Abstract
The worldwide epidemic of diabetes and metabolic syndrome in the last few decades cannot be fully accounted for only by changes in the lifestyle factors, such as sedentary lifestyle and overeating. Besides genetic factors, there must be other causes to explain this rapid change. They could not be infectious in nature and induce insulin resistance as key biochemical abnormality. Mitochondrial dysfunction could be underlying mechanism behind the insulin resistance, thus metabolic syndrome. Then there have been increasing number of reports suggesting that chronic exposure to and accumulation of endocrine disrupting chemicals (EDCs), especially so-called the persistent organic pollutants (POPs) within the body might be associated with metabolic syndrome. Combining two concepts, we developed new “EDCs-induced mitochondrial dysfunction hypothesis of metabolic syndrome”. In this review we suggest that classifying those chemicals into 5 groups might be clinically useful considering their removal or avoidance; POPs, non-persistent organic pollutants, heavy metals, air pollutants and drugs. We will also discuss briefly how those insights could be applied to clinical medicine.
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Acknowledgments
This work was supported in part by MIC & IITA through the IT Leading R & D Support Project.
Conflict of interest statement
Disclosure: The authors do not have any financial relationship with organizations. Dr. HK Lee owns a part of patent (PCT/KR2011/006583) for the application of cell based arylhydrocarbon receptor ligands assay to the diagnosis of metabolic syndrome. The authors have full control of all primary data and that we agree to allow the journal to review our data if requested.
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Kim, J.T., Lee, H.K. Metabolic syndrome and the environmental pollutants from mitochondrial perspectives. Rev Endocr Metab Disord 15, 253–262 (2014). https://doi.org/10.1007/s11154-014-9297-5
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DOI: https://doi.org/10.1007/s11154-014-9297-5