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Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses
The impact of chronic cadmium exposure and slow accumulation on the occurrence and development of diabetes is controversial for human populations. Islets of Langerhans play a prominent role in the etiology of the disease, including by their ability to secrete insulin. Conversion of glucose increase...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6027415/ https://www.ncbi.nlm.nih.gov/pubmed/29565305 http://dx.doi.org/10.3390/toxics6020020 |
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author | Jacquet, Adeline Cottet-Rousselle, Cécile Arnaud, Josiane Julien Saint Amand, Kevin Ben Messaoud, Raoua Lénon, Marine Demeilliers, Christine Moulis, Jean-Marc |
author_facet | Jacquet, Adeline Cottet-Rousselle, Cécile Arnaud, Josiane Julien Saint Amand, Kevin Ben Messaoud, Raoua Lénon, Marine Demeilliers, Christine Moulis, Jean-Marc |
author_sort | Jacquet, Adeline |
collection | PubMed |
description | The impact of chronic cadmium exposure and slow accumulation on the occurrence and development of diabetes is controversial for human populations. Islets of Langerhans play a prominent role in the etiology of the disease, including by their ability to secrete insulin. Conversion of glucose increase into insulin secretion involves mitochondria. A rat model of pancreatic β-cells was exposed to largely sub-lethal levels of cadmium cations applied for the longest possible time. Cadmium entered cells at concentrations far below those inducing cell death and accumulated by factors reaching several hundred folds the basal level. The mitochondria reorganized in response to the challenge by favoring fission as measured by increased circularity at cadmium levels already ten-fold below the median lethal dose. However, the energy charge and respiratory flux devoted to adenosine triphosphate synthesis were only affected at the onset of cellular death. The present data indicate that mitochondria participate in the adaptation of β-cells to even a moderate cadmium burden without losing functionality, but their impairment in the long run may contribute to cellular dysfunction, when viability and β-cells mass are affected as observed in diabetes. |
format | Online Article Text |
id | pubmed-6027415 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-60274152018-07-13 Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses Jacquet, Adeline Cottet-Rousselle, Cécile Arnaud, Josiane Julien Saint Amand, Kevin Ben Messaoud, Raoua Lénon, Marine Demeilliers, Christine Moulis, Jean-Marc Toxics Article The impact of chronic cadmium exposure and slow accumulation on the occurrence and development of diabetes is controversial for human populations. Islets of Langerhans play a prominent role in the etiology of the disease, including by their ability to secrete insulin. Conversion of glucose increase into insulin secretion involves mitochondria. A rat model of pancreatic β-cells was exposed to largely sub-lethal levels of cadmium cations applied for the longest possible time. Cadmium entered cells at concentrations far below those inducing cell death and accumulated by factors reaching several hundred folds the basal level. The mitochondria reorganized in response to the challenge by favoring fission as measured by increased circularity at cadmium levels already ten-fold below the median lethal dose. However, the energy charge and respiratory flux devoted to adenosine triphosphate synthesis were only affected at the onset of cellular death. The present data indicate that mitochondria participate in the adaptation of β-cells to even a moderate cadmium burden without losing functionality, but their impairment in the long run may contribute to cellular dysfunction, when viability and β-cells mass are affected as observed in diabetes. MDPI 2018-03-22 /pmc/articles/PMC6027415/ /pubmed/29565305 http://dx.doi.org/10.3390/toxics6020020 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Jacquet, Adeline Cottet-Rousselle, Cécile Arnaud, Josiane Julien Saint Amand, Kevin Ben Messaoud, Raoua Lénon, Marine Demeilliers, Christine Moulis, Jean-Marc Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses |
title | Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses |
title_full | Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses |
title_fullStr | Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses |
title_full_unstemmed | Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses |
title_short | Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses |
title_sort | mitochondrial morphology and function of the pancreatic β-cells ins-1 model upon chronic exposure to sub-lethal cadmium doses |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6027415/ https://www.ncbi.nlm.nih.gov/pubmed/29565305 http://dx.doi.org/10.3390/toxics6020020 |
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