Small-intestinal mucosal protein synthesis and whole-body protein turnover in alcoholic liver disease

We used stable-isotope-labelled amino acids to measure the effects of alcoholic liver disease (ALD) on whole-body protein turnover and small-intestinal mucosal protein synthesis. Groups comprising eight patients with ALD and eight healthy control subjects were studied. They received primed, continuous intravenous infusions of L-[1-¹³C]leucine after an overnight fast; after 4 h, duodenal biopsies were obtained via endoscopy. Protein synthesis was calculated from protein labelling relative to intracellular leucine enrichment. Rates of duodenal mucosal protein synthesis were 2.58±0.32%·h^-1 (mean±S.D.) in the normal subjects and 2.04±0.18%·h^-1 in the ALD patients (P< 0.003), despite the fact that the protein synthetic capacity (μg of RNA/mg of protein) was higher in ALD patients (160±14 compared with 137±6 μg/mg; P < 0.003). The mucosal cell size (protein/DNA ratio) was lower in ALD patients (9.23±0.91 compared with 13±2.2 μg/mg; P< 0.002). Although the mean rates of whole-body protein turnover were not significantly different between the two groups (204±18 and 196±44 μmol leucine·h^-1·kg^-1 for ALD and control subjects respectively), there was, in the ALD patients, an inverse relationship between the rate of small-intestinal mucosal protein synthesis and the severity of ALD; furthermore, there was a direct relationship between the rate of whole-body protein turnover and the severity of ALD. Thus there was an inverse relationship between the rate of small-intestinal mucosal protein synthesis and the rate of whole-body protein turnover in ALD patients, which was not seen in the normal subjects.