Persistent Organic Pollutant Exposure Leads to Insulin Resistance Syndrome
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Persistent Organic Pollutant Exposure Leads to Insulin Resistance Syndrome. / Ruzzin, Jérôme; Petersen, Rasmus; Meugnier, Emmanuelle; Madsen, Lise; Lock, Erik-Jan; Lillefosse, Haldis; Ma, Tao; Pesenti, Sandra; Sonne, Si Brask; Marstrand, Troels Torben; Malde, Marian Kjellevod; Du, Zhen-Yu; Chavey, Carine; Fajas, Lluis; Lundebye, Anne-Katrine; Brand, Christian Lehn; Vidal, Hubert; Kristiansen, Karsten; Frøyland, Livar.
In: Environmental Health Perspectives, Vol. 118, No. 4, 2010, p. 465-71.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Persistent Organic Pollutant Exposure Leads to Insulin Resistance Syndrome
AU - Ruzzin, Jérôme
AU - Petersen, Rasmus
AU - Meugnier, Emmanuelle
AU - Madsen, Lise
AU - Lock, Erik-Jan
AU - Lillefosse, Haldis
AU - Ma, Tao
AU - Pesenti, Sandra
AU - Sonne, Si Brask
AU - Marstrand, Troels Torben
AU - Malde, Marian Kjellevod
AU - Du, Zhen-Yu
AU - Chavey, Carine
AU - Fajas, Lluis
AU - Lundebye, Anne-Katrine
AU - Brand, Christian Lehn
AU - Vidal, Hubert
AU - Kristiansen, Karsten
AU - Frøyland, Livar
N1 - Keywords: contaminants, farmed salmon, metabolic syndrome, nonalcoholic fatty liver, obesity, pollution, public health, type 2 diabetes
PY - 2010
Y1 - 2010
N2 - BACKGROUND: The incidence of the insulin resistance syndrome has increased at analarming rate worldwide creating a serious challenge to public health care in the 21stcentury. Recently, epidemiological studies have associated the prevalence of type 2diabetes with elevated body burdens of persistent organic pollutants (POPs). However,experimental evidence demonstrating a causal link between POPs and the developmentof insulin resistance is lacking.OBJECTIVE: We investigated whether exposure to POPs contributes to insulinresistance and metabolic disorders.METHODS: Wistar rats were exposed for 28 days to lipophilic POPs through theconsumption of high-fat diet containing either refined or crude fish oil obtained fromfarmed Atlantic salmon. Furthermore, differentiated adipocytes were exposed to severalPOP mixtures that mimicked the relative abundance of organic pollutants present incrude salmon oil. We measured body weight, whole-body insulin sensitivity, POPaccumulation, lipid and glucose homeostasis, gene expression and performedmicroarray analysis.RESULTS: Adult male rats exposed to crude, but not refined, salmon oil developedinsulin resistance, abdominal obesity and hepatosteatosis. The contribution of POPs toinsulin resistance was confirmed in cultured adipocytes where POPs, especiallyorganochlorine pesticides, led to robust inhibition of insulin action. Moreover, POPsinduced down-regulation of insulin-induced gene-1 (Insig-1) and Lpin1 genes, twomaster regulators of lipid homeostasis.CONCLUSION: Our findings, for the first time, provide evidence that exposure toPOPs commonly present in food chains leads to insulin resistance and associatedmetabolic disorders.
AB - BACKGROUND: The incidence of the insulin resistance syndrome has increased at analarming rate worldwide creating a serious challenge to public health care in the 21stcentury. Recently, epidemiological studies have associated the prevalence of type 2diabetes with elevated body burdens of persistent organic pollutants (POPs). However,experimental evidence demonstrating a causal link between POPs and the developmentof insulin resistance is lacking.OBJECTIVE: We investigated whether exposure to POPs contributes to insulinresistance and metabolic disorders.METHODS: Wistar rats were exposed for 28 days to lipophilic POPs through theconsumption of high-fat diet containing either refined or crude fish oil obtained fromfarmed Atlantic salmon. Furthermore, differentiated adipocytes were exposed to severalPOP mixtures that mimicked the relative abundance of organic pollutants present incrude salmon oil. We measured body weight, whole-body insulin sensitivity, POPaccumulation, lipid and glucose homeostasis, gene expression and performedmicroarray analysis.RESULTS: Adult male rats exposed to crude, but not refined, salmon oil developedinsulin resistance, abdominal obesity and hepatosteatosis. The contribution of POPs toinsulin resistance was confirmed in cultured adipocytes where POPs, especiallyorganochlorine pesticides, led to robust inhibition of insulin action. Moreover, POPsinduced down-regulation of insulin-induced gene-1 (Insig-1) and Lpin1 genes, twomaster regulators of lipid homeostasis.CONCLUSION: Our findings, for the first time, provide evidence that exposure toPOPs commonly present in food chains leads to insulin resistance and associatedmetabolic disorders.
U2 - 10.1289/ehp.0901321
DO - 10.1289/ehp.0901321
M3 - Journal article
C2 - 20064776
VL - 118
SP - 465
EP - 471
JO - Environmental Health Perspectives
JF - Environmental Health Perspectives
SN - 0091-6765
IS - 4
ER -
ID: 17581399