The Effect of Diesel Exhaust Particles on Adipose Tissue Mitochondrial Function and Inflammatory Status
Air pollution poses a significant global health risk, with fine particulate matter (PM ) such as diesel exhaust particles (DEPs) being of particular concern due to their potential to drive systemic toxicities through bloodstream infiltration. The association between PM exposure and an increased prev...
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| Veröffentlicht in: | International journal of molecular sciences 2024-04, Vol.25 (8), p.4322 |
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| description | Air pollution poses a significant global health risk, with fine particulate matter (PM
) such as diesel exhaust particles (DEPs) being of particular concern due to their potential to drive systemic toxicities through bloodstream infiltration. The association between PM
exposure and an increased prevalence of metabolic disorders, including obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM), is evident against a backdrop of rising global obesity and poor metabolic health. This paper examines the role of adipose tissue in mediating the effects of PM
on metabolic health. Adipose tissue, beyond its energy storage function, is responsive to inhaled noxious stimuli, thus disrupting metabolic homeostasis and responding to particulate exposure with pro-inflammatory cytokine release, contributing to systemic inflammation. The purpose of this study was to characterize the metabolic response of adipose tissue in mice exposed to either DEPs or room air (RA), exploring both the adipokine profile and mitochondrial bioenergetics. In addition to a slight change in fat mass and a robust shift in adipocyte hypertrophy in the DEP-exposed animals, we found significant changes in adipose mitochondrial bioenergetics. Furthermore, the DEP-exposed animals had a significantly higher expression of adipose inflammatory markers compared with the adipose from RA-exposed mice. Despite the nearly exclusive focus on dietary factors in an effort to better understand metabolic health, these results highlight the novel role of environmental factors that may contribute to the growing global burden of poor metabolic health. |
| doi_str_mv | 10.3390/ijms25084322 |
| format | Article |
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exposure and an increased prevalence of metabolic disorders, including obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM), is evident against a backdrop of rising global obesity and poor metabolic health. This paper examines the role of adipose tissue in mediating the effects of PM
on metabolic health. Adipose tissue, beyond its energy storage function, is responsive to inhaled noxious stimuli, thus disrupting metabolic homeostasis and responding to particulate exposure with pro-inflammatory cytokine release, contributing to systemic inflammation. The purpose of this study was to characterize the metabolic response of adipose tissue in mice exposed to either DEPs or room air (RA), exploring both the adipokine profile and mitochondrial bioenergetics. In addition to a slight change in fat mass and a robust shift in adipocyte hypertrophy in the DEP-exposed animals, we found significant changes in adipose mitochondrial bioenergetics. Furthermore, the DEP-exposed animals had a significantly higher expression of adipose inflammatory markers compared with the adipose from RA-exposed mice. Despite the nearly exclusive focus on dietary factors in an effort to better understand metabolic health, these results highlight the novel role of environmental factors that may contribute to the growing global burden of poor metabolic health.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25084322</identifier><identifier>PMID: 38673906</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adipocytes ; Adipocytes - drug effects ; Adipocytes - metabolism ; Adipokines - metabolism ; Adipose Tissue - drug effects ; Adipose Tissue - metabolism ; Adipose tissues ; Air Pollutants - adverse effects ; Air Pollutants - toxicity ; Air pollution ; Animals ; Bioenergetics ; Body fat ; Cytokines ; Diabetes ; Energy Metabolism - drug effects ; Inflammation ; Inflammation - chemically induced ; Inflammation - metabolism ; Inflammation - pathology ; Insulin resistance ; Male ; Metabolic disorders ; Metabolic syndrome ; Mice ; Mice, Inbred C57BL ; Mitochondria - drug effects ; Mitochondria - metabolism ; Morphology ; Obesity ; Outdoor air quality ; Particulate Matter - adverse effects ; Particulate Matter - toxicity ; Pollutants ; Respiration ; Tumor necrosis factor-TNF ; Type 2 diabetes ; Vehicle Emissions - toxicity</subject><ispartof>International journal of molecular sciences, 2024-04, Vol.25 (8), p.4322</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 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 (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c381t-758df510a9043fab9bf77546c1569e7c0d2a09ec93117421fae5fdf3622757923</cites><orcidid>0000-0002-0931-3025</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38673906$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Warren, Cali E</creatorcontrib><creatorcontrib>Campbell, Kennedy M</creatorcontrib><creatorcontrib>Kirkham, Madison N</creatorcontrib><creatorcontrib>Saito, Erin R</creatorcontrib><creatorcontrib>Remund, Nicole P</creatorcontrib><creatorcontrib>Cayabyab, Kevin B</creatorcontrib><creatorcontrib>Kim, Iris J</creatorcontrib><creatorcontrib>Heimuli, Micah S</creatorcontrib><creatorcontrib>Reynolds, Paul R</creatorcontrib><creatorcontrib>Arroyo, Juan A</creatorcontrib><creatorcontrib>Bikman, Benjamin T</creatorcontrib><title>The Effect of Diesel Exhaust Particles on Adipose Tissue Mitochondrial Function and Inflammatory Status</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Air pollution poses a significant global health risk, with fine particulate matter (PM
) such as diesel exhaust particles (DEPs) being of particular concern due to their potential to drive systemic toxicities through bloodstream infiltration. The association between PM
exposure and an increased prevalence of metabolic disorders, including obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM), is evident against a backdrop of rising global obesity and poor metabolic health. This paper examines the role of adipose tissue in mediating the effects of PM
on metabolic health. Adipose tissue, beyond its energy storage function, is responsive to inhaled noxious stimuli, thus disrupting metabolic homeostasis and responding to particulate exposure with pro-inflammatory cytokine release, contributing to systemic inflammation. The purpose of this study was to characterize the metabolic response of adipose tissue in mice exposed to either DEPs or room air (RA), exploring both the adipokine profile and mitochondrial bioenergetics. In addition to a slight change in fat mass and a robust shift in adipocyte hypertrophy in the DEP-exposed animals, we found significant changes in adipose mitochondrial bioenergetics. Furthermore, the DEP-exposed animals had a significantly higher expression of adipose inflammatory markers compared with the adipose from RA-exposed mice. Despite the nearly exclusive focus on dietary factors in an effort to better understand metabolic health, these results highlight the novel role of environmental factors that may contribute to the growing global burden of poor metabolic health.</description><subject>Adipocytes</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>Adipokines - metabolism</subject><subject>Adipose Tissue - drug effects</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose tissues</subject><subject>Air Pollutants - adverse effects</subject><subject>Air Pollutants - toxicity</subject><subject>Air pollution</subject><subject>Animals</subject><subject>Bioenergetics</subject><subject>Body fat</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Energy Metabolism - drug effects</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Insulin resistance</subject><subject>Male</subject><subject>Metabolic disorders</subject><subject>Metabolic syndrome</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Morphology</subject><subject>Obesity</subject><subject>Outdoor air quality</subject><subject>Particulate Matter - adverse effects</subject><subject>Particulate Matter - toxicity</subject><subject>Pollutants</subject><subject>Respiration</subject><subject>Tumor necrosis factor-TNF</subject><subject>Type 2 diabetes</subject><subject>Vehicle Emissions - toxicity</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkc1rGzEQxUVoyfet5yLoJYc40cdqtTqa1GkMKSnEOS-ydhTL7EqupIXmv49M0sYJZQ4zDL_3ePAQ-kLJBeeKXLr1kJggTcUZ20OHtGJsQkgtP-3cB-gopTUhjDOh9tEBb2pZtPUhelysAM-sBZNxsPi7gwQ9nv1Z6TFl_EvH7EwPCQePp53bhAR44VIaAf90OZhV8F10usfXozfZFUr7Ds-97fUw6BziE77POo_pBH22uk9w-rqP0cP1bHF1M7m9-zG_mt5ODG9onkjRdFZQohWpuNVLtbRSiqo2VNQKpCEd00SBUZxSWTFqNQjbWV4zJoVUjB-jsxffTQy_R0i5HVwy0PfaQxhTy0klVaVEQwv67QO6DmP0Jd2WqhWlXJA36lH30DpvQ47abE3bqSwxlCS8KtTFf6gyHQzOBA_Wlf87wfmLwMSQUgTbbqIbdHxqKWm3vba7vRb862vWcTlA9w_-WyR_BpRvm7c</recordid><startdate>20240401</startdate><enddate>20240401</enddate><creator>Warren, Cali E</creator><creator>Campbell, Kennedy M</creator><creator>Kirkham, Madison N</creator><creator>Saito, Erin R</creator><creator>Remund, Nicole P</creator><creator>Cayabyab, Kevin B</creator><creator>Kim, Iris J</creator><creator>Heimuli, Micah S</creator><creator>Reynolds, Paul R</creator><creator>Arroyo, Juan A</creator><creator>Bikman, Benjamin T</creator><general>MDPI AG</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0931-3025</orcidid></search><sort><creationdate>20240401</creationdate><title>The Effect of Diesel Exhaust Particles on Adipose Tissue Mitochondrial Function and Inflammatory Status</title><author>Warren, Cali E ; Campbell, Kennedy M ; Kirkham, Madison N ; Saito, Erin R ; Remund, Nicole P ; Cayabyab, Kevin B ; Kim, Iris J ; Heimuli, Micah S ; Reynolds, Paul R ; Arroyo, Juan A ; Bikman, Benjamin T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-758df510a9043fab9bf77546c1569e7c0d2a09ec93117421fae5fdf3622757923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adipocytes</topic><topic>Adipocytes - 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) such as diesel exhaust particles (DEPs) being of particular concern due to their potential to drive systemic toxicities through bloodstream infiltration. The association between PM
exposure and an increased prevalence of metabolic disorders, including obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM), is evident against a backdrop of rising global obesity and poor metabolic health. This paper examines the role of adipose tissue in mediating the effects of PM
on metabolic health. Adipose tissue, beyond its energy storage function, is responsive to inhaled noxious stimuli, thus disrupting metabolic homeostasis and responding to particulate exposure with pro-inflammatory cytokine release, contributing to systemic inflammation. The purpose of this study was to characterize the metabolic response of adipose tissue in mice exposed to either DEPs or room air (RA), exploring both the adipokine profile and mitochondrial bioenergetics. In addition to a slight change in fat mass and a robust shift in adipocyte hypertrophy in the DEP-exposed animals, we found significant changes in adipose mitochondrial bioenergetics. Furthermore, the DEP-exposed animals had a significantly higher expression of adipose inflammatory markers compared with the adipose from RA-exposed mice. Despite the nearly exclusive focus on dietary factors in an effort to better understand metabolic health, these results highlight the novel role of environmental factors that may contribute to the growing global burden of poor metabolic health.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38673906</pmid><doi>10.3390/ijms25084322</doi><orcidid>https://orcid.org/0000-0002-0931-3025</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes Adipocytes - drug effects Adipocytes - metabolism Adipokines - metabolism Adipose Tissue - drug effects Adipose Tissue - metabolism Adipose tissues Air Pollutants - adverse effects Air Pollutants - toxicity Air pollution Animals Bioenergetics Body fat Cytokines Diabetes Energy Metabolism - drug effects Inflammation Inflammation - chemically induced Inflammation - metabolism Inflammation - pathology Insulin resistance Male Metabolic disorders Metabolic syndrome Mice Mice, Inbred C57BL Mitochondria - drug effects Mitochondria - metabolism Morphology Obesity Outdoor air quality Particulate Matter - adverse effects Particulate Matter - toxicity Pollutants Respiration Tumor necrosis factor-TNF Type 2 diabetes Vehicle Emissions - toxicity |
| title | The Effect of Diesel Exhaust Particles on Adipose Tissue Mitochondrial Function and Inflammatory Status |
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