Hypothetical model. Bmal1 loss leads to chronic activation of Akt, under both basal states, as well as in response to insulin. Chronic Akt activation is associated with mTOR activation, and concomitant attenuation of autophagy and augmentation of protein synthesis. Bmal1 loss, also leads to decreased I-1 levels, which is anticipated to activate PP1; PP1 decreases phosphorylation of AS160 and GSK3β, leading to a concomitant decrease and increase in activity, respectively. Consistent with decreased AS160 and GSK3β phosphorylation, Bmal1 loss leads to diminished glucose utilization. Directionality of arrows indicate activity status of protein/process. Thickness of line signifies magnitude of relationship.