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Toxics
Volume 6
Issue 2
10.3390/toxics6020020
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Article

Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses

by
Adeline Jacquet
1,
Cécile Cottet-Rousselle
1,
Josiane Arnaud
1,2,
Kevin Julien Saint Amand
1,
Raoua Ben Messaoud
1,
Marine Lénon
1,
Christine Demeilliers
1 and
Jean-Marc Moulis
1,3,*
1
Laboratory of Fundamental and Applied Bioenergetics (LBFA), Inserm, Universite Grenoble Alpes, 38000 Grenoble, France
2
Biochemistry, Molecular Biology and Environmental Toxicology (SB2TE), Grenoble University Hospital, CS 10217, 38043 Grenoble, France
3
CEA-Grenoble, Bioscience and Biotechnology Institute (BIG), 38054 Grenoble, France
*
Author to whom correspondence should be addressed.
Toxics 2018, 6(2), 20; https://doi.org/10.3390/toxics6020020
Received: 19 February 2018 / Revised: 12 March 2018 / Accepted: 20 March 2018 / Published: 22 March 2018
(This article belongs to the Special Issue Cadmium Sources and Toxicity)
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Abstract

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. View Full-Text
Keywords: mitochondrial network; image analysis; mitochondrial morphology; bioenergetics; sub-lethal exposure; toxicological mechanism; cadmium mitochondrial network; image analysis; mitochondrial morphology; bioenergetics; sub-lethal exposure; toxicological mechanism; cadmium
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
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MDPI and ACS Style

Jacquet, A.; Cottet-Rousselle, C.; Arnaud, J.; Julien Saint Amand, K.; Ben Messaoud, R.; Lénon, M.; Demeilliers, C.; Moulis, J.-M. Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses. Toxics 2018, 6, 20. https://doi.org/10.3390/toxics6020020

AMA Style

Jacquet A, Cottet-Rousselle C, Arnaud J, Julien Saint Amand K, Ben Messaoud R, Lénon M, Demeilliers C, Moulis J-M. Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses. Toxics. 2018; 6(2):20. https://doi.org/10.3390/toxics6020020

Chicago/Turabian Style

Jacquet, Adeline, Cécile Cottet-Rousselle, Josiane Arnaud, Kevin Julien Saint Amand, Raoua Ben Messaoud, Marine Lénon, Christine Demeilliers, and Jean-Marc Moulis. 2018. "Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses" Toxics 6, no. 2: 20. https://doi.org/10.3390/toxics6020020

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