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Daily energy and substrate metabolism in patients with cirrhosis
Author(s) -
Greco Aldo V.,
Mingrone Geltrude,
Benedetti Giuseppe,
Capristo Esmeralda,
Tataranni Pietro A.,
Gasbarrini Giovanni
Publication year - 1998
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510270205
Subject(s) - energy metabolism , cirrhosis , substrate (aquarium) , medicine , metabolism , intensive care medicine , biology , ecology
Twenty‐four‐hour energy expenditure (EE) and substrate oxidation (respiratory chamber), and whole‐body glucose uptake and oxidation rates (euglycemic hyperinsulinemic clamp [EHC] and indirect calorimetry) were measured in 10 male patients with posthepatitis, Child B cirrhosis, and 8 healthy male controls matched for age, body size, and body composition. Twenty‐four‐hour EE was higher in cirrhotic patients than in controls (8,567 ± 764 vs. 6,825 ± 507 kJ/d; P < .001). Resting energy expenditure (REE) was also higher in cirrhotic patients than in controls (7,881 ± 1,125 vs. 5,868 ± 489 kJ/d; P < .01). Twenty‐four‐hour respiratory quotient (RQ) (trend) and fasting RQ (0.76 ± 0.05 vs. 0.82 ± 0.04; P < .05) were lower in cirrhotic patients than in controls, reflecting higher lipid oxidation rates in the former group. Whole‐body glucose uptake was markedly reduced in cirrhotic patients when compared with controls (22.4 ± 3.2 vs. 44.5 ± 7.6 mmol/kg/min; P < .001). Carbohydrate oxidation rates, computed during the last 40 minutes of the clamp, were 8.5 ± 1.1 mmol/kg/min in cirrhotic patients and 22.6 ± 6.1 mmol/kg/min in controls ( P < .001). Nonoxidative glucose disposal was 13.9 ± 2.5 mmol/kg/min in cirrhotic patients and 22.0 ± 5.5 mmol/kg/min in normal controls ( P < .01). In conclusion, our data indicate that patients with Child B cirrhosis who still maintain a nutritional status (i.e., body composition) comparable with healthy controls are characterized by a cluster of metabolic defects that include hypermetabolism, increased lipid utilization, and insulin resistance. This suggests that the above metabolic syndrome precedes and probably leads to malnutrition in the natural history of the liver disease. In fact, in spite of the absence of a significant difference in caloric intake between cirrhotic patients and normal controls, the elevated 24‐hour EE might allow for a relevant weight loss in cirrhotic patients, because, with time, the differences may be cumulative. However, whether this hypermetabolism can lead to a real weight loss remains to be evaluated in a longitudinal study.