Persistent organic pollutants and diabetes: a review of the epidemiological evidence.
Identifieur interne : 001595 ( Ncbi/Merge ); précédent : 001594; suivant : 001596Persistent organic pollutants and diabetes: a review of the epidemiological evidence.
Auteurs : D J Magliano [Australie] ; V H Y. Loh [Australie] ; J L Harding [Australie] ; J. Botton [France] ; J E Shaw [Australie]Source :
- Diabetes & metabolism [ 1878-1780 ] ; 2014.
Descripteurs français
- KwdFr :
- Diabète de type 2 (), Diabète de type 2 (métabolisme), Diabète de type 2 (épidémiologie), Diabète de type 2 (étiologie), Dibenzodioxines polychlorées (effets indésirables), Exposition environnementale (effets indésirables), Facteurs de risque, Femelle, Foie (métabolisme), Herbicides (effets indésirables), Humains, Hydrocarbures chlorés (effets indésirables), Insuline (sécrétion), Liaison aux protéines (), Mâle, Pancréas (métabolisme), Polluants atmosphériques d'origine professionnelle (effets indésirables), Polluants environnementaux (effets indésirables), Polychlorobiphényles (effets indésirables), Prévalence, Tissu adipeux (métabolisme), Transporteurs de glucose par diffusion facilitée (métabolisme), Épidémiosurveillance.
- MESH :
- effets indésirables : Dibenzodioxines polychlorées, Exposition environnementale, Herbicides, Hydrocarbures chlorés, Polluants atmosphériques d'origine professionnelle, Polluants environnementaux, Polychlorobiphényles.
- métabolisme : Diabète de type 2, Foie, Pancréas, Tissu adipeux, Transporteurs de glucose par diffusion facilitée.
- sécrétion : Insuline.
- épidémiologie : Diabète de type 2.
- étiologie : Diabète de type 2.
- Diabète de type 2, Facteurs de risque, Femelle, Humains, Liaison aux protéines, Mâle, Prévalence, Épidémiosurveillance.
English descriptors
- KwdEn :
- Adipose Tissue (metabolism), Air Pollutants, Occupational (adverse effects), Diabetes Mellitus, Type 2 (chemically induced), Diabetes Mellitus, Type 2 (epidemiology), Diabetes Mellitus, Type 2 (etiology), Diabetes Mellitus, Type 2 (metabolism), Environmental Exposure (adverse effects), Environmental Pollutants (adverse effects), Epidemiological Monitoring, Female, Glucose Transport Proteins, Facilitative (metabolism), Herbicides (adverse effects), Humans, Hydrocarbons, Chlorinated (adverse effects), Insulin (secretion), Liver (metabolism), Male, Pancreas (metabolism), Polychlorinated Biphenyls (adverse effects), Polychlorinated Dibenzodioxins (adverse effects), Prevalence, Protein Binding (drug effects), Risk Factors.
- MESH :
- chemical , adverse effects : Air Pollutants, Occupational, Environmental Pollutants, Herbicides, Hydrocarbons, Chlorinated, Polychlorinated Biphenyls, Polychlorinated Dibenzodioxins.
- adverse effects : Environmental Exposure.
- chemically induced : Diabetes Mellitus, Type 2.
- drug effects : Protein Binding.
- epidemiology : Diabetes Mellitus, Type 2.
- etiology : Diabetes Mellitus, Type 2.
- metabolism : Adipose Tissue, Diabetes Mellitus, Type 2, Glucose Transport Proteins, Facilitative, Liver, Pancreas.
- chemical , secretion : Insulin.
- Epidemiological Monitoring, Female, Humans, Male, Prevalence, Risk Factors.
Abstract
The prevalence of diabetes and obesity has increased rapidly over the last few decades in both developed and developing countries. While it is intuitively appealing to suggest that lifestyle risk factors such as decreased physical activity and adoption of poor diets can explain much of the increase, the evidence to support this is poor. Given this, there has been an impetus to look more widely than traditional lifestyle and biomedical risk factors, especially those risk factors, which arise from the environment. Since the industrial revolution, there has been an introduction of many chemicals into our environment, which have now become environmental pollutants. There has been growing interest in one key class of environmental pollutants known as persistent organic pollutants (POPs) and their potential role in the development of diabetes. This review will summarise and appraise the current epidemiological evidence relating POPs to diabetes and highlight gaps and flaws in this evidence.
DOI: 10.1016/j.diabet.2013.09.006
PubMed: 24262435
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pubmed:24262435Le document en format XML
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<term>Diabetes Mellitus, Type 2 (epidemiology)</term>
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<term>Diabetes Mellitus, Type 2 (metabolism)</term>
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<term>Hydrocarbons, Chlorinated (adverse effects)</term>
<term>Insulin (secretion)</term>
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<term>Pancreas (metabolism)</term>
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<term>Diabète de type 2 (métabolisme)</term>
<term>Diabète de type 2 (épidémiologie)</term>
<term>Diabète de type 2 (étiologie)</term>
<term>Dibenzodioxines polychlorées (effets indésirables)</term>
<term>Exposition environnementale (effets indésirables)</term>
<term>Facteurs de risque</term>
<term>Femelle</term>
<term>Foie (métabolisme)</term>
<term>Herbicides (effets indésirables)</term>
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<term>Polluants environnementaux</term>
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<front><div type="abstract" xml:lang="en">The prevalence of diabetes and obesity has increased rapidly over the last few decades in both developed and developing countries. While it is intuitively appealing to suggest that lifestyle risk factors such as decreased physical activity and adoption of poor diets can explain much of the increase, the evidence to support this is poor. Given this, there has been an impetus to look more widely than traditional lifestyle and biomedical risk factors, especially those risk factors, which arise from the environment. Since the industrial revolution, there has been an introduction of many chemicals into our environment, which have now become environmental pollutants. There has been growing interest in one key class of environmental pollutants known as persistent organic pollutants (POPs) and their potential role in the development of diabetes. This review will summarise and appraise the current epidemiological evidence relating POPs to diabetes and highlight gaps and flaws in this evidence.</div>
</front>
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<Abstract><AbstractText>The prevalence of diabetes and obesity has increased rapidly over the last few decades in both developed and developing countries. While it is intuitively appealing to suggest that lifestyle risk factors such as decreased physical activity and adoption of poor diets can explain much of the increase, the evidence to support this is poor. Given this, there has been an impetus to look more widely than traditional lifestyle and biomedical risk factors, especially those risk factors, which arise from the environment. Since the industrial revolution, there has been an introduction of many chemicals into our environment, which have now become environmental pollutants. There has been growing interest in one key class of environmental pollutants known as persistent organic pollutants (POPs) and their potential role in the development of diabetes. This review will summarise and appraise the current epidemiological evidence relating POPs to diabetes and highlight gaps and flaws in this evidence.</AbstractText>
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<MeshHeading><DescriptorName UI="D062665" MajorTopicYN="N">Epidemiological Monitoring</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051246" MajorTopicYN="N">Glucose Transport Proteins, Facilitative</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006540" MajorTopicYN="N">Herbicides</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006843" MajorTopicYN="N">Hydrocarbons, Chlorinated</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName>
<QualifierName UI="Q000557" MajorTopicYN="N">secretion</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010179" MajorTopicYN="N">Pancreas</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011078" MajorTopicYN="N">Polychlorinated Biphenyls</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000072317" MajorTopicYN="N">Polychlorinated Dibenzodioxins</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015995" MajorTopicYN="N">Prevalence</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes</Keyword>
<Keyword MajorTopicYN="N">Dioxin</Keyword>
<Keyword MajorTopicYN="N">Persistent organic pollutants</Keyword>
<Keyword MajorTopicYN="N">Polychlorinated biphenyls</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year>
<Month>08</Month>
<Day>19</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2013</Year>
<Month>09</Month>
<Day>26</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2013</Year>
<Month>09</Month>
<Day>26</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2013</Year>
<Month>11</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2013</Year>
<Month>11</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2014</Year>
<Month>11</Month>
<Day>13</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">24262435</ArticleId>
<ArticleId IdType="pii">S1262-3636(13)00179-1</ArticleId>
<ArticleId IdType="doi">10.1016/j.diabet.2013.09.006</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>Australie</li>
<li>France</li>
</country>
<region><li>Victoria (État)</li>
<li>Île-de-France</li>
</region>
<settlement><li>Melbourne</li>
<li>Villejuif</li>
</settlement>
</list>
<tree><country name="Australie"><region name="Victoria (État)"><name sortKey="Magliano, D J" sort="Magliano, D J" uniqKey="Magliano D" first="D J" last="Magliano">D J Magliano</name>
</region>
<name sortKey="Harding, J L" sort="Harding, J L" uniqKey="Harding J" first="J L" last="Harding">J L Harding</name>
<name sortKey="Loh, V H Y" sort="Loh, V H Y" uniqKey="Loh V" first="V H Y" last="Loh">V H Y. Loh</name>
<name sortKey="Shaw, J E" sort="Shaw, J E" uniqKey="Shaw J" first="J E" last="Shaw">J E Shaw</name>
</country>
<country name="France"><region name="Île-de-France"><name sortKey="Botton, J" sort="Botton, J" uniqKey="Botton J" first="J" last="Botton">J. Botton</name>
</region>
</country>
</tree>
</affiliations>
</record>
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