B cell activation and differentiation are associated with marked changes in proliferative and effector functions. Each stage of B cell differentiation thus has unique metabolic demands. New studies have provided insight on how nutrient uptake and usage by B cells are regulated by B cell receptor signals, autophagy, mammalian target of rapamycin, and transcriptional control of transporters and rate-limiting enzymes. A recurring theme is that these pathways play distinct roles ranging from survival to antibody production, depending on the B cell fate. We review recently published data that define how these pathways control metabolic flux in B cells, with a particular emphasis on genetic and in vivo evidence. We further discuss how lessons from T cells can guide future directions.