Propranolol decreases splanchnic triacylglycerol storage in burn patients receiving a high-carbohydrate diet.
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.


BACKGROUND
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 micromol/kg/min, whereas the rates of oxidation and VLDL-TG secretion were only 0.12 +/- 0.11 and 0.003 +/- 0.02 micromol/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 micromol/kg/min without propranolol to 0.76 +/- 0.58 micromol/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.
Morio
Beatrice
B
University of Texas Medical Branch, Department of Surgery, Shriners Burns Hospital, Metabolism Unit, Galveston, Texas 77550, USA.
Irtun
Oivind
O
Herndon
David N
DN
Wolfe
Robert R
RR
D000293:Adolescent; D000319:Adrenergic beta-Antagonists / Q000378:metabolism / Q000494:pharmacology*; D000328:Adult; D002056:Burns / Q000150:complications / Q000178:diet therapy* / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D005234:Fatty Liver / Q000150:complications / Q000503:physiopathology / Q000517:prevention & control; D005260:Female; D006801:Humans; D008079:Lipoproteins, VLDL / Q000097:blood / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D019308:Palmitic Acid / Q000097:blood / Q000378:metabolism; D011433:Propranolol / Q000378:metabolism / Q000494:pharmacology*; D013152:Splanchnic Circulation / Q000187:drug effects*; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood / Q000378:metabolism*
D000319:Adrenergic beta-Antagonists; D004040:Dietary Carbohydrates; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride; D019308:Palmitic Acid; D011433:Propranolol