Association of Dioxin and Other Persistent Organic Pollutants (POPs) with Diabetes: Epidemiological Evidence and New Mechanisms of Beta Cell Dysfunction

Abstract

The worldwide explosion of the rates of diabetes and other metabolic diseases in the last few decades cannot be fully explained only by changes in the prevalence of classical lifestyle-related risk factors, such as physical inactivity and poor diet. For this reason, it has been recently proposed that other “nontraditional” risk factors could contribute to the diabetes epidemics. In particular, an increasing number of reports indicate that chronic exposure to and accumulation of a low concentration of environmental pollutants (especially the so-called persistent organic pollutants (POPs)) within the body might be associated with diabetogenesis. In this review, the epidemiological evidence suggesting a relationship between dioxin and other POPs exposure and diabetes incidence will be summarized, and some recent developments on the possible underlying mechanisms, with particular reference to dioxin, will be presented and discussed.

Two persistent organic pollutants which act through different xenosensors (alpha-endosulfan and 2,3,7,8 tetrachlorodibenzo-p-dioxin) interact in a mixture and downregulate multiple genes involved in human hepatocyte lipid and glucose metabolism

“…Further, it is not clear whether toxicant-associated steatohepatitis develops in humans exposed to TCDD [104] and although there appears to be an association between dioxin and type 2 diabetes a causal link is not necessarily implied [5,10,105,106]. Continued investigation in a variety of model systems clearly seems warranted to further elucidate the mechanisms of action of these pollutants in humans.…”

Persistent organic pollutants and biomarkers of diabetes risk in a cohort of Great Lakes sport caught fish consumers

“…Possible biologic pathways through which POPs could affect diabetes incidence have been hypothesized, including insulin resistance (Kern et al 2004), pancreatic beta cell destruction (De Tata 2014), mitochondrial dysfunction (Lee 2011), alterations in steroid metabolism (Persky et al 2011;Persky et al 2012), antagonism of PPARγ expression (Remillard and Bunce 2002), and induction of low grade chronic inflammation (Fujiyoshi et al 2006), oxidative stress (Lee et al 2008), and autoimmunity (Langer et al 2002). This study explored some of these potential pathways using biomarkers of diabetes risk.…”

The Prevention and Treatment of Type 2 Diabetes Mellitus with a Plant-Based Diet

“…Research strongly implicates Beta-cell mitochondrial dysfunction in the pathogenies of type 2 diabetes [105,106]. Research shows an association between POPs and mitochondrial dysfunction in the Beta cells [104][105][106][107]. One study showed a strong association, with a dose-response relationship with organochlorine POPs and diabetic peripheral neuropathy.…”

“…Adipose tissue is a common site of POPs accumulation where they can induce adverse effects on human health [104]. Research strongly implicates Beta-cell mitochondrial dysfunction in the pathogenies of type 2 diabetes [105,106].…”