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Increased leukotriene B4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy
BACKGROUND AND AIM: A low-grade inflammation is associated with cardiac autonomic neuropathy (CAN) and increased concentration of leukotriene B4 (LTB4) was found in individuals with type 1 diabetes and definitive CAN. This cross-sectional study evaluated plasma concentration of LTB4 and of other inf...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7663893/ https://www.ncbi.nlm.nih.gov/pubmed/33292560 http://dx.doi.org/10.1186/s13098-020-00606-3 |
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author | Neves, Jose Antonio Januario De Matos, Mozânia Reis Ramalho, Theresa Santos-Bezerra, Daniele Pereira Cavalcante, Cristiane Das Graças Dias Alpino Peixoto, Renata D’ Queiroz, Márcia Silva Jancar, Sonia Correa-Giannella, Maria Lucia |
author_facet | Neves, Jose Antonio Januario De Matos, Mozânia Reis Ramalho, Theresa Santos-Bezerra, Daniele Pereira Cavalcante, Cristiane Das Graças Dias Alpino Peixoto, Renata D’ Queiroz, Márcia Silva Jancar, Sonia Correa-Giannella, Maria Lucia |
author_sort | Neves, Jose Antonio Januario |
collection | PubMed |
description | BACKGROUND AND AIM: A low-grade inflammation is associated with cardiac autonomic neuropathy (CAN) and increased concentration of leukotriene B4 (LTB4) was found in individuals with type 1 diabetes and definitive CAN. This cross-sectional study evaluated plasma concentration of LTB4 and of other inflammatory mediators, namely, tumor necrosis factor (TNF), interleukin (IL)1B, and IL10 in individuals with type 2 diabetes (T2D) and different degrees of CAN, and correlated these inflammatory mediators with the degree of glycemic control and with a surrogate marker of insulin resistance. METHODS: TNF, IL1B, IL10 and LTB4 plasma concentrations were measured in 129 T2D subjects (62% women with [median] age of 63 years, disease duration of 8 years and HbA1c of 7.3%) with or without CAN. The Lipid accumulation product index was used as a surrogate marker of insulin resistance. RESULTS: LTB4 concentration was significantly higher in those presenting incipient CAN (69.7 ± 16.6 pg mL(-1)) and definitive CAN (71.5 ± 15.7 pg mL(-1)) versus those without CAN (57.0 ± 13.9 pg mL(-1)). The groups without CAN and with incipient CAN were pooled (group without definitive CAN) and compared to those with definitive CAN. LTB4 concentration was higher in the latter group, as well as TNF concentration, while IL10 concentration was lower in this group. After adjustment for confounding variables, only LTB4 concentration remained significantly different between the groups with and without definitive CAN. Plasma concentration of LTB4 did not correlate with the degree of glycemic control. After sorting the participants by sex, a borderline weak correlation was found between LTB4 and the Lipid accumulation product index in women. CONCLUSION: In the T2D setting, circulating LTB4 concentration seems to be associated with cardiovascular dysautonomia. |
format | Online Article Text |
id | pubmed-7663893 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-76638932020-11-13 Increased leukotriene B4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy Neves, Jose Antonio Januario De Matos, Mozânia Reis Ramalho, Theresa Santos-Bezerra, Daniele Pereira Cavalcante, Cristiane Das Graças Dias Alpino Peixoto, Renata D’ Queiroz, Márcia Silva Jancar, Sonia Correa-Giannella, Maria Lucia Diabetol Metab Syndr Short Report BACKGROUND AND AIM: A low-grade inflammation is associated with cardiac autonomic neuropathy (CAN) and increased concentration of leukotriene B4 (LTB4) was found in individuals with type 1 diabetes and definitive CAN. This cross-sectional study evaluated plasma concentration of LTB4 and of other inflammatory mediators, namely, tumor necrosis factor (TNF), interleukin (IL)1B, and IL10 in individuals with type 2 diabetes (T2D) and different degrees of CAN, and correlated these inflammatory mediators with the degree of glycemic control and with a surrogate marker of insulin resistance. METHODS: TNF, IL1B, IL10 and LTB4 plasma concentrations were measured in 129 T2D subjects (62% women with [median] age of 63 years, disease duration of 8 years and HbA1c of 7.3%) with or without CAN. The Lipid accumulation product index was used as a surrogate marker of insulin resistance. RESULTS: LTB4 concentration was significantly higher in those presenting incipient CAN (69.7 ± 16.6 pg mL(-1)) and definitive CAN (71.5 ± 15.7 pg mL(-1)) versus those without CAN (57.0 ± 13.9 pg mL(-1)). The groups without CAN and with incipient CAN were pooled (group without definitive CAN) and compared to those with definitive CAN. LTB4 concentration was higher in the latter group, as well as TNF concentration, while IL10 concentration was lower in this group. After adjustment for confounding variables, only LTB4 concentration remained significantly different between the groups with and without definitive CAN. Plasma concentration of LTB4 did not correlate with the degree of glycemic control. After sorting the participants by sex, a borderline weak correlation was found between LTB4 and the Lipid accumulation product index in women. CONCLUSION: In the T2D setting, circulating LTB4 concentration seems to be associated with cardiovascular dysautonomia. BioMed Central 2020-11-12 /pmc/articles/PMC7663893/ /pubmed/33292560 http://dx.doi.org/10.1186/s13098-020-00606-3 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Short Report Neves, Jose Antonio Januario De Matos, Mozânia Reis Ramalho, Theresa Santos-Bezerra, Daniele Pereira Cavalcante, Cristiane Das Graças Dias Alpino Peixoto, Renata D’ Queiroz, Márcia Silva Jancar, Sonia Correa-Giannella, Maria Lucia Increased leukotriene B4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy |
title | Increased leukotriene B4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy |
title_full | Increased leukotriene B4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy |
title_fullStr | Increased leukotriene B4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy |
title_full_unstemmed | Increased leukotriene B4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy |
title_short | Increased leukotriene B4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy |
title_sort | increased leukotriene b4 plasma concentration in type 2 diabetes individuals with cardiovascular autonomic neuropathy |
topic | Short Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7663893/ https://www.ncbi.nlm.nih.gov/pubmed/33292560 http://dx.doi.org/10.1186/s13098-020-00606-3 |
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