The obesogenic effects of polyunsaturated fatty acids are dependent ...

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Ruzzin et al. salmon oil induced a significant inhibition of insulin-dependent glucose uptake. These data provide compelling evidence that exposure to POPs increases the risk of developing insulin resistance and metabolic disorders. Despite intense investigations and establishment of both preventive and therapeutic strategies, insulin resistance–associated meta bolic diseases such as type 2 diabetes, obesity, and non alcoholic fatty liver disease have reached alarming proportions worldwide (Angulo 2002; Ford et al. 2004; Zimmet et al. 2001). By 2015, the World Health Organization (WHO) estimates that > 1.5 billion people will be overweight and that 338 million people will die from chronic diseases such as diabetes and heart disease (WHO 2005). Although physical inactivity and regular intake of highenergy diets are recognized contributors (Hill and Peters 1998; Roberts and Barnard 2005), these lifestyle factors can only partially explain the explosive and uncontrolled global increase in metabolic diseases. Recently, the development of insulin resistance and inflammation was found to be exacerbated in humans and animals exposed to air pollution (Kelishadi et al. 2009; Sun et al. 2009). Furthermore, the widespread environmental contaminant bisphenol A was reported to impair pancreatic beta cells and trigger insulin resistance (Alonso- Magdalena et al. 2006). Our data, together with the finding that type 2 diabetics accumulate significant body burdens of POPs (Lee et al. 2006), provide additional evidence that global environmental pollution contributes to the epidemic of insulin resistance–associated metabolic diseases. Although rats chronically fed the HFC diet for 28 days were exposed to a relatively high intake of organic pollutants, the POPs Nuclear receptors (AhR, CAR, PXR, ) TLR5, ROCK2, CD14, and YWHAZ PGC1α Insig-1 Lpin1 SREBP1c FAS concentrations of PCDDs/PCDFs and indicator PCBs in adipose tissue of these animals did not exceed those observed in Northern Europeans 40–50 years of age (Kiviranta et al. 2005), thereby indicating that doses of POP exposure sufficient to induce detrimental health effects were not excessive. Whether the exposure to lower levels of POPs would induce similar detrimental effects as those observed in the present study remains to be investigated. Dietary interventions are current strategies to prevent or treat metabolic diseases, and nutritional guidelines are usually based on energy density and glycemic index of the diet; however, the levels of POPs present in food has received less attention. Given that POPs are ubiquitous in food chains (Fisher 1999), such under estimation may interfere with the expected beneficial effects of some dietary recommendations and lead to poor outcomes. For instance, the presence of POPs in food products may, to some extent, explain the conflicting results regarding the protective effects of n-3 polyunsaturated fatty acids against the incidence of myocardial infarction (Guallar et al. 1999; Rissanen et al. 2000). Overall, better understanding of the interactions between POPs and nutrients will help improve nutritional education of patients with insulin resistance syndrome. To protect consumer health, the presence of contaminants in food is internationally regulated. In the European Union legislation, certain POPs including dioxins and dioxin-like PCBs are regulated in foodstuffs (European Union 2006). Risk assessment of these organic pollutants is based on the ability of individual compounds to produce hetero geneous toxic and biological effects through the binding of the aryl hydrocarbon receptor. Interestingly, Chronic low-grade inflammation Mitochondrial function Fatty acid oxidation Lipogenesis Insulin resistance syndrome Figure 4. Schematic representation of the possible mechanisms behind the development of the insulin resistance syndrome induced by POP exposure. POPs may activate nuclear receptors including aryl hydrocarbon receptor (AhR), pregnane X receptor (PXR), constitutive androstane receptor (CAR), or yet unknown receptors. POP exposure may induce the regulation of genes involved in the inflammatory pathway, mitochondrial function, lipid oxidation, and lipogenesis, thereby contributing to the development of the insulin resistance syndrome. we found that cultured adipo cytes exposed to a PCDF or PCDD mixture have normal insulin action, even though the TEQ of these mixtures could be up to 3,500 times higher than the TEQ of the non-ortho-substituted and monoortho-substituted PCB mixtures that impaired insulin action. These findings demonstrate that risk assessment based on WHO TEQs assigned to dioxins and dioxin-like PCBs is unlikely to reflect the risk of insulin resistance and the possible development of metabolic disorders. Although the production of organochlorine pesticides has been restricted since the 1970s, the global production and use of pesticides are poorly controlled (Jorgenson 2001; Nweke and Sanders 2009), and the presence of these environmental chemicals in seafood still remains unregulated in European countries (European Union 2008). Of the POP mixtures tested in vitro, organochlorine pesticides were the most potent disruptors of insulin action. This powerful inhibitory effect of pesticides on insulin action likely explains the common finding emerging from several independent cross-sectional studies reporting an association between type 2 diabetes and the body burdens of p,p´-DDE, oxychlordane, or trans-nonachlor (Lee et al. 2006; Rignell- Hydbom et al. 2007; Turyk et al. 2009). Therefore, widespread pesticide exposure to humans appears to be of particular global concern in relation to public health. We draw two main conclusions from these observations. First, exposure to POPs present in the environment and food chains are capable of causing insulin resistance and impair both lipid and glucose metabolism, thus supporting the notion that these chemicals are potential contributors to the rise in prevalence of insulin resistance and associated disorders (Figure 4). Second, although beneficial, the presence of n-3 polyunsaturated fatty acids in crude salmon oil (in the HFC diet) could not counteract the deleterious metabolic effects induced by POP exposure. Altogether, our data provide novel insights regarding the ability of POPs to mediate insulin resistance– associated metabolic abnormalities and provide solid evidence reinforcing the importance of international agreements to limit the release of POPs to minimize public health risks. References Alonso-Magdalena P, Morimoto S, Ripoll C, Fuentes E, Nadal A. 2006. The estrogenic effect of bisphenol A disrupts pancreatic β-cell function in vivo and induces insulin resistance. Environ Health Perspect 114:106–112. Angulo P. 2002. Nonalcoholic fatty liver disease. N Engl J Med 346(16):1221–1231. Atlas E, Giam CS. 1981. Global transport of organic pollutants: ambient concentrations in the remote marine atmosphere. Science 211(4478):163–165. Begum N, Sandu OA, Ito M, Lohmann SM, Smolenski A. 2002. Active Rho kinase (ROK-α) associates with insulin receptor substrate-1 and inhibits insulin signaling in vascular smooth muscle cells. J Biol Chem 277(8):6214–6222. 470 v o l u m e 118 | number 4 | April 2010 • Environmental Health Perspectives
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The obesogenic effects of polyunsat
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Table of Contents Acknowledgement .
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Abstract in Danish Polyumættede n-
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Polyunsaturated fatty acids in the
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was more than 3 times higher in the
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gluconeogenesis and ureagenesis (Fi
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high dietary PUFAs, the modulation
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In a pair of population studies, an
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18. Massiera, F. et al. Arachidonic
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54. Xu, J. et al. Polyunsaturated f
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Annexes 1. Ma T, Liaset B, Hao Q, P
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Fish Oil, Sucrose and Obesity Obesi
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Fish Oil, Sucrose and Obesity Figur
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Fish Oil, Sucrose and Obesity Table
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Fish Oil, Sucrose and Obesity 6. Ma
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Carbohydrate source and insulin sec
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20 21 22 23 24 25 26 27 28 29 30 31
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68 69 70 71 72 73 74 75 76 77 78 79
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114 115 116 117 118 119 120 121 122
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208 209 210 211 212 213 214 215 216
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302 303 304 305 306 307 308 309 310
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350 351 FIGURE LEGENDS 352 353 354
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398 399 400 401 402 403 404 subunit
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446 447 448 449 450 451 gamma, coac
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484 485 486 TABLE 1. Macronutrient
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Energy (kJ/g) 17.16 25.12 25.12 25.
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561 562 563 564 565 566 567 568 569
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Page 74 and 75: Cyclooxygenases and UCP1 Although i
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Page 88 and 89: hydrolysate (SPH), would be protect
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