Eicosapentaenoic acid ethyl ester supplementation in cachectic cancer patients and healthy subjects: effects on lipolysis and lipid oxidation

S.D. van Zuijdgeest Leeuwen, P.C. Dagnelie*, J.D.L. Wattimena, J.W.O. van den Berg, A. van der Gaast, G.R. Swart, J.H.P. Wilson

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Background & aims: Recent reports suggest that weight loss in cachectic cancer patients may be inhibited by supplementation of the n-3 fatty acid eicosapentaenoic acid (20.5n-3, EPA), presumably due to inhibition of lipolysis. The aim of the present double-blind, randomized trial was to assess whether short-term oral EPA ethyl ester (EE) supplementation inhibits lipolysis and lipid oxidation in weight-losing cancer patients and in healthy subjects. Methods: Seventeen weight losing, cancer patients of different tumor types, and 16 healthy subjects were randomized to receive EPA-EE (6 g/d) or placebo (oleic acid (OA)-EE; 6 g/d) for seven days. At baseline (day 0) and during supplementation (days 2 and 7) whole-body lipolysis and palmitic acid release were measured in the overnight fasting state using [1, 1, 2, 3, 3-H-2(5)] glycerol and [1-C-13] palmitic acid. Palmitate oxidation was determined by measuring (CO2)-C-13 enrichment in expired breath. Results: No significant effects of EPA-EE on whole-body lipolysis, palmitic acid release, or palmitate oxidation were detected in cancer patients nor in healthy subjects in comparison with OA-EE. EPA-EE supplementation reduced plasma-free fatty acid and triacylglycerol concentrations significantly in healthy subjects bur not in cancer patients. Conclusion: We conclude that supplementation of EPA-EE does not significantly inhibit lipolysis or lipid oxidation in weight-losing cancer patients or in healthy subjects during short-term supplementation when using OA-EE as a placebo supplement.
Original languageEnglish
Pages (from-to)417-423
Number of pages7
JournalClinical Nutrition
Volume19
DOIs
Publication statusPublished - 1 Jan 2000

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