Adipose tissue-liver crosstalk during pathologic changes caused by vinyl chloride metabolites in mice.
Adipocytes
/ drug effects
Adipose Tissue, White
/ drug effects
Animals
Diet, High-Fat
/ adverse effects
Inflammation
/ chemically induced
Lipid Metabolism
/ drug effects
Lipids
Liver
/ drug effects
Male
Mice
Mice, Inbred C57BL
Non-alcoholic Fatty Liver Disease
/ metabolism
Obesity
/ chemically induced
Vinyl Chloride
/ toxicity
Hepatotoxicity
Metabolic syndrome
PVC
Plastic
Saturated fat
TASH
Journal
Toxicology and applied pharmacology
ISSN: 1096-0333
Titre abrégé: Toxicol Appl Pharmacol
Pays: United States
ID NLM: 0416575
Informations de publication
Date de publication:
15 07 2020
15 07 2020
Historique:
received:
06
03
2020
revised:
06
05
2020
accepted:
19
05
2020
pubmed:
24
5
2020
medline:
19
8
2020
entrez:
24
5
2020
Statut:
ppublish
Résumé
Volatile organic compounds (VOCs), such as vinyl chloride (VC), can be directly toxic at high concentrations. However, we have shown that 'nontoxic' exposures to VC and its metabolite chloroethanol (CE) enhances experimental non-alcoholic fatty liver disease (NAFLD), suggesting an unpredicted interaction. Importantly, VOC exposure has been identified as a potential risk factor for the development of obesity and its sequelae in humans. As there is a known axis between adipose and hepatic tissue in NAFLD, the impact of CE on white adipose tissue (WAT) inflammation and lipolysis was investigated. Mice were administered CE (or vehicle) once, after 10 weeks of being fed high-fat or low-fat diet (LFD). CE significantly enhanced hepatic steatosis and inflammation caused by HFD. HFD significantly increased the size of epididymal fat pads, which was enhanced by CE. The relative size of adipocyte lipid droplets increased by HFD + CE, which was also correlated with increased expression of lipid-associated proteins (e.g., PLINs). CE also enhanced HFD-induced indices of WAT inflammation, and ER stress. Hepatic-derived circulating FGF21, a major modulator of WAT lipolysis, which is hypothesized to thereby regulate hepatic steatosis, was significantly increased by CE in animals fed HFD. Taken together these data support the hypothesis that environmental toxicant exposure can exacerbate the severity of NAFLD/NASH, involving the liver-adipose axis in this process. Specifically, CE enhances local inflammation and alters lipid metabolism and WAT-mediated hepatic steatosis due to changes in WAT lipolysis.
Identifiants
pubmed: 32445754
pii: S0041-008X(20)30192-7
doi: 10.1016/j.taap.2020.115068
pmc: PMC7450542
mid: NIHMS1598430
pii:
doi:
Substances chimiques
Lipids
0
Vinyl Chloride
WD06X94M2D
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
115068Subventions
Organisme : NIDDK NIH HHS
ID : R03 DK107912
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM113226
Pays : United States
Organisme : NIDDK NIH HHS
ID : K01 DK096042
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES031531
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA021978
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA028436
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK120531
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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