy |
title_fullStr |
Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy |
title_full_unstemmed |
Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy |
title_sort |
Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy |
author |
Filimonova,Tamara |
author_facet |
Filimonova,Tamara Karakulova,Yulia |
author_role |
author |
author2 |
Karakulova,Yulia |
author2_role |
author |
dc.contributor.author.fl_str_mv |
Filimonova,Tamara Karakulova,Yulia |
dc.subject.por.fl_str_mv |
Diabetic neuropathies Brain-derived neurotrophic factor Receptor, trkB Obesity |
topic |
Diabetic neuropathies Brain-derived neurotrophic factor Receptor, trkB Obesity |
description |
ABSTRACT 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. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082021000100234 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082021000100234 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.31744/einstein_journal/2021ao6256 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Instituto Israelita de Ensino e Pesquisa Albert Einstein |
publisher.none.fl_str_mv |
Instituto Israelita de Ensino e Pesquisa Albert Einstein |
dc.source.none.fl_str_mv |
einstein (São Paulo) v.19 2021 reponame:Einstein (São Paulo) instname:Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE) instacron:IIEPAE |
instname_str |
Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE) |
instacron_str |
IIEPAE |
institution |
IIEPAE |
reponame_str |
Einstein (São Paulo) |
collection |
Einstein (São Paulo) |
repository.name.fl_str_mv |
Einstein (São Paulo) - Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE) |
repository.mail.fl_str_mv |
||revista@einstein.br |
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1752129910588047360 |