Diet-induced thermogenesis in patients with liver cirrhosis

Summary. Diet-induced thermogenesis after ingestion of a mixed meal was investigated in eight patients with documented liver cirrhosis and in eight age- and sex-matched healthy controls. Respiratory gas exchange was measured continuously for one hour in the basal state and for three hours after ingestion of a mixed liquid meal, consisting of 17% kJ protein, 28% kJ lipids and 55% kJ carbohydrates and dispensed to correspond to 60% of the individually computed energy expenditure. Arterial substrate and hormone concentrations were determined before and at timed intervals for three hours after the meal. Urine was collected for determination of nitrogen excretion. The patients' oxygen uptake, energy expenditure and respiratory quotient were similar to those of the controls in the basal state. After the meal, pulmonary oxygen uptake and energy expenditure rose markedly in both groups during the first hour and were subsequently stable. The average increase in oxygen uptake above basal during the whole study period was 21·2 ± 1·8% and 22·3 ± 1·2% (NS) in patients and controls, respectively. The corresponding increase in energy expenditure was 24·8 ± 2·0% in the patients and 24·9 ± 1·4% in the controls (NS). The respiratory quotient was elevated throughout the postprandial period in both groups but the quotient was significantly higher in the patients (P<0·05–0·001), suggesting a greater proportion of carbohydrate oxidation. The basal arterial concentrations of insulin and glucagon were significantly higher in the patients. After the meal the insulin level increased 10- to 20–fold in both groups. Glucose concentration rose significantly in both groups to a maximum of 8·82 ± 1·00 and 8·03 ± 0·95 mmol/l in patients and controls, respectively, at 60 min after the meal. This was accompanied by a fall in the levels of glycerol and ketone bodies in both groups, indicating decreased lipolysis. It is concluded that both the basal energy expenditure and the thermogenic response to a mixed meal are similar in patients with liver cirrhosis and in healthy controls. The patients' carbohydrate oxidation rose to a greater extent after the meal, probably as a consequence of excessive increases in insulin concentration, demonstrating that insulin resistance in these patients may be compensated for by postprandial hyperinsulinaemia.