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Research Article Free access | 10.1172/JCI114854

Whole-body lipolysis and triglyceride-fatty acid cycling in cachectic patients with esophageal cancer.

S Klein and R R Wolfe

Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.

Find articles by Klein, S. in: PubMed | Google Scholar

Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.

Find articles by Wolfe, R. in: PubMed | Google Scholar

Published November 1, 1990 - More info

Published in Volume 86, Issue 5 on November 1, 1990
J Clin Invest. 1990;86(5):1403–1408. https://doi.org/10.1172/JCI114854.
© 1990 The American Society for Clinical Investigation
Published November 1, 1990 - Version history
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Abstract

Whole-body lipolytic rates and the rate of triglyceride-fatty acid cycling (reesterification of fatty acids released during lipolysis) were measured with stable isotopic tracers in the basal state and during beta-adrenergic blockade with propranolol infusion in five cachectic patients with squamous cell carcinoma of the esophagus, five cachectic cancer-free, nutritionally-matched control patients, and 10 healthy volunteers. Resting energy expenditure and plasma catecholamines were normal in all three groups. The basal rate of glycerol appearance in blood in the patients with cancer (2.96 +/- 0.45 mumol.kg-1.min-1) was similar to that in the nutritionally matched controls (3.07 +/- 0.28 mumol.kg-1.min-1), but 48% greater than in the normal-weight volunteers (2.00 +/- 0.16 mumol.kg-1.min-1) (P = 0.028). The antilipolytic effect of propranolol and the rate of triglyceride-fatty acid cycling in the patients with cancer were also similar in the cachectic control group and approximately 50% greater than in the normal-weight volunteers, but the differences were not statistically significant because of the variability in the data. We conclude that the increase in lipolysis and triglyceride-fatty acid cycling in "unstressed" cachectic patients with esophageal cancer is due to alterations in their nutritional status rather than the presence of tumor itself. Increased beta-adrenergic activity may be an important contributor to the stimulation of lipolysis.

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