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Am J Physiol Endocrinol Metab 282: E304-E311, 2002; doi:10.1152/ajpendo.00333.2001
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Vol. 282, Issue 2, E304-E311, February 2002

Impairment of albumin and whole body postprandial protein synthesis in compensated liver cirrhosis

P. Tessari1,3, R. Barazzoni1, E. Kiwanuka1, G. Davanzo1, G. De Pergola3, R. Orlando2, M. Vettore1, and M. Zanetti1

1 Department of Clinical and Experimental Medicine, Chair of Metabolism, and 2 Department of Internal Medicine, University of Padova, 35128 Padua; and 3 Department of Internal Medicine and Endocrinology, University of Bari, 70124 Bari, Italy

To investigate the anabolic effects of feeding in cirrhosis, we measured albumin fractional synthesis rate (FSR) and whole body protein synthesis in six nondiabetic patients with stable liver cirrhosis (three in the Child-Pugh classification Class A, three in Class B) and in seven normal control subjects, before and after administration of a 4-h mixed meal. Leucine tracer precursor-product relationships and whole body kinetics were employed at steady state. Basal levels of postabsorptive albumin concentration and FSR, whole body leucine rate of appearance, oxidation, and nonoxidative leucine disposal (NOLD, approx protein synthesis) were similar in the two groups. However, after the meal, in the patients neither albumin FSR (from 8.5 ± 1.5 to 8.8 ± 1.8 %/day) nor NOLD (from 1.69 ± 0.22 to 1.55 ± 0.26 µmol · kg-1 · min-1) changed (P = nonsignificant vs. basal), whereas they increased in control subjects (albumin FSR: from 10.9 ± 1.5 to 15.9 ± 1.9 %/day, P < 0.002; NOLD: from 1.80 ± 0.14 to 2.10 ± 0.19 µmol · kg-1 · min-1, P = 0.032). Thus mixed meal ingestion did not stimulate either albumin FSR or whole body protein synthesis in compensated liver cirrhosis. The mechanism(s) maintaining normoalbuminemia at this disease stage need to be further investigated.

albumin synthesis; nonoxidative leucine disposal; meal ingestion; alpha -ketoisocaproate; specific activity; compensated cirrhosis


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