Persistent organic pollutant exposure leads to insulin resistance syndrome.

Details

Serval ID
serval:BIB_16619B1D658F
Type
Article: article from journal or magazin.
Collection
Publications
Title
Persistent organic pollutant exposure leads to insulin resistance syndrome.
Journal
Environmental Health Perspectives
Author(s)
Ruzzin J., Petersen R., Meugnier E., Madsen L., Lock E.J., Lillefosse H., Ma T., Pesenti S., Sonne S.B., Marstrand T.T., Malde M.K., Du Z.Y., Chavey C., Fajas L., Lundebye A.K., Brand C.L., Vidal H., Kristiansen K., Frøyland L.
ISSN
1552-9924 (Electronic)
ISSN-L
0091-6765
Publication state
Published
Issued date
2010
Volume
118
Number
4
Pages
465-471
Language
english
Abstract
BACKGROUND: The incidence of the insulin resistance syndrome has increased at an alarming rate worldwide, creating a serious challenge to public health care in the 21st century. Recently, epidemiological studies have associated the prevalence of type 2 diabetes with elevated body burdens of persistent organic pollutants (POPs). However, experimental evidence demonstrating a causal link between POPs and the development of insulin resistance is lacking.
OBJECTIVE: We investigated whether exposure to POPs contributes to insulin resistance and metabolic disorders.
METHODS: Sprague-Dawley rats were exposed for 28 days to lipophilic POPs through the consumption of a high-fat diet containing either refined or crude fish oil obtained from farmed Atlantic salmon. In addition, differentiated adipocytes were exposed to several POP mixtures that mimicked the relative abundance of organic pollutants present in crude salmon oil. We measured body weight, whole-body insulin sensitivity, POP accumulation, lipid and glucose homeostasis, and gene expression and we performed microarray analysis.
RESULTS: Adult male rats exposed to crude, but not refined, salmon oil developed insulin resistance, abdominal obesity, and hepatosteatosis. The contribution of POPs to insulin resistance was confirmed in cultured adipocytes where POPs, especially organochlorine pesticides, led to robust inhibition of insulin action. Moreover, POPs induced down-regulation of insulin-induced gene-1 (Insig-1) and Lpin1, two master regulators of lipid homeostasis.
CONCLUSION: Our findings provide evidence that exposure to POPs commonly present in food chains leads to insulin resistance and associated metabolic disorders.
Keywords
3T3-L1 Cells, Animals, Carbohydrate Metabolism/drug effects, Environmental Pollutants/toxicity, Glucose/metabolism, Glucose Clamp Technique, Hydrocarbons, Chlorinated/toxicity, Insulin Resistance, Lipid Metabolism/drug effects, Male, Metabolic Syndrome X/chemically induced, Metabolic Syndrome X/metabolism, Mice, Oligonucleotide Array Sequence Analysis, Pesticides/toxicity, Polymerase Chain Reaction, Rats, Rats, Sprague-Dawley
Pubmed
Web of science
Create date
07/03/2013 15:56
Last modification date
20/08/2019 12:45
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