Chronic liver disease and transplantation — uncovering the role of the liver in ingestive behaviour

Abstract

The liver is an important metabolic sensor relaying humoral and neural signalling via the brain stem to the hypothalamus. The integration of this information in the higher centres ultimately controls the composition, duration and frequency of nutritional intake. In chronic liver disease, alterations in oxidative metabolism and impairment of the liver's metabolic role may affect changes in ingestive behaviour and nutritional status. In cirrhosis undernutrition is prevalent, whereas following transplantation rapid weight gain is observed. Liver transplant recipients lose all extrinsic hepatic innervation and the absence of humoral and neural responses relayed via hepatic afferents could affect energy homeostasis and contribute to weight gain. Recent in vivo work suggests that patients with hepatocellular cirrhosis have the greatest metabolic disturbances, poorest intakes and nutritional status when compared with patients with cholestatic cirrhosis. Stratification of patients by disease severity had no differential effect. Conversely following transplantation, patients' weights significantly exceed pre-illness values. Evidence suggests that these patients exhibit an energy economy and a shift to increased energy intake from fat. It may be postulated that the liver transplant procedure per se is implicated in development of obesity. The sensing of energy metabolism and food intake are likely to be different in liver cirrhosis and after transplantation. Changes in energy intake and body composition evident in liver cirrhosis and liver transplantation are consistent with its role as an energy sensor.