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A Review of Diabetes Mellitus and Exposure to the Environmental Toxicant Cadmium with an Emphasis on Likely Mechanisms of Action
There is increasing interest in how exposure to environmental substances can contribute to the onset of Type II diabetes mellitus (T2DM). Impaired insulin release is a hallmark of type I diabetes mellitus and is involved in the progression of T2DM. Both epidemiological and experimental studies show...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Bentham Science Publishers
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5002940/ https://www.ncbi.nlm.nih.gov/pubmed/26264451 http://dx.doi.org/10.2174/1573399811666150812142922 |
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author | Edwards, Joshua Ackerman, Christopher |
author_facet | Edwards, Joshua Ackerman, Christopher |
author_sort | Edwards, Joshua |
collection | PubMed |
description | There is increasing interest in how exposure to environmental substances can contribute to the onset of Type II diabetes mellitus (T2DM). Impaired insulin release is a hallmark of type I diabetes mellitus and is involved in the progression of T2DM. Both epidemiological and experimental studies show that exposure to the environmental pollutant cadmium (Cd), is associated with hyperglycemia, T2DM and reduced serum insulin. The goal of this review is to examine likely mechanisms of action of Cd-induced dysglycemia based on experimental studies in the literature and from the most recent findings in the Edwards lab. The primary focus of this review will examine how Cd may cause islet dysfunction and subsequent impaired insulin release. Recent findings in the Edwards lab indicate that Cd causes time-dependent and statistically significant changes in fasting leptin, Glucose-dependent Insulinotropic Polypeptide (GIP) and pancreas polypeptide hormone levels in a subchronic animal model of Cd-induced hyperglycemia. This review summarizes the most likely cellular mechanisms by which the ubiquitous environmental contaminant Cd disrupts glucose homeostasis. While individual cellular effects of Cd are reviewed it is likely that no one single mechanism is involved, rather multiple mechanisms exist and work synergistically resulting in islet dysfunction and ultimately dysglycemia. |
format | Online Article Text |
id | pubmed-5002940 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Bentham Science Publishers |
record_format | MEDLINE/PubMed |
spelling | pubmed-50029402016-08-31 A Review of Diabetes Mellitus and Exposure to the Environmental
Toxicant Cadmium with an Emphasis on Likely Mechanisms of Action Edwards, Joshua Ackerman, Christopher Curr Diabetes Rev Article There is increasing interest in how exposure to environmental substances can contribute to the onset of Type II diabetes mellitus (T2DM). Impaired insulin release is a hallmark of type I diabetes mellitus and is involved in the progression of T2DM. Both epidemiological and experimental studies show that exposure to the environmental pollutant cadmium (Cd), is associated with hyperglycemia, T2DM and reduced serum insulin. The goal of this review is to examine likely mechanisms of action of Cd-induced dysglycemia based on experimental studies in the literature and from the most recent findings in the Edwards lab. The primary focus of this review will examine how Cd may cause islet dysfunction and subsequent impaired insulin release. Recent findings in the Edwards lab indicate that Cd causes time-dependent and statistically significant changes in fasting leptin, Glucose-dependent Insulinotropic Polypeptide (GIP) and pancreas polypeptide hormone levels in a subchronic animal model of Cd-induced hyperglycemia. This review summarizes the most likely cellular mechanisms by which the ubiquitous environmental contaminant Cd disrupts glucose homeostasis. While individual cellular effects of Cd are reviewed it is likely that no one single mechanism is involved, rather multiple mechanisms exist and work synergistically resulting in islet dysfunction and ultimately dysglycemia. Bentham Science Publishers 2016-09 2016-09 /pmc/articles/PMC5002940/ /pubmed/26264451 http://dx.doi.org/10.2174/1573399811666150812142922 Text en © 2016 Bentham Science Publishers https://creativecommons.org/licenses/by-nc/4.0/legalcode This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode ), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited. |
spellingShingle | Article Edwards, Joshua Ackerman, Christopher A Review of Diabetes Mellitus and Exposure to the Environmental Toxicant Cadmium with an Emphasis on Likely Mechanisms of Action |
title | A Review of Diabetes Mellitus and Exposure to the Environmental
Toxicant Cadmium with an Emphasis on Likely Mechanisms of Action |
title_full | A Review of Diabetes Mellitus and Exposure to the Environmental
Toxicant Cadmium with an Emphasis on Likely Mechanisms of Action |
title_fullStr | A Review of Diabetes Mellitus and Exposure to the Environmental
Toxicant Cadmium with an Emphasis on Likely Mechanisms of Action |
title_full_unstemmed | A Review of Diabetes Mellitus and Exposure to the Environmental
Toxicant Cadmium with an Emphasis on Likely Mechanisms of Action |
title_short | A Review of Diabetes Mellitus and Exposure to the Environmental
Toxicant Cadmium with an Emphasis on Likely Mechanisms of Action |
title_sort | review of diabetes mellitus and exposure to the environmental
toxicant cadmium with an emphasis on likely mechanisms of action |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5002940/ https://www.ncbi.nlm.nih.gov/pubmed/26264451 http://dx.doi.org/10.2174/1573399811666150812142922 |
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