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Periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on Klotho
AIMS/INTRODUCTION: Recent studies have shown that periodontitis can contribute to adipose tissue inflammation and subsequent systemic insulin resistance in the obese rat model. However, the related inflammatory mechanism is not yet clear. The present study aims to investigate the effects of periodon...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4847883/ https://www.ncbi.nlm.nih.gov/pubmed/27330715 http://dx.doi.org/10.1111/jdi.12410 |
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author | Liu, Yihua Zhang, Qiuli |
author_facet | Liu, Yihua Zhang, Qiuli |
author_sort | Liu, Yihua |
collection | PubMed |
description | AIMS/INTRODUCTION: Recent studies have shown that periodontitis can contribute to adipose tissue inflammation and subsequent systemic insulin resistance in the obese rat model. However, the related inflammatory mechanism is not yet clear. The present study aims to investigate the effects of periodontitis on the function of pancreatic β‐cells with pro‐inflammatory cytokines‐related immune mechanism in a mouse model. MATERIALS AND METHODS: C57BL/6‐db/db and inbred C57BL/6 mice were chosen here to establish a mouse model with periodontitis, which was induced by ligatures for 8 weeks. Glucose‐stimulated insulin secretion was introduced to evaluate the function of pancreatic islets and β‐cells. Serum levels of pro‐inflammatory cytokines and Klotho were also measured, and the correlation between immunostimulation and Klotho level was deeply investigated in vitro. RESULTS: Pancreatic β‐cell failure, with insulin resistance, was observed in db/db mice, while periodontitis could aggravate β‐cell dysfunction‐related features. Serum levels of interleukin (IL)‐12 and Klotho showed a negatively synergistic change, whereas the expression of Klotho was also inhibited under IL‐12 treatment in MIN6 β‐cells or isolated islets. Furthermore, IL‐12‐induced immune stimulation and also decreased insulin secretion were proven to be reversed by Klotho overexpression. CONCLUSIONS: Periodontitis aggravated pancreatic β‐cell failure in diabetic mice. Further in vitro studies showed IL‐12 regulation on Klotho, while Klotho also acted as an inhibitor on IL‐12, indicating the potential of Klotho for preserving pancreatic β‐cell function in diabetes. |
format | Online Article Text |
id | pubmed-4847883 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-48478832016-06-21 Periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on Klotho Liu, Yihua Zhang, Qiuli J Diabetes Investig Articles AIMS/INTRODUCTION: Recent studies have shown that periodontitis can contribute to adipose tissue inflammation and subsequent systemic insulin resistance in the obese rat model. However, the related inflammatory mechanism is not yet clear. The present study aims to investigate the effects of periodontitis on the function of pancreatic β‐cells with pro‐inflammatory cytokines‐related immune mechanism in a mouse model. MATERIALS AND METHODS: C57BL/6‐db/db and inbred C57BL/6 mice were chosen here to establish a mouse model with periodontitis, which was induced by ligatures for 8 weeks. Glucose‐stimulated insulin secretion was introduced to evaluate the function of pancreatic islets and β‐cells. Serum levels of pro‐inflammatory cytokines and Klotho were also measured, and the correlation between immunostimulation and Klotho level was deeply investigated in vitro. RESULTS: Pancreatic β‐cell failure, with insulin resistance, was observed in db/db mice, while periodontitis could aggravate β‐cell dysfunction‐related features. Serum levels of interleukin (IL)‐12 and Klotho showed a negatively synergistic change, whereas the expression of Klotho was also inhibited under IL‐12 treatment in MIN6 β‐cells or isolated islets. Furthermore, IL‐12‐induced immune stimulation and also decreased insulin secretion were proven to be reversed by Klotho overexpression. CONCLUSIONS: Periodontitis aggravated pancreatic β‐cell failure in diabetic mice. Further in vitro studies showed IL‐12 regulation on Klotho, while Klotho also acted as an inhibitor on IL‐12, indicating the potential of Klotho for preserving pancreatic β‐cell function in diabetes. John Wiley and Sons Inc. 2015-11-05 2016-05 /pmc/articles/PMC4847883/ /pubmed/27330715 http://dx.doi.org/10.1111/jdi.12410 Text en © 2015 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Articles Liu, Yihua Zhang, Qiuli Periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on Klotho |
title | Periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on Klotho |
title_full | Periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on Klotho |
title_fullStr | Periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on Klotho |
title_full_unstemmed | Periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on Klotho |
title_short | Periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on Klotho |
title_sort | periodontitis aggravated pancreatic β‐cell dysfunction in diabetic mice through interleukin‐12 regulation on klotho |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4847883/ https://www.ncbi.nlm.nih.gov/pubmed/27330715 http://dx.doi.org/10.1111/jdi.12410 |
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