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

S Klein, RR Wolfe - The Journal of clinical investigation, 1990 - Am Soc Clin Investig
The Journal of clinical investigation, 1990Am Soc Clin Investig
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 …
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.
The Journal of Clinical Investigation