Literature DB >> 24963112

Exposure to persistent organic pollutants: relationship with abnormal glucose metabolism and visceral adiposity.

Eveline L Dirinck1, Alin C Dirtu2, Malarvannan Govindan2, Adrian Covaci2, Luc F Van Gaal3, Philippe G Jorens4.   

Abstract

OBJECTIVE: The contribution of persistent organic pollutants (POPs) to the pandemic of type 2 diabetes mellitus and obesity has been assumed but remains speculative. Our study aimed at investigating the relationship of POP levels with detailed markers of glucose metabolism and body composition. RESEARCH DESIGN AND METHODS: Glucose tolerance was determined in a group of normal-weight and obese individuals. Fat distribution was assessed with abdominal computed tomography (CT) scanning, determining subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). Selected POPs (28 polychlorinated biphenyls [PCBs] and the pesticide p,p'-dichlorodiphenyldichloroethylene [p,p'-DDE]) were measured in serum. In a subset of obese individuals undergoing bariatric surgery, POPs were also measured in adipose tissue.
RESULTS: Among obese participants, serum and adipose tissue levels of POPs were significantly correlated to glucose levels during an oral glucose tolerance test. Logistic regression using a model including age, age(2), sex, family history of diabetes, BMI, CT-VAT, smoking behavior, physical activity level score, and a POP level identified serum levels of PCB153, the sum of PCBs and p,p'-DDE as significant predictors of abnormal glucose tolerance (odds ratio 4.6, 4.8, and 3.4, respectively; P < 0.05). Adipose tissue levels of p,p'-DDE were also significant predictors (odds ratio 81.6; P < 0.05). Serum levels of PCBs were inversely related to BMI, while serum and adipose tissue levels of all POPs were positively related to the CT-VAT/SAT ratio, suggesting an important role for the visceral fat compartment in POP dynamics.
CONCLUSIONS: Our findings further sustain the theory that exposure to environmentally relevant levels of POPs may exert both a diabetogenic and obesogenic effect.
© 2014 by the American Diabetes Association.

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Year:  2014        PMID: 24963112     DOI: 10.2337/dc13-2329

Source DB:  PubMed          Journal:  Diabetes Care        ISSN: 0149-5992            Impact factor:   19.112


  19 in total

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8.  Co-morditities of environmental diseases: A common cause.

Authors:  Harold I Zeliger
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9.  Circulating persistent organic pollutants and body fat distribution: Evidence from NHANES 1999-2004.

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10.  Environmental exposure to BDE47 is associated with increased diabetes prevalence: Evidence from community-based case-control studies and an animal experiment.

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