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

We used stable-isotope-labelled amino acids to measure the effects of alcoh olic liver disease (ALD) on whole-body protein turnover and small-intestina l mucosal protein synthesis. Groups comprising eight patients with ALD and eight healthy control subjects were studied. They received primed, continuo us intravenous infusions of L-[I-C-13]leucine after an overnight fast; afte r 4 h, duodenal biopsies were obtained via endoscopy. Protein synthesis was calculated from protein labelling relative to intracellular leucine enrich ment. 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 AL D patients (P < 0.003), despite the fact that the protein synthetic capacit y (mu g of RNA/mg of protein) was higher in ALD patients (160 +/- 14 compar ed with 137 +/- 6 mu g/mg; P < 0.003). The mucosal cell size (protein/DNA r atio) was lower in ALD patients (9.23 +/- 0.91 compared with 13 +/- 2.2 mu g/mg; P < 0.002). Although the mean rates of whole-body protein turnover we re not significantly different between the two groups (204 +/- 18 and 196 /- 44 mu mol 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; fur thermore, there was a direct relationship between the rate of whole-body pr otein tu mover and the severity of ALD. Thus there was an inverse relations hip 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.