Environmental pollution and diabetes: a neglected association

Department of Biochemistry, Hopkins Building, University of Cambridge, Cambridge CB2 1QW, UK.
The Lancet (Impact Factor: 45.22). 02/2008; 371(9609):287-8. DOI: 10.1016/S0140-6736(08)60147-6
Source: PubMed
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Available from: Oliver Andrzej Hodgson Jones, Feb 07, 2014
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    • "Indeed, there is growing evidence suggesting a connection between particulate air pollution and T2DM occurrence and progression [5] [6]. Regulated pollutants thought to have an effect on the risk of T2DM include among others, particulate matter pollutants of 2.5 mm in aerodynamic diameter (PM 2.5 ) or less, which are derived from fossil-fuel combustion by motor vehicles and stationary sources such as power plants [7] [8]. These micro particles are potential health hazardous molecules because of their small size, that confers them the capacity to enter the airways, leading to their deposition on the pulmonary alveolocapillary membrane and therefore increasing their likelihood to trigger a systemic inflammatory response [9]. "
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    ABSTRACT: Aim Whether exposure to relatively high levels of air pollution is associated with diabetes occurrence remains unclear. To assess and quantify the association between exposure to major air pollutants and risk of type 2 diabetes. Methods PubMed and EMBASE databases (through September 2013) were searched using a combination of terms related to exposure to gaseous (NO2 and NOx) or particulate matter pollutants (PM2.5, PM10 and PM10-2.5) and type 2 diabetes. Descriptive and quantitative information were extracted from selected studies. We used random-effects models meta-analysis to derive overall risk estimates per type of pollutant. Results We included ten studies (five cross-sectional and five prospective), assessing the effects of air pollutants on the occurrence of diabetes. In prospective investigations, the overall effect on diabetes occurrence was significant for both NO2 (adjusted hazard ratio [HR], 1.13; 95% confidence interval [95%CI], 1.01-1.22; p < 0.001; I2 = 36.4%, p-heterogeneity= 0.208) and PM2.5 (HR, 1.11; 95%CI, 1.03-1.20; p < 0.001; I2 = 0.0%, p-heterogeneity= 0.827). Odds ratios were reported by two cross-sectional studies which revealed similar associations between both NO2 and PM2.5 with type 2 diabetes. Across studies, risk estimates were generally adjusted for age, gender, body mass index and cigarette smoking. Conclusions Available evidence supports a prospective association of main air pollutants with an increased risk for type 2 diabetes. This finding may have implications for population-based strategies to reduce diabetes risk.
    Full-text · Article · Sep 2014 · Diabetes Research and Clinical Practice
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    • "However, an understanding of the reason behind tissue mitochondrial deficit is lacking [3] [4] [5]. Epidemiologic studies suggest that persistent organic pollutants (POPs) or synthetic endocrine-disrupting chemicals might play an important role in the diabetes pandemic [6] [7]. POPsinduced adipogenesis and obesity in experimental models posited environmental obesogen hypothesis: certain environmental pollutants induce weight gain. "
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    ABSTRACT: Serum concentrations of environmental pollutants have been positively correlated with diabetes and metabolic syndrome in epidemiologic studies. In turn, abnormal mitochondrial function has been associated with the diseases. The relationships between these variables, however, have not been studied. We developed novel cell-based aryl hydrocarbon receptor (AhR) agonist bioassay system without solvent extraction process and analyzed whether low-dose circulating AhR ligands in human serum are associated with parameters of metabolic syndrome and mitochondrial function. Serum AhR ligand activities were measured as serum 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalent (sTCDDeq) in pM using 10 μL human sera from 97 Korean participants (47 with glucose intolerance and 50 matched controls, average age of 46.6 ± 9.9 years, 53 male and 45 female). sTCDDeq were higher in participants with glucose intolerance than normal controls and were positively associated (P < 0.01) with obesity, blood pressure, serum triglyceride, and fasting glucose, but not with HDL-cholesterol. Body mass index was in a positive linear relationship with serum AhR ligands in healthy participants. When myoblast cells were incubated with human sera, ATP generating power of mitochondria became impaired in an AhR ligand concentration-dependent manner. Our results support that circulating AhR ligands may directly reduce mitochondrial function in tissues, leading to weight gain, glucose intolerance, and metabolic syndrome. Our rapid cell-based assay using minute volume of human serum may provide one of the best monitoring systems for circulating AhR ligands, good clinical biomarkers for the progress of disease and therapeutic efficacy. © 2013 BioFactors, 2013.
    Full-text · Article · Jul 2013 · BioFactors
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    • "Infections with adenovirus have been linked to insulin resistance and obesity (Atkinson 2007). Similarly, the increased load of organic pollutants such as polychlorinated biphenyl (Trasande et al., 2012), pesticides and herbicides, and heavy metals such as cadmium, arsenic, mercury, and lead (known water pollutants), increase the production of inflammatory cytokines and enhance insulin resistance, obesity, and development of T2D (Jones et al., 2008), and chronic renal failure. Gluten intolerance or celiac disease is another relatively common condition that triggers chronic systemic inflammation. "

    Full-text · Article · Jan 2013
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