Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Jacquet, Adeline, Cottet-Rousselle, Cécile, Arnaud, Josiane, Julien Saint Amand, Kevin, Ben Messaoud, Raoua, Lénon, Marine, Demeilliers, Christine, Moulis, Jean-Marc
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
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
_version_ 1783336606262886400
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
work_keys_str_mv AT jacquetadeline mitochondrialmorphologyandfunctionofthepancreaticbcellsins1modeluponchronicexposuretosublethalcadmiumdoses
AT cottetroussellececile mitochondrialmorphologyandfunctionofthepancreaticbcellsins1modeluponchronicexposuretosublethalcadmiumdoses
AT arnaudjosiane mitochondrialmorphologyandfunctionofthepancreaticbcellsins1modeluponchronicexposuretosublethalcadmiumdoses
AT juliensaintamandkevin mitochondrialmorphologyandfunctionofthepancreaticbcellsins1modeluponchronicexposuretosublethalcadmiumdoses
AT benmessaoudraoua mitochondrialmorphologyandfunctionofthepancreaticbcellsins1modeluponchronicexposuretosublethalcadmiumdoses
AT lenonmarine mitochondrialmorphologyandfunctionofthepancreaticbcellsins1modeluponchronicexposuretosublethalcadmiumdoses
AT demeillierschristine mitochondrialmorphologyandfunctionofthepancreaticbcellsins1modeluponchronicexposuretosublethalcadmiumdoses
AT moulisjeanmarc mitochondrialmorphologyandfunctionofthepancreaticbcellsins1modeluponchronicexposuretosublethalcadmiumdoses