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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–...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Polish Society of Experimental and Clinical Immunology
2014
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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. |
format | Online Article Text |
id | pubmed-4439999 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Polish Society of Experimental and Clinical Immunology |
record_format | MEDLINE/PubMed |
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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