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Clinical Trial
. 1996 Jun;223(6):777-87; discussion 787-9.
doi: 10.1097/00000658-199606000-00016.

Beta-blockade lowers peripheral lipolysis in burn patients receiving growth hormone. Rate of hepatic very low density lipoprotein triglyceride secretion remains unchanged

Affiliations
Clinical Trial

Beta-blockade lowers peripheral lipolysis in burn patients receiving growth hormone. Rate of hepatic very low density lipoprotein triglyceride secretion remains unchanged

A Aarsland et al. Ann Surg. 1996 Jun.

Abstract

Objective: The purpose of this study was to determine the effect of propranolol on peripheral lipolysis in massively burned children during treatment with recombinant human growth hormone (rhGH), and to ascertain whether decreased free fatty acid availability for re-esterification would alter the hepatic rate of secretion of triglycerides (TGs) bound to very low density lipoproteins (VLDLs).

Background: Fatty liver occurs in severely burned patients, often resulting in a twofold increase in liver size. This could be the result of an imbalance between increased provision of free fatty acids from peripheral lipolysis, coupled with no increase in fat oxidation, and insufficient rate of secretion of TGs from the liver.

Methods: In a cross-over study, six burned children were treated with either rhGH or rhGH plus propranolol. On the sixth day of treatment, isotopic tracer infusions were conducted to determine the rate of release of free fatty acid (Ra FFA) from peripheral tissue and the rate of secretion of VLDL-bound TGs by the liver.

Results: Exogenous rhGH increased Ra FFA in children with large third-degree burns. Propranolol decreased Ra FFA, but the rate of secretion of fatty acids in the form of VLDL-TG from the liver was maintained. Plasma FFA, as opposed to fatty acids newly synthesized in the liver, were the primary precursors for hepatic triglyceride synthesis.

Conclusions: The administration of propranolol to burned children receiving rhGH is safe, has salutary cardiovascular effects, decreases the release of FFA from adipose tissue and increases the efficiency of the liver in secreting fatty acids as VLDL TGs.

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