Mary Turyk1, Giamila Fantuzzi2, Victoria Persky3, Sally Freels3, Anissa Lambertino3, Maria Pini4, Davina H Rhodes5, Henry A Anderson6. 1. University of Illinois at Chicago, Division of Epidemiology and Biostatistics, School of Public Health, 1603 W. Taylor Street, Chicago, IL 60612, United States. Electronic address: mturyk1@uic.edu. 2. University of Illinois at Chicago, Department of Kinesiology and Nutrition, College of Applied Health Sciences, 1919 W. Taylor Street, Chicago, IL 60612, United States. 3. University of Illinois at Chicago, Division of Epidemiology and Biostatistics, School of Public Health, 1603 W. Taylor Street, Chicago, IL 60612, United States. 4. University of Illinois at Chicago, Department of Kinesiology and Nutrition, College of Applied Health Sciences, 1919 W. Taylor Street, Chicago, IL 60612, United States; Université Pierre et Marie Curie-Paris6, Centre de Recherche des Cordeliers, UMRS 872, Paris F-75006, France; Institute of Cardiometabolism and Nutrition (ICAN), Pitié-Salpêtrière Hospital, Paris F-75013, France. 5. University of Illinois at Chicago, Department of Kinesiology and Nutrition, College of Applied Health Sciences, 1919 W. Taylor Street, Chicago, IL 60612, United States; Department of Human Nutrition, Kansas State University, Manhattan, KS 66506, United States. 6. Wisconsin Division of Public Health, 1 W. Wilson St., Room 150, Madison, WI 53702, United States.
Abstract
BACKGROUND: Exposure to persistent organic pollutants (POPs) is associated with increased diabetes risk, although the mechanism of action is not well delineated. METHODS: We investigated established diabetes biomarkers that could implicate potential mechanistic pathways, including C-reactive protein (CRP), a marker of systemic inflammation; gamma glutamyl transferase (GGT), a liver enzyme associated with oxidative stress; and adiponectin, an adipokine modulating glucose regulation and fatty acid oxidation. These biomarkers as well as hemoglobin A1c (HA1c), and POPs [polychlorinated biphenyls (PCBs), p,p-dichlorodiphenyldichloroethylene (DDE) and polybrominated diphenyl ethers (PBDEs)] were measured in a cohort of Great Lakes sport caught fish (GLSCF) consumers. We examined associations of POPs and fish consumption with HA1c and incident diabetes, and evaluated mediation and moderation by the diabetes biomarkers. RESULTS: Odds of incident diabetes were elevated with exposure to DDE and PCBs. DDE and PCB 118 were positively, and fish meals were inversely, associated with HA1c. CRP was inversely associated with saltwater and total fish meals, particularly in persons with higher adiposity, but did not mediate the associations of fish meals with HA1c. There were few associations of POPs with adiponectin, CRP and GGT, with the exception of positive associations of PCB 118 with GGT, PBDEs with GGT in older persons, and PBDEs with adiponectin. Adiponectin, CRP and GGT did not mediate associations of DDE and PCBs with HA1c or incident diabetes. However, the association of DDE with HA1c was stronger in persons with higher CRP, GGT and BMI, and lower adiponectin, while the association of PCB 118 with HA1c was stronger in persons with higher GGT. CONCLUSIONS: These findings suggest that adiponectin, CRP and GGT did not mediate effects of POPs on diabetes or HA1c. However, POPs may have stronger effects on blood glucose in persons at higher risk for diabetes.
BACKGROUND: Exposure to persistent organic pollutants (POPs) is associated with increased diabetes risk, although the mechanism of action is not well delineated. METHODS: We investigated established diabetes biomarkers that could implicate potential mechanistic pathways, including C-reactive protein (CRP), a marker of systemic inflammation; gamma glutamyl transferase (GGT), a liver enzyme associated with oxidative stress; and adiponectin, an adipokine modulating glucose regulation and fatty acid oxidation. These biomarkers as well as hemoglobin A1c (HA1c), and POPs [polychlorinated biphenyls (PCBs), p,p-dichlorodiphenyldichloroethylene (DDE) and polybrominated diphenyl ethers (PBDEs)] were measured in a cohort of Great Lakes sport caught fish (GLSCF) consumers. We examined associations of POPs and fish consumption with HA1c and incident diabetes, and evaluated mediation and moderation by the diabetes biomarkers. RESULTS: Odds of incident diabetes were elevated with exposure to DDE and PCBs. DDE and PCB 118 were positively, and fish meals were inversely, associated with HA1c. CRP was inversely associated with saltwater and total fish meals, particularly in persons with higher adiposity, but did not mediate the associations of fish meals with HA1c. There were few associations of POPs with adiponectin, CRP and GGT, with the exception of positive associations of PCB 118 with GGT, PBDEs with GGT in older persons, and PBDEs with adiponectin. Adiponectin, CRP and GGT did not mediate associations of DDE and PCBs with HA1c or incident diabetes. However, the association of DDE with HA1c was stronger in persons with higher CRP, GGT and BMI, and lower adiponectin, while the association of PCB 118 with HA1c was stronger in persons with higher GGT. CONCLUSIONS: These findings suggest that adiponectin, CRP and GGT did not mediate effects of POPs on diabetes or HA1c. However, POPs may have stronger effects on blood glucose in persons at higher risk for diabetes.
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