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Background: The objective of this study was to evaluate changes in resting energy expenditure (REE), body composition and metabolic parameters, and to investigate predictors of the results in seriously obese patients after Roux-en-Y gastric bypass (RYGBP).Methods: 31 patients (BMI 44.4 ± 4.8 kg/m 2 ; 27 female, 4 male; 37.3 ± 11.1 y) were evaluated at baseline and 6 months after RYGBP. Weight, REE, waist circumference (WC), fat mass (FM) and fat-free mass (FFM), physical activity, food intake, fasting glucose (GLU), insulin (INS), HOMA-IR and lipid concentrations were measured. Results: At 6 months, percentage of weight loss (%WL) was 29.0 ± 4.4% and percentage of excess weight loss was (%EWL) 59.7 ± 12.3%. FM loss corresponded to 77.1 ± 12.2% of the weight loss. REE decreased from 33.4 ± 4.1 to 30.1±2.6 kcal/kg FFM (P<0.05). Significant decreases (P<0.001) were observed in GLU, INS, HOMA-IR, LDL-cholesterol and triglycerides. %EWL was correlated with baseline INS (r=0.44; P=0.014), baseline HOMA (r=0.43; P=0.017), change in %FM (r=0.67; P<0.001) and change in WC (r=0.5; P<0.01). Decrease in REE/FFM (%) was positively correlated with baseline REE/FFM% (r=0.51; P<0.005) and change in %FM (r=0.69; P<0.001). Initial REE/FFM, baseline energy balance and FM change explain 90% of REE/FFM decrease.Conclusion: RYGBP was an effective procedure to induce significant weight loss, fat mass loss and improvement in metabolic parameters in the short term. Metabolic adaptation was not related to FFM wasting but to a higher baseline REE. Fasting hyperinsulinemia was the best single predictor of weight loss after RYGBP.

Environmental factors, including pesticides, have been linked to autism and neurodegeneration risk using retrospective epidemiological studies. Here we sought to prospectively identify chemicals that share transcriptomic signatures with neurological disorders, by exposing mouse cortical neuron-enriched cultures to hundreds of chemicals commonly found in the environment and on food. We find that rotenone, a pesticide associated with Parkinson's disease risk, and certain fungicides, including pyraclostrobin, trifloxystrobin, famoxadone and fenamidone, produce transcriptional changes in vitro that are similar to those seen in brain samples from humans with autism, advanced age and neurodegeneration (Alzheimer's disease and Huntington's disease). These chemicals stimulate free radical production and disrupt microtubules in neurons, effects that can be reduced by pretreating with a microtubule stabilizer, an antioxidant, or with sulforaphane. Our study provides an approach to prospectively identify environmental chemicals that transcriptionally mimic autism and other brain disorders.

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