Metabolic syndrome and the environmental pollutants from mitochondrial perspectives

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.

Gestational diabetes and offspring birth size at elevated environmental pollutant exposures

“…Exposure to certain POPs, such as DDE, PFOS and PFOA, has been previously proposed to alter the secretion and function of human sex steroids and thyroid hormones (Berg et al 2016; Ferguson et al 2012), induce inflammation, mitochondrial dysfunction and oxidative stress (Kim and Lee 2014; Myre and Imbeault 2014), promote adipogenesis through activation of the peroxisome proliferator activated receptor gamma (PPARγ) (Janesick and Blumberg 2016), and alter lipid peroxidation and pancreatic beta cell function (Al-Eryani et al 2015). Findings from experimental studies also support an interference of mercury exposure to lipid peroxidation and pancreatic beta cell function (Chen et al 2006 and 2010; Moreira et al 2012), though data on metabolic effects of mercury are sparse (Heindel et al 2016).…”

Cardio Metabolic Syndrome: A Global Epidemic

“…Simple measures such as reducing non-physical and sedentary activities; TV watching, video gaming or non-work related computer use to a limit of one hour per day, could potentially reduce the prevalence of CMS in the US adult population by 30-35% [70]. Sedentary living with low or no exercise leads to insulin resistance and secondary hyperinsulinemia, type II diabetes and the associated obesity, hypertension, hyperlipidemia and the ultimate common and undesired clinical outcome of atherosclerosis [105].…”

Effects of Environmental Exposures on Fetal and Childhood Growth Trajectories

“…Environmental stressors, such as PCFs exposure, may result in a ‘thrifty phenotype’ that stores excess calories too efficient. 53 …”