Study Finds Exposure to Chemical Pollutants Increases Fat
Rats exposed to high levels of chemical pollutants in fish oil could
not regulate fat properly

Links to original paper:

http://ehp03.niehs.nih.gov/article/f...89/ehp.0901321
or
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854721/

"In this study, we demonstrate for the first time a causal
relationship between POPs and insulin resistance in rats. In vivo,
chronic exposure to low doses of POPs commonly found in food chains
induced severe impairment of whole-body insulin action and contributed
to the development of abdominal obesity and hepatosteatosis. Treatment
in vitro of differentiated adipocytes with nanomolar concentrations of
POP mixtures mimicking those found in crude 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 metabolic
diseases such as type 2 diabetes, obesity, and nonalcoholic 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 high-energy 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 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 underestimation 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
heterogeneous toxic and biological effects through the binding of the
aryl hydrocarbon receptor. Interestingly, we found that cultured
adipocytes 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 mono-ortho-
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."