Altered interorgan response to feeding in patients with chronic obstructive pulmonary disease |
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Authors: | Engelen Mariëlle P K J Rutten Erica P A De Castro Carmen L N Wouters Emiel F M Schols Annemie M W J Deutz Nicolaas E P |
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Affiliation: | Department of Respiratory Medicine and Surgery, Maastricht University, Maastricht, Netherlands. mpkj.engelen@ah.unimaas.nl |
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Abstract: | BACKGROUND: Previously, we reported increased values for whole-body protein turnover in patients with chronic obstructive pulmonary disease (COPD) in the postabsorptive state. OBJECTIVE: The objective was to investigate whether intake of a carbohydrate-protein meal influences whole-body protein turnover differently in COPD patients and control subjects. DESIGN: Eight normal-weight patients with moderate COPD and 8 healthy control subjects were examined in the postabsorptive state and after 2 h of repeatedly ingesting a maltodextrin casein-based protein meal (0.02 g x kg body wt(-1) x 20 min(-1)). Combined simultaneous, continuous, intravenous infusion of L-[ring-2H5]-phenylalanine and L-[ring-2H2]-tyrosine tracer and oral repeated ingestion of 1-13C-phenylalanine were performed to measure whole-body protein synthesis (WbPS) and first-pass splanchnic extraction of phenylalanine. Endogenous rate of appearance of phenylalanine as the measure of whole-body protein breakdown (WbPB) and netWbPS was calculated as WbPS--WbPB. Arterialized venous blood was sampled for amino acid enrichment and concentration analyses. RESULTS: Feeding induced an increase in WbPS and a reduction in WbPB. The reduction in WbPB was larger in the COPD group than in the control group (P < 0.05) and was related to the lower splanchnic extraction of phenylalanine in the patients. Consequently, netWbPS increased more after feeding in the COPD group than in the control group (P < 0.05). CONCLUSION: Feeding induces more protein anabolism in normal-weight patients with moderate COPD than in healthy control subjects. This is probably because these COPD patients are characterized by an adaptive interorgan response to feeding to prevent or delay weight loss at this disease stage. |
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