Obesity is associated with risk of cognitive dysfunction, neurodegenerative disorders and impaired neuroplasticity. We evaluated the effect of bariatric surgery (RYGB) on brain glucose utilization, cognitive function, visual neuroplasticity (VNP) and peripheral glucose metabolism. Thirteen non-diabetic obese subjects with no history of psychiatric illness, psychoactive drug use and major brain disorders were recruited. Subjects underwent a 75gr OGTT during a 60min FDG dynamic brain PET study, standardized neurocognitive tests and VNP by psychophysical technique at baseline and 6-months after RYGB. Plasma glucose, insulin, c-peptide, GLP-1, GIP, VIP, BDNF and leptin were measured during OGTT. After RYGB, BMI declined (p<0.001) and insulin sensitivity improved (p=0.006). Cerebral glucose metabolic rate (CMRg by voxel-wise paired analysis) declined in several brain regions (p=0.005). Token and Trail Making Test score change correlated with CMRg change in several areas of the brain (all p≤0.03). After RYGB, VNP increased (p=0.008) and correlated with CMRg change in orbitofrontal cortex (p=0.03) and hippocampus (p=0.03). CMRg of several cortical and subcortical areas correlated with HOMA-IR (p<0.001) but not with BMI. GLP-1/GIP levels increased (p<0.002) with no correlation with CMRg, VIP or BDNF levels. These results show that bariatric surgery modulates CMRg in brain areas involved in cognitive function and neuroplasticity.