Environmental risk factors of type 2 diabetes—an exposome approach
Type 2 diabetes is one of the major chronic diseases accounting for a substantial proportion of disease burden in Western countries. The majority of the burden of type 2 diabetes is attributed to environmental risks and modifiable risk factors such as lifestyle. The environment we live in, and chang...
Gespeichert in:
Veröffentlicht in: | Diabetologia 2022-02, Vol.65 (2), p.263-274 |
---|---|
Hauptverfasser: | , , , , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 274 |
---|---|
container_issue | 2 |
container_start_page | 263 |
container_title | Diabetologia |
container_volume | 65 |
creator | Beulens, Joline W. J. Pinho, Maria G. M. Abreu, Taymara C. den Braver, Nicole R. Lam, Thao M. Huss, Anke Vlaanderen, Jelle Sonnenschein, Tabea Siddiqui, Noreen Z. Yuan, Zhendong Kerckhoffs, Jules Zhernakova, Alexandra Brandao Gois, Milla F. Vermeulen, Roel C. H. |
description | Type 2 diabetes is one of the major chronic diseases accounting for a substantial proportion of disease burden in Western countries. The majority of the burden of type 2 diabetes is attributed to environmental risks and modifiable risk factors such as lifestyle. The environment we live in, and changes to it, can thus contribute substantially to the prevention of type 2 diabetes at a population level. The ‘exposome’ represents the (measurable) totality of environmental, i.e. nongenetic, drivers of health and disease. The external exposome comprises aspects of the built environment, the social environment, the physico-chemical environment and the lifestyle/food environment. The internal exposome comprises measurements at the epigenetic, transcript, proteome, microbiome or metabolome level to study either the exposures directly, the imprints these exposures leave in the biological system, the potential of the body to combat environmental insults and/or the biology itself. In this review, we describe the evidence for environmental risk factors of type 2 diabetes, focusing on both the general external exposome and imprints of this on the internal exposome. Studies provided established associations of air pollution, residential noise and area-level socioeconomic deprivation with an increased risk of type 2 diabetes, while neighbourhood walkability and green space are consistently associated with a reduced risk of type 2 diabetes. There is little or inconsistent evidence on the contribution of the food environment, other aspects of the social environment and outdoor temperature. These environmental factors are thought to affect type 2 diabetes risk mainly through mechanisms incorporating lifestyle factors such as physical activity or diet, the microbiome, inflammation or chronic stress. To further assess causality of these associations, future studies should focus on investigating the longitudinal effects of our environment (and changes to it) in relation to type 2 diabetes risk and whether these associations are explained by these proposed mechanisms.
Graphical abstract |
doi_str_mv | 10.1007/s00125-021-05618-w |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2617591282</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2617591282</sourcerecordid><originalsourceid>FETCH-LOGICAL-c419t-d3b83f6edf116cdc3e146e6d07a26b2952a163342767a000bd70850faee893e63</originalsourceid><addsrcrecordid>eNp9kL1OwzAQxy0EoqXwAgzIErPBZydOMiIoH1IlFpDYLCe5QEobBzuldOMheEKeBJcU2JhuuP_H3Y-QQ-AnwHly6jkHETMugPFYQcqWW2QIkRSMRyLdJsP1nkGqHgZkz_sp51zGkdolAxklmVCQDcnFuHmtnW3m2HRmRl3tn2llis46T21Fu1WLVNCyNjl26D_fP0xD8a213s6RmrZ11hRP-2SnMjOPB5s5IveX47vzaza5vbo5P5uwIoKsY6XMU1kpLCsAVZSFRIgUqpInRqhcZLEwoKSMRKISE47Ny4SnMa8MYppJVHJEjvvcUPuyQN_pqV24JlTq8E0SZyBSEVSiVxXOeu-w0q2r58atNHC9Bqd7cDqA09_g9DKYjjbRi3yO5a_lh1QQyF7gw6p5RPfX_U_sFwo2eZQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2617591282</pqid></control><display><type>article</type><title>Environmental risk factors of type 2 diabetes—an exposome approach</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Beulens, Joline W. J. ; Pinho, Maria G. M. ; Abreu, Taymara C. ; den Braver, Nicole R. ; Lam, Thao M. ; Huss, Anke ; Vlaanderen, Jelle ; Sonnenschein, Tabea ; Siddiqui, Noreen Z. ; Yuan, Zhendong ; Kerckhoffs, Jules ; Zhernakova, Alexandra ; Brandao Gois, Milla F. ; Vermeulen, Roel C. H.</creator><creatorcontrib>Beulens, Joline W. J. ; Pinho, Maria G. M. ; Abreu, Taymara C. ; den Braver, Nicole R. ; Lam, Thao M. ; Huss, Anke ; Vlaanderen, Jelle ; Sonnenschein, Tabea ; Siddiqui, Noreen Z. ; Yuan, Zhendong ; Kerckhoffs, Jules ; Zhernakova, Alexandra ; Brandao Gois, Milla F. ; Vermeulen, Roel C. H.</creatorcontrib><description>Type 2 diabetes is one of the major chronic diseases accounting for a substantial proportion of disease burden in Western countries. The majority of the burden of type 2 diabetes is attributed to environmental risks and modifiable risk factors such as lifestyle. The environment we live in, and changes to it, can thus contribute substantially to the prevention of type 2 diabetes at a population level. The ‘exposome’ represents the (measurable) totality of environmental, i.e. nongenetic, drivers of health and disease. The external exposome comprises aspects of the built environment, the social environment, the physico-chemical environment and the lifestyle/food environment. The internal exposome comprises measurements at the epigenetic, transcript, proteome, microbiome or metabolome level to study either the exposures directly, the imprints these exposures leave in the biological system, the potential of the body to combat environmental insults and/or the biology itself. In this review, we describe the evidence for environmental risk factors of type 2 diabetes, focusing on both the general external exposome and imprints of this on the internal exposome. Studies provided established associations of air pollution, residential noise and area-level socioeconomic deprivation with an increased risk of type 2 diabetes, while neighbourhood walkability and green space are consistently associated with a reduced risk of type 2 diabetes. There is little or inconsistent evidence on the contribution of the food environment, other aspects of the social environment and outdoor temperature. These environmental factors are thought to affect type 2 diabetes risk mainly through mechanisms incorporating lifestyle factors such as physical activity or diet, the microbiome, inflammation or chronic stress. To further assess causality of these associations, future studies should focus on investigating the longitudinal effects of our environment (and changes to it) in relation to type 2 diabetes risk and whether these associations are explained by these proposed mechanisms.
Graphical abstract</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-021-05618-w</identifier><identifier>PMID: 34792619</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Air pollution ; Built environment ; Chronic illnesses ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - epidemiology ; Environmental Exposure - adverse effects ; Environmental factors ; Environmental health ; Environmental risk ; Epigenetics ; Exposome ; Green infrastructure ; Health risks ; Human Physiology ; Humans ; Internal Medicine ; Lifestyles ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Microbiomes ; Noise pollution ; Physical activity ; Proteomes ; Review ; Risk Factors ; Social environment ; Transcription ; Urban environments</subject><ispartof>Diabetologia, 2022-02, Vol.65 (2), p.263-274</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-d3b83f6edf116cdc3e146e6d07a26b2952a163342767a000bd70850faee893e63</citedby><cites>FETCH-LOGICAL-c419t-d3b83f6edf116cdc3e146e6d07a26b2952a163342767a000bd70850faee893e63</cites><orcidid>0000-0003-4928-0851 ; 0000-0003-3326-5243 ; 0000-0002-7240-726X ; 0000-0001-6592-9548 ; 0000-0002-9096-692X ; 0000-0002-4574-0841 ; 0000-0003-2699-2303 ; 0000-0003-4082-8163 ; 0000-0002-6345-251X ; 0000-0002-4181-0937 ; 0000-0001-7918-2481 ; 0000-0001-9063-3407 ; 0000-0001-9065-6916</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00125-021-05618-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00125-021-05618-w$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34792619$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Beulens, Joline W. J.</creatorcontrib><creatorcontrib>Pinho, Maria G. M.</creatorcontrib><creatorcontrib>Abreu, Taymara C.</creatorcontrib><creatorcontrib>den Braver, Nicole R.</creatorcontrib><creatorcontrib>Lam, Thao M.</creatorcontrib><creatorcontrib>Huss, Anke</creatorcontrib><creatorcontrib>Vlaanderen, Jelle</creatorcontrib><creatorcontrib>Sonnenschein, Tabea</creatorcontrib><creatorcontrib>Siddiqui, Noreen Z.</creatorcontrib><creatorcontrib>Yuan, Zhendong</creatorcontrib><creatorcontrib>Kerckhoffs, Jules</creatorcontrib><creatorcontrib>Zhernakova, Alexandra</creatorcontrib><creatorcontrib>Brandao Gois, Milla F.</creatorcontrib><creatorcontrib>Vermeulen, Roel C. H.</creatorcontrib><title>Environmental risk factors of type 2 diabetes—an exposome approach</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Type 2 diabetes is one of the major chronic diseases accounting for a substantial proportion of disease burden in Western countries. The majority of the burden of type 2 diabetes is attributed to environmental risks and modifiable risk factors such as lifestyle. The environment we live in, and changes to it, can thus contribute substantially to the prevention of type 2 diabetes at a population level. The ‘exposome’ represents the (measurable) totality of environmental, i.e. nongenetic, drivers of health and disease. The external exposome comprises aspects of the built environment, the social environment, the physico-chemical environment and the lifestyle/food environment. The internal exposome comprises measurements at the epigenetic, transcript, proteome, microbiome or metabolome level to study either the exposures directly, the imprints these exposures leave in the biological system, the potential of the body to combat environmental insults and/or the biology itself. In this review, we describe the evidence for environmental risk factors of type 2 diabetes, focusing on both the general external exposome and imprints of this on the internal exposome. Studies provided established associations of air pollution, residential noise and area-level socioeconomic deprivation with an increased risk of type 2 diabetes, while neighbourhood walkability and green space are consistently associated with a reduced risk of type 2 diabetes. There is little or inconsistent evidence on the contribution of the food environment, other aspects of the social environment and outdoor temperature. These environmental factors are thought to affect type 2 diabetes risk mainly through mechanisms incorporating lifestyle factors such as physical activity or diet, the microbiome, inflammation or chronic stress. To further assess causality of these associations, future studies should focus on investigating the longitudinal effects of our environment (and changes to it) in relation to type 2 diabetes risk and whether these associations are explained by these proposed mechanisms.
Graphical abstract</description><subject>Air pollution</subject><subject>Built environment</subject><subject>Chronic illnesses</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - epidemiology</subject><subject>Environmental Exposure - adverse effects</subject><subject>Environmental factors</subject><subject>Environmental health</subject><subject>Environmental risk</subject><subject>Epigenetics</subject><subject>Exposome</subject><subject>Green infrastructure</subject><subject>Health risks</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Lifestyles</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Microbiomes</subject><subject>Noise pollution</subject><subject>Physical activity</subject><subject>Proteomes</subject><subject>Review</subject><subject>Risk Factors</subject><subject>Social environment</subject><subject>Transcription</subject><subject>Urban environments</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kL1OwzAQxy0EoqXwAgzIErPBZydOMiIoH1IlFpDYLCe5QEobBzuldOMheEKeBJcU2JhuuP_H3Y-QQ-AnwHly6jkHETMugPFYQcqWW2QIkRSMRyLdJsP1nkGqHgZkz_sp51zGkdolAxklmVCQDcnFuHmtnW3m2HRmRl3tn2llis46T21Fu1WLVNCyNjl26D_fP0xD8a213s6RmrZ11hRP-2SnMjOPB5s5IveX47vzaza5vbo5P5uwIoKsY6XMU1kpLCsAVZSFRIgUqpInRqhcZLEwoKSMRKISE47Ny4SnMa8MYppJVHJEjvvcUPuyQN_pqV24JlTq8E0SZyBSEVSiVxXOeu-w0q2r58atNHC9Bqd7cDqA09_g9DKYjjbRi3yO5a_lh1QQyF7gw6p5RPfX_U_sFwo2eZQ</recordid><startdate>20220201</startdate><enddate>20220201</enddate><creator>Beulens, Joline W. J.</creator><creator>Pinho, Maria G. M.</creator><creator>Abreu, Taymara C.</creator><creator>den Braver, Nicole R.</creator><creator>Lam, Thao M.</creator><creator>Huss, Anke</creator><creator>Vlaanderen, Jelle</creator><creator>Sonnenschein, Tabea</creator><creator>Siddiqui, Noreen Z.</creator><creator>Yuan, Zhendong</creator><creator>Kerckhoffs, Jules</creator><creator>Zhernakova, Alexandra</creator><creator>Brandao Gois, Milla F.</creator><creator>Vermeulen, Roel C. H.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0003-4928-0851</orcidid><orcidid>https://orcid.org/0000-0003-3326-5243</orcidid><orcidid>https://orcid.org/0000-0002-7240-726X</orcidid><orcidid>https://orcid.org/0000-0001-6592-9548</orcidid><orcidid>https://orcid.org/0000-0002-9096-692X</orcidid><orcidid>https://orcid.org/0000-0002-4574-0841</orcidid><orcidid>https://orcid.org/0000-0003-2699-2303</orcidid><orcidid>https://orcid.org/0000-0003-4082-8163</orcidid><orcidid>https://orcid.org/0000-0002-6345-251X</orcidid><orcidid>https://orcid.org/0000-0002-4181-0937</orcidid><orcidid>https://orcid.org/0000-0001-7918-2481</orcidid><orcidid>https://orcid.org/0000-0001-9063-3407</orcidid><orcidid>https://orcid.org/0000-0001-9065-6916</orcidid></search><sort><creationdate>20220201</creationdate><title>Environmental risk factors of type 2 diabetes—an exposome approach</title><author>Beulens, Joline W. J. ; Pinho, Maria G. M. ; Abreu, Taymara C. ; den Braver, Nicole R. ; Lam, Thao M. ; Huss, Anke ; Vlaanderen, Jelle ; Sonnenschein, Tabea ; Siddiqui, Noreen Z. ; Yuan, Zhendong ; Kerckhoffs, Jules ; Zhernakova, Alexandra ; Brandao Gois, Milla F. ; Vermeulen, Roel C. H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-d3b83f6edf116cdc3e146e6d07a26b2952a163342767a000bd70850faee893e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Air pollution</topic><topic>Built environment</topic><topic>Chronic illnesses</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - epidemiology</topic><topic>Environmental Exposure - adverse effects</topic><topic>Environmental factors</topic><topic>Environmental health</topic><topic>Environmental risk</topic><topic>Epigenetics</topic><topic>Exposome</topic><topic>Green infrastructure</topic><topic>Health risks</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Lifestyles</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Microbiomes</topic><topic>Noise pollution</topic><topic>Physical activity</topic><topic>Proteomes</topic><topic>Review</topic><topic>Risk Factors</topic><topic>Social environment</topic><topic>Transcription</topic><topic>Urban environments</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Beulens, Joline W. J.</creatorcontrib><creatorcontrib>Pinho, Maria G. M.</creatorcontrib><creatorcontrib>Abreu, Taymara C.</creatorcontrib><creatorcontrib>den Braver, Nicole R.</creatorcontrib><creatorcontrib>Lam, Thao M.</creatorcontrib><creatorcontrib>Huss, Anke</creatorcontrib><creatorcontrib>Vlaanderen, Jelle</creatorcontrib><creatorcontrib>Sonnenschein, Tabea</creatorcontrib><creatorcontrib>Siddiqui, Noreen Z.</creatorcontrib><creatorcontrib>Yuan, Zhendong</creatorcontrib><creatorcontrib>Kerckhoffs, Jules</creatorcontrib><creatorcontrib>Zhernakova, Alexandra</creatorcontrib><creatorcontrib>Brandao Gois, Milla F.</creatorcontrib><creatorcontrib>Vermeulen, Roel C. H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Beulens, Joline W. J.</au><au>Pinho, Maria G. M.</au><au>Abreu, Taymara C.</au><au>den Braver, Nicole R.</au><au>Lam, Thao M.</au><au>Huss, Anke</au><au>Vlaanderen, Jelle</au><au>Sonnenschein, Tabea</au><au>Siddiqui, Noreen Z.</au><au>Yuan, Zhendong</au><au>Kerckhoffs, Jules</au><au>Zhernakova, Alexandra</au><au>Brandao Gois, Milla F.</au><au>Vermeulen, Roel C. H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Environmental risk factors of type 2 diabetes—an exposome approach</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2022-02-01</date><risdate>2022</risdate><volume>65</volume><issue>2</issue><spage>263</spage><epage>274</epage><pages>263-274</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Type 2 diabetes is one of the major chronic diseases accounting for a substantial proportion of disease burden in Western countries. The majority of the burden of type 2 diabetes is attributed to environmental risks and modifiable risk factors such as lifestyle. The environment we live in, and changes to it, can thus contribute substantially to the prevention of type 2 diabetes at a population level. The ‘exposome’ represents the (measurable) totality of environmental, i.e. nongenetic, drivers of health and disease. The external exposome comprises aspects of the built environment, the social environment, the physico-chemical environment and the lifestyle/food environment. The internal exposome comprises measurements at the epigenetic, transcript, proteome, microbiome or metabolome level to study either the exposures directly, the imprints these exposures leave in the biological system, the potential of the body to combat environmental insults and/or the biology itself. In this review, we describe the evidence for environmental risk factors of type 2 diabetes, focusing on both the general external exposome and imprints of this on the internal exposome. Studies provided established associations of air pollution, residential noise and area-level socioeconomic deprivation with an increased risk of type 2 diabetes, while neighbourhood walkability and green space are consistently associated with a reduced risk of type 2 diabetes. There is little or inconsistent evidence on the contribution of the food environment, other aspects of the social environment and outdoor temperature. These environmental factors are thought to affect type 2 diabetes risk mainly through mechanisms incorporating lifestyle factors such as physical activity or diet, the microbiome, inflammation or chronic stress. To further assess causality of these associations, future studies should focus on investigating the longitudinal effects of our environment (and changes to it) in relation to type 2 diabetes risk and whether these associations are explained by these proposed mechanisms.
Graphical abstract</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>34792619</pmid><doi>10.1007/s00125-021-05618-w</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-4928-0851</orcidid><orcidid>https://orcid.org/0000-0003-3326-5243</orcidid><orcidid>https://orcid.org/0000-0002-7240-726X</orcidid><orcidid>https://orcid.org/0000-0001-6592-9548</orcidid><orcidid>https://orcid.org/0000-0002-9096-692X</orcidid><orcidid>https://orcid.org/0000-0002-4574-0841</orcidid><orcidid>https://orcid.org/0000-0003-2699-2303</orcidid><orcidid>https://orcid.org/0000-0003-4082-8163</orcidid><orcidid>https://orcid.org/0000-0002-6345-251X</orcidid><orcidid>https://orcid.org/0000-0002-4181-0937</orcidid><orcidid>https://orcid.org/0000-0001-7918-2481</orcidid><orcidid>https://orcid.org/0000-0001-9063-3407</orcidid><orcidid>https://orcid.org/0000-0001-9065-6916</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0012-186X |
ispartof | Diabetologia, 2022-02, Vol.65 (2), p.263-274 |
issn | 0012-186X 1432-0428 |
language | eng |
recordid | cdi_proquest_journals_2617591282 |
source | MEDLINE; Springer Nature - Complete Springer Journals |
subjects | Air pollution Built environment Chronic illnesses Diabetes Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - epidemiology Environmental Exposure - adverse effects Environmental factors Environmental health Environmental risk Epigenetics Exposome Green infrastructure Health risks Human Physiology Humans Internal Medicine Lifestyles Medicine Medicine & Public Health Metabolic Diseases Microbiomes Noise pollution Physical activity Proteomes Review Risk Factors Social environment Transcription Urban environments |
title | Environmental risk factors of type 2 diabetes—an exposome approach |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T17%3A53%3A54IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Environmental%20risk%20factors%20of%20type%202%20diabetes%E2%80%94an%20exposome%20approach&rft.jtitle=Diabetologia&rft.au=Beulens,%20Joline%20W.%20J.&rft.date=2022-02-01&rft.volume=65&rft.issue=2&rft.spage=263&rft.epage=274&rft.pages=263-274&rft.issn=0012-186X&rft.eissn=1432-0428&rft_id=info:doi/10.1007/s00125-021-05618-w&rft_dat=%3Cproquest_cross%3E2617591282%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2617591282&rft_id=info:pmid/34792619&rfr_iscdi=true |