Objective: To quantify the various components of splanchnic free fatty acid and very-low-density lipoprotein-triacylglycerol (VLDL-TAG) metabolism in order to gain insight into the mechanisms responsible for the development of fatty liver in severely burned patients, and to determine if decreasing free fatty acid availability by use of propranolol could potentially reduce hepatic fatty acid accumulation. Summary Background Data: Hepatic fat accumulation results from an imbalance between fatty acid uptake, oxidation, and release via VLDL-TAG. Fatty acid delivery is accelerated in burn patients because of stimulated lipolysis. Since propranolol decreases lipolysis, it should also decrease hepatic fatty acid uptake and thus TAG synthesis. Methods: Stable isotope-labeled tracers and regional catheterization enabled quantification of various parameters of lipid metabolism across the splanchnic bed in severely burned patients. The acute effects of propranolol treatment were studied in all patients, and in a subgroup of patients the chronic (3 weeks) effects of propranolol were assessed. Results: The rate of splanchnic uptake of palmitate was 1.68±1.3 μmol/kg/min, whereas the rates of oxidation and VLDL-TG secretion were only 0.12 ± 0.11 and 0.003 ± 0.02 μmol/kg/ min, respectively. Propranolol significantly reduced palmitate delivery, and thus palmitate uptake, without significantly affecting oxidation or VLDL-TAG secretion. Thus, palmitate storage was reduced from 1.53 ± 1.30 μmol/kg/min without propranolol to 0.76 ± 0.58 μmol/kg/min after propranolol. Conclusions: Hepatic fat storage in burn patients is due to low rates of both fatty acid oxidation and VLDL-TAG secretion. Propranolol can decrease hepatic fat storage by limiting fatty acid delivery.
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