Abstract
Persistent organic pollutants (POPs) such as organochlorine (OC) pesticides, polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs) have become wide-spread environmental contaminants as a consequence of their extensive use, long-range transport, and persistence. Because POPs are highly resistant to metabolic degradation, humans bioaccumulate these lipophilic and hydrophobic pollutants in fatty tissues for many years. Previous studies have demonstrated that POPs including PCBs are involved in the development of diabetes mellitus (DM) type 2 and insulin resistance. Numerous epidemiological studies suggest an association between POP burden and DM type 2/metabolic syndrome. In addition, several experimental studies have provided additional evidence supporting the association between POP exposure and DM type 2 or insulin resistance. Epidemiological and experimental studies have provided compelling evidence indicating that exposure to POPs increases the risk of developing insulin resistance and metabolic disorders. However, the detailed molecular mechanism underlying POP-induced insulin resistance is yet to be elucidated. In this article, we review literature that has reported on the association between POP burden and insulin resistance and the mechanism underlying POP-induced insulin resistance, and discuss implications for public health.
Highlights
According to State of the Science of Endocrine Disrupting Chemicals—2012 published by the WHO in 2012 [1], chronic exposure of lower concentrations of Persistent organic pollutants (POPs) has been shown to lead to female reproductive dysfunction [11,12], testicular cancer [13,14], breast cancer [15], prostate cancer [16], decreased semen quality [17,18,19], increased cryptorchidism and hypospadias at birth [20,21], and cognitive and behavioral deficits caused by developmental exposure [22,23,24]
Experimental studies could offer a suitable target for interventions targeting polychlorinated biphenyls (PCBs)-induced insulin resistance
Numerous epidemiological studies have provided compelling evidence indicating that exposure to POPs increases the risk of developing insulin resistance and metabolic disorders
Summary
The awareness of POPs was the result of large-scale casualties caused by the exposure to high concentrations of POPs in the early 20th century. According to State of the Science of Endocrine Disrupting Chemicals—2012 published by the WHO in 2012 [1], chronic exposure of lower concentrations of POPs has been shown to lead to female reproductive dysfunction [11,12], testicular cancer [13,14], breast cancer [15], prostate cancer [16], decreased semen quality [17,18,19], increased cryptorchidism and hypospadias at birth [20,21], and cognitive and behavioral deficits caused by developmental exposure [22,23,24] These neurodevelopmental disorders have been linked to severe forms of thyroid hormone deficiencies, and the decrease of thyroid function has been associated with PCBs, PBDEs, phthalates, bisphenol A, and perfluorinated chemicals in some epidemiological studies [25]. Sufficient epidemiological and experimental evidence has shown that PCB exposure is associated with motor and cognitive deficits in humans and animal models [37]
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