Aim 1: To test the hypothesis that acute bromocriptine administration will 1a) increase homeostatic mechanisms of satiation (meal termination), and 1b) alter neural, behavioral and perceived hedonic drivers of eating behavior, both contributing to a decrease in palatable food intake in those at high risk for T2DM. We expect bromocriptine to modify endocrine-mediated satiation signaling via suppressed prolactin, augmented adiponectin, amylin, glucagon like peptide-1 (GLP1), and decrease postprandial plasma glucose and insulin. We expect that, it will contribute to decreased ad lib palatable food intake, as well as promote healthy blood sugar. We also expect that bromocriptine will increase BOLD response during palatable food intake in dopaminergic brain regions thought to encode reward, decrease food specific impulsivity, and increase perceptual hedonic food ratings. Aim 2: Test whether the DRD2 TaqIA A1 allele, which is associated with reduced dopamine-D2 receptor density and dopamine signaling, moderates the impact of bromocriptine on homeostatic and hedonic drivers of food intake. This will provide critical information whether individual genetic predisposition alters the effectiveness of this medication, and may provide a foundation for individualized T2DM treatment.