Profound metal-related changes in the supply of metabolites to t he liver and in the hepatic metabolism occur, and there is ample evidence that neural signals from hepatic metabolic sensors can affect eating. Hepatic afferent nerves presumably represent glucosensors which contribute to the control of eating by monitoring their own glucose utilization. Yet, the nature of the putative sensors that respond to the oxidation of other metabolites than glucose had not been identified. ATP and sodium pump activity may link hepatic oxidative metabolism and membrane potential, because hepatic phosphate-trapping by 2,5-anhydro-mannitol, and inhibition of sodium pump activity by ouabain is associated with a stimulation of eating. Hepatocyte membrane potential is also subject to changes in transmembranal potassium flow through volumetrically controlled membranal potassium channels. Yet it is unknown if and how hepatocytes are linked to afferent nerves. It is also unclear how the effects of glucagon and insulin fit into the hepatic metabolic control of eating. Glucagon appears to induce satiety through its actions in the liver, but the involved mechanism is still unclear. Recent studies suggest that insulin, which has mainly been explored as a centrally acting long-term satiety signal, has an immediate effect on meal size, but is presently unknown whether an hepatic action of insulin is involved.