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HOPPE, ANDREA A., AND GALE B. CAREY. Polybrominated diphenyl ethers as endocrine disruptors of adipocyte metabolism. Obesity. 2007;15:2942-2950. Objective: Obesity is thought to result from poor diet and insufficient exercise. An additional factor may be endocrine-disrupting environmental chemicals that contaminate the air, water, and food supply. We tested the hypothesis that a class of lipid-soluble flame retardant chemicals known to accumulate in adipose tissue, polybrominated diphenyl ethers (PBDEs), disrupts insulin and isoproterenol sensitivity of isolated rat adipocytes. Research Methods and Procedures: Six-week-old Sprague-Dawley rats were gavaged daily with 14 mg/kg body weight (BW) pentabrominated diphenyl ether (penta-BDE) in corn oil (n ϭ 24) or corn oil alone (n ϭ 24). At 2 and 4 weeks of treatment, epididymal fat pad adipocytes were isolated, and isoproterenol-stimulated lipolysis, insulin-stimulated glucose oxidation, and adipocyte size were measured. Results: There was no alteration in adipocyte metabolism after 2 weeks of in vivo penta-BDE treatment, but after 4 weeks of treatment, adipocytes averaged a 30% increase in isoproterenol-stimulated lipolysis and a 59% decrease in insulin-stimulated glucose oxidation, compared with control. There were no differences in average rat BW and adipocyte size between treated and control rats, but plasma total thyroxine level in 2-and 4-week treated rats was 30% of control. Discussion: Daily exposure of rats to 14 mg/kg BW penta-BDE for 4 weeks has no effect on animal or adipocyte size but significantly alters insulin and isoproterenol-stimulated metabolism of isolated adipocytes. These alterations, hallmark features of metabolic obesity, suggest the need for further research on the contribution of lipid-soluble, endocrine-disrupting environmental chemicals to the obesity epidemic.

Objective: The present study evaluated the restaurant and dining venues on and near post-secondary campuses varying in institution size. Design: The Nutrition Environment Measures Survey for Restaurants (NEMS-R) was modified to evaluate restaurants as fast food, sit down and fast casual; and campus dining venues as dining halls, student unions and snack bar/cafés. ANOVA with post hoc Tukey's B and T tests were used to distinguish differences between dining venues and associated institutions by size. Setting: The study was conducted at fifteen US post-secondary institutions, 2009-2011. Subjects: Data presented are from a sample of 175 restaurants and sixty-eight on-campus dining venues. Results: There were minimal differences in dining halls by institution size, although medium-sized institutions as compared with small-sized institutions offered significantly more healthful side dish/salad bar items. Dining halls scored significantly higher than student unions or snack bar/cafés on healthful entrées, side dish/salad bar and beverages offerings, but they also had the most barriers to healthful dietary habits (i.e. all-you-can-eat). No differences were found by restaurant type for NEMS-R scores for total restaurant dining environment or healthful entrées and barriers. Snack bars had more healthful side dishes (P 5 0?002) and fast-food restaurants had the highest level of facilitators (i.e. nutrition information; P 5 0?002). Conclusions: Based on this evaluation in fifteen institutions, the full campus dining environment provides limited support for healthy eating and obesity prevention. The quality of campus dining environments can be improved via healthful offerings, providing nutrition information and other supports to facilitate healthy eating and prevent unwanted weight gain.

Furniture flammability standards are typically met with chemical flame retardants (FRs). FRs can migrate out of products into dust and are linked to cancer, neurological impairment, and endocrine disruption. We collected 95 dust samples from dormitory common areas and student rooms on two U.S. college campuses adhering to two different furniture flammability standards: Technical Bulletin 117 (TB117) and Technical Bulletin 133 (TB133). Because TB133 requires furniture to withstand a much-more-demanding test flame than TB117, we hypothesized that spaces with TB133 furniture would have higher levels of FRs in dust. We found all 47 targeted FRs, including 12 polybrominated diphenyl ether (PBDE) congeners, 19 other brominated FRs, 11 phosphorus FRs (PFRs), 2 Dechlorane-Plus (DP) isomers, and 3 hexabromocyclododecane (HBCDD) isomers in the 95 dust samples. We measured the highest reported U.S. concentrations for a number of FRs, including BDE 209 (up to 990 000 ng/g), which may be used to meet the TB133 standard. We prioritized 16 FRs and analyzed levels in relation to flammability standard as well as presence and age of furniture and electronics. Adherence to TB133 was associated with higher concentrations of BDE 209, decabromodiphenylethane (DBDPE), DPs, and HBCDD compared to adherence to TB117 in univariate models (p < 0.05). Student dormitory rooms tended to have higher levels of some FRs compared to common rooms, likely a result of the density of furniture and electronics. As flammability standards are updated, it is critical to understand their impact on exposure and health risks.

Xenobiotics such as phenobarbital, 2,3,7,8-tetrachlorodibenzo-p-dioxin, and Aroclor 1254 significantly suppress the activity of a key gluconeogenic and glyceroneogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK), suggesting that xenobiotics disrupt hepatic glucose and fat metabolism. The effects of polybrominated diphenyl ethers (PBDE), a family of synthetic flame-retardant chemicals, on PEPCK activity is unknown. This study investigated the effect of DE-71, a commercial PBDE mixture, on PEPCK enzyme kinetics. Forty-eight 1-mo-old male Wistar rats were gavaged daily with either corn oil or corn oil containing 14 mg/kg DE-71 for 3, 14, or 28 d (n = 8/group). At each time point, fasting plasma glucose, insulin, and C-peptide were measured and hepatic PEPCK activity, lipid content, and three cytochrome P-450 enzymes (CYP1A, -2B, and -3A) were assayed. PBDE treatment for 28 d significantly decreased PEPCK Vmax ( μ mol/min/g liver weight) by 43% and increased liver lipid by 20%, compared to control. CYP1A, -2B, and -3A Vmax values were enhanced by 5-, 6-, and 39-fold, respectively, at both 14 and 28 d in treated rats compared to control. There was a significant inverse and temporal correlation between CYP3A and PEPCK Vmax for the treatment group. Fasting plasma glucose, insulin, and C-peptide levels were not markedly affected by treatment, but the glucose:insulin ratio was significantly higher in treated compared to control rats. Data suggest that in vivo PBDE treatment compromises liver glucose and lipid metabolism, and may influence whole-body insulin sensitivity.