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Influence of Whole Body Protein Turnover Rate on Resting Energy Expenditure in Patients with Cancer¹

Departments of Medical Oncology [K. C. H. F., J. A. P.], Surgery [D. T. H., J. D., H. J. G. B.], Clinical Biochemistry [A. S., D. S.], and Postgraduate Medical Education [K. C. C.], University of Glasgow, Glasgow, United Kingdom; and Department of Health Physics, Scottish Universities Research and Reactor Centre, East Kilbride [T. P.] United Kingdom

Whole body protein turnover and resting energy expenditure are measured simultaneously in weight stable and weight losing patients with lung (n = 22) or colorectal cancer (n = 38). These results were compared with those from weight stable and weight losing non-cancer controls (n = 22). Rates of whole body protein turnover were calculated from the plateau isotopic enrichment of urinary ammonia and urea following a primed, continuous, 24-h infusion of [¹⁵N]glycine. Resting energy expenditure was measured by indiret calorimetry.

All groups of cancer patients had significantly elevated rates of whole body protein turnover (P < 0.05) and synthesized, on average, 1.9 g/kg/day more protein compared with weight stable non-cancer controls. In contrast, the resting energy expenditure of cancer patients and controls was similar. Moreover, there was no correlation between individual rates of whole body protein turnover. Thus, although cancer patients had rates of whole body protein turnover which were 50–70% greater than controls, this did not result in a measurable increase in resting energy expenditure. The assumption that elevation of whole body protein turnover or resting energy expenditure causes weight loss in cancer patients must be an oversimplification.

An acute phase protein response was observed in the majority of cancer patients. Although the presence of such an inflammatory response did not correlate with the rate of whole body protein turnover, the role of inflammatory mediators in the pathogenesis of disturbed protein metabolism in cancer patients merits further investigation.

¹ This work was supported in part by a grant from the Cancer Research Campaign.

² To whom requests for reprints should be addressed, at Department of Medical Oncology, 1 Horselethill Road, Glasgow G12 9LX, United Kingdom.

Received 6/15/87. Revised 12/ 1/88. Accepted 1/26/88.

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