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Diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4

Toll-like receptor 4 has an important role in inflammation and immunity. Whether TLR4 signaling contributes to the link between insulin resistance and islet β cell dysfunction is an unanswered question. Here, we show that in the face of the same high-fat continuous stimulation for 24 weeks, in TLR4–...

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Autores principales: Li, Juan, Chen, Shufen, Qiang, Juan, Wang, Xin, Chen, Lei, Zou, Dajin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Polish Society of Experimental and Clinical Immunology 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439999/
https://www.ncbi.nlm.nih.gov/pubmed/26155140
http://dx.doi.org/10.5114/ceji.2014.45940
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author Li, Juan
Chen, Shufen
Qiang, Juan
Wang, Xin
Chen, Lei
Zou, Dajin
author_facet Li, Juan
Chen, Shufen
Qiang, Juan
Wang, Xin
Chen, Lei
Zou, Dajin
author_sort Li, Juan
collection PubMed
description Toll-like receptor 4 has an important role in inflammation and immunity. Whether TLR4 signaling contributes to the link between insulin resistance and islet β cell dysfunction is an unanswered question. Here, we show that in the face of the same high-fat continuous stimulation for 24 weeks, in TLR4–/– HF mice, the weight, fraction of the liver, epididymal fat pad fraction, as well as blood glucose and insulin levels were lower than in the WT HF group. In TLR4–/– HF mice, the O(2) consumption, CO(2) production and activities were higher than in the WT HF group. Glucose tolerance test, insulin tolerance test and insulin release test suggest that the impaired insulin secretion was significantly improved in TLR4–/– HF mice, compared with the WT HF group. In TLR4–/– HF mice, islet β cell ultrastructure was not damaged in the face of the same high-fat continuous stimulation, compared to that in the WT HF group. By detecting glucose-stimulated insulin secretion in the primary islet, insulin secretion of TLR4–/– HF mice was better than that of the WT HF group, and in the TLR4–/– HF group, at the mRNA level, islet interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and monocyte chemotactic protein 1 (MCP-1) were significantly lower than in the WT HF group. There was the islet macrophage infiltration in the WT HF group, but no significant macrophage infiltration in the TLR4–/– HF group. These data suggest that the damaged islet functions of the high fat diet-induced obesity mice may be linked to the TLR4 expression level, and the recruitment of macrophages into the islets.
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spelling pubmed-44399992015-07-07 Diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4 Li, Juan Chen, Shufen Qiang, Juan Wang, Xin Chen, Lei Zou, Dajin Cent Eur J Immunol Original Article Toll-like receptor 4 has an important role in inflammation and immunity. Whether TLR4 signaling contributes to the link between insulin resistance and islet β cell dysfunction is an unanswered question. Here, we show that in the face of the same high-fat continuous stimulation for 24 weeks, in TLR4–/– HF mice, the weight, fraction of the liver, epididymal fat pad fraction, as well as blood glucose and insulin levels were lower than in the WT HF group. In TLR4–/– HF mice, the O(2) consumption, CO(2) production and activities were higher than in the WT HF group. Glucose tolerance test, insulin tolerance test and insulin release test suggest that the impaired insulin secretion was significantly improved in TLR4–/– HF mice, compared with the WT HF group. In TLR4–/– HF mice, islet β cell ultrastructure was not damaged in the face of the same high-fat continuous stimulation, compared to that in the WT HF group. By detecting glucose-stimulated insulin secretion in the primary islet, insulin secretion of TLR4–/– HF mice was better than that of the WT HF group, and in the TLR4–/– HF group, at the mRNA level, islet interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and monocyte chemotactic protein 1 (MCP-1) were significantly lower than in the WT HF group. There was the islet macrophage infiltration in the WT HF group, but no significant macrophage infiltration in the TLR4–/– HF group. These data suggest that the damaged islet functions of the high fat diet-induced obesity mice may be linked to the TLR4 expression level, and the recruitment of macrophages into the islets. Polish Society of Experimental and Clinical Immunology 2014-10-14 2014 /pmc/articles/PMC4439999/ /pubmed/26155140 http://dx.doi.org/10.5114/ceji.2014.45940 Text en Copyright © Central European Journal of Immunology 2014 http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Li, Juan
Chen, Shufen
Qiang, Juan
Wang, Xin
Chen, Lei
Zou, Dajin
Diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4
title Diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4
title_full Diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4
title_fullStr Diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4
title_full_unstemmed Diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4
title_short Diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4
title_sort diet-induced obesity mediates a proinflammatory response in pancreatic β cell via toll-like receptor 4
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439999/
https://www.ncbi.nlm.nih.gov/pubmed/26155140
http://dx.doi.org/10.5114/ceji.2014.45940
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