Low Dose Organochlorine Pesticides and Polychlorinated Biphenyls Predict Obesity, Dyslipidemia, and Insulin Resistance among People Free of Diabetes

Department of Preventative Medicine, School of Medicine, Kyungpook National University, Daegu, Korea.
PLoS ONE (Impact Factor: 3.23). 01/2011; 6(1):e15977. DOI: 10.1371/journal.pone.0015977
Source: PubMed


There is emerging evidence that background exposure to persistent organic pollutants (POPs) are important in the development of conditions predisposing to diabetes as well as of type 2 diabetes itself. We recently reported that low dose POPs predicted incident type 2 diabetes in a nested case-control study. The current study examined if low dose POPs predicted future adiposity, dyslipidemia, and insulin resistance among controls without diabetes in that study.
The 90 controls were diabetes-free during 20 years follow-up. They were a stratified random sample, enriched with overweight and obese persons. POPs measured in 1987-88 (year 2) sera included 8 organochlorine (OC) pesticides, 22 polychlorinated biphenyls (PCBs), and 1 polybrominated biphenyl (PBB). Body mass index (BMI), triglycerides, HDL-cholesterol, LDL-cholesterol, and homeostasis model assessment value for insulin resistance (HOMA-IR) were study outcomes at 2005-06 (year 20). The evolution of study outcomes during 18 years by categories of serum concentrations of POPs at year 2 was evaluated by adjusting for the baseline values of outcomes plus potential confounders. Parallel to prediction of type 2 diabetes, many statistically significant associations of POPs with dysmetabolic conditions appeared at low dose, forming inverted U-shaped dose-response relations. Among OC pesticides, p,p'-DDE most consistently predicted higher BMI, triglycerides, and HOMA-IR and lower HDL-cholesterol at year 20 after adjusting for baseline values. Oxychlordane, trans-nonachlor, and hexachlorobenzene also significantly predicted higher triglycerides. Persistent PCBs with ≥7 chlorides predicted higher BMI, triglycerides, and HOMA-IR and lower HDL-cholesterol at year 20 with similar dose-response curves.
Simultaneous exposure to various POPs in the general population may contribute to development of obesity, dyslipidemia, and insulin resistance, common precursors of type 2 diabetes and cardiovascular diseases. Although obesity is a primary cause of these metabolic abnormalities, POPs exposure may contribute to excess adiposity and other features of dysmetabolism.

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    • "Another theory suggests endocrine disruptors , including pesticides, mimic natural lipophilic hormones and mediate their effects through altering various nuclear receptor transcription factors by functioning as agonist ligands to create disturbances in the body's homeostatic hormonal controls that impact key adipogenic factors, fat depot size, and function (Grun and Blumberg 2006; Yoon et al. 2014). Human cross-sectional studies identified increased body weight with higher blood and/or tissue levels of endocrine disruptors, including pesticides (Brauner et al. 2012; Lee et al. 2011; Kanazawa et al. 2012; Elobeid et al. 2010; Raafat et al. 2012). One study compared current blood levels of organochlorine (OC) pesticides with change in weight from age 20 yr (self-reported) to time of enrollment (measured) and found the sum of the pesticide concentrations was significantly positively related to the estimated weight change (4.3 kg more weight gain in quintile 5 vs. quintile 1) (Lind et al. 2013). "
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    • "When DDT and DDE are stored in adipose tissue, other tissues are protected from their exposure and resulting toxicity ; however, these chronic exposures within adipose tissue raise the possibility of specific toxicity to adipose tissue [22]. Consistent with adipose as a target tissue of toxicity, DDT and DDE are reported to have disruptive effects on lipid homeostasis associated with obesity observed in rodents and humans [23] [24] [30] [34] [37] [41]. Because endocrine disruption has been implicated in these adverse metabolic effects of exposure to DDT and DDE [23] [34], it is possible that the mobilization of DDT and DDE from adipose tissue during weight loss could also contribute to DDT and DDE metabolic toxicity by targeting non-adipose tissues [2] [19] [21] [22] [31]. "
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