BACKGROUND: Conflicting data are available concerning energy metabolism in liver disease. Changes should be most pronounced in acute hepatic failure in which loss of 85% of liver cell mass is reported. Metabolic rate could be decreased due to impairment in liver mass but may also be increased as a result of systemic-mediator actions. To clarify this issue we studied energy metabolism in acute hepatic failure. METHODS: Energy metabolism was evaluated by indirect calorimetry in 12 patients with acute liver failure and 22 sex-, age-, and body size-matched healthy individuals. In controls and 5 patients, studies were performed in the postabsorptive state; the remaining 7 patients received glucose at a rate of 8 mumol/kg body weight.min to prevent hypoglycemia. RESULTS: Resting energy expenditure was increased in acute liver failure compared with healthy controls (5.1 +/- 0.14 kJ.min-1 x 1.73 m-2 vs. 3.97 +/- 0.08 kJ.min-1 x 1.73 m-2; mean +/- SEM; P < 0.001). Respiratory quotient and oxidation rates for major fuels were not different between the total patient-group and controls. In patients without glucose supply, energy derived from fat was higher and from carbohydrate lower than in healthy controls and patients with glucose supply. CONCLUSIONS: Energy expenditure is increased in acute liver failure. Altered substrate oxidation can be normalized by glucose supply.
BACKGROUND: Conflicting data are available concerning energy metabolism in liver disease. Changes should be most pronounced in acute hepatic failure in which loss of 85% of liver cell mass is reported. Metabolic rate could be decreased due to impairment in liver mass but may also be increased as a result of systemic-mediator actions. To clarify this issue we studied energy metabolism in acute hepatic failure. METHODS: Energy metabolism was evaluated by indirect calorimetry in 12 patients with acute liver failure and 22 sex-, age-, and body size-matched healthy individuals. In controls and 5 patients, studies were performed in the postabsorptive state; the remaining 7 patients received glucose at a rate of 8 mumol/kg body weight.min to prevent hypoglycemia. RESULTS: Resting energy expenditure was increased in acute liver failure compared with healthy controls (5.1 +/- 0.14 kJ.min-1 x 1.73 m-2 vs. 3.97 +/- 0.08 kJ.min-1 x 1.73 m-2; mean +/- SEM; P < 0.001). Respiratory quotient and oxidation rates for major fuels were not different between the total patient-group and controls. In patients without glucose supply, energy derived from fat was higher and from carbohydrate lower than in healthy controls and patients with glucose supply. CONCLUSIONS: Energy expenditure is increased in acute liver failure. Altered substrate oxidation can be normalized by glucose supply.
Authors: Mathias Plauth; William Bernal; Srinivasan Dasarathy; Manuela Merli; Lindsay D Plank; Tatjana Schütz; Stephan C Bischoff Journal: Clin Nutr Date: 2019-01-16 Impact factor: 7.324
Authors: Valentin Fuhrmann; Nikolaus Kneidinger; Harald Herkner; Gottfried Heinz; Mariam Nikfardjam; Anja Bojic; Peter Schellongowski; Bernhard Angermayr; Reinhard Kitzberger; Joanna Warszawska; Ulrike Holzinger; Peter Schenk; Christian Madl Journal: Intensive Care Med Date: 2009-06-09 Impact factor: 17.440