Nutritional hepatic steatosis and mortality after burn injury in rats

• Published in: Clinical nutrition (Edinburgh, Scotland) Vol. 17; no. 6; pp. 293 - 299
• Main Authors: Mittendorfer, B., Jeschke, M.G., Wolf, S.E., Sidossis, L.S.
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01-12-1998; Elsevier
• Subjects: Alkaline Phosphatase - blood; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animal Nutritional Physiological Phenomena; Animals; Biological and medical sciences; burn; Burns - complications; Burns - mortality; carbohydrate; Dietary Carbohydrates - administration & dosage; Disease Models, Animal; Emergency and intensive care: burns; fat; Fatty Acids, Nonesterified - blood; Fatty Liver - etiology; Fatty Liver - mortality; Intensive care medicine; Liver - enzymology; Liver - pathology; liver, steatosis; Male; Medical sciences; Random Allocation; Rats; Rats, Wistar; Starvation - complications; Triglycerides - analysis; United States; North America; America; fat; burn; liver, steatosis; carbohydrate; Animal model; Starvation; Rat; Liver; Mortality; Rodentia; Hepatic disease; Triglyceride; Trauma; Steatosis; Burn; Vertebrata; Mammalia; Food intake; Animal; Digestive diseases; Qualitative analysis; Nutritional status; Comparative study
• ISSN: 0261-5614; 1532-1983
• DOI: 10.1016/S0261-5614(98)80322-1

Abstract
To investigate the effects of diet composition and starvation on hepatic steatosis and mortality after severe burn injury in rats.
Experiment 1: rats received either normal chow (55% of energy carbohydrates, 14% fat, 31% protein), a high-fat (40% carbohydrates, 40% fat, 20% protein), or a high-carbohydrate diet (81% carbohydrates, 4% fat, 15% protein) ad libitum for 6 days. Another three groups received these diets ad libitum for 6 days after 48 h starvation. Experiment 2: mortality after 60% total body surface area scald burn was determined in a control group of rats and a group with nutritionally induced hepatic steatosis. Hepatic steatosis was induced by feeding the rats a high-fat diet (40% carbohydrates, 4% fat, 15% protein) ad libitum for 6 days.
Without starvation, liver triglyceride content (mg/g liver) increased in response to the high-fat diet (25.6±6.9) compared to normal chow (9.4±3.8;
P < 0.05); the high-carbohydrate diet had no influence on liver triglyceride content (12.4±3.7). Refeeding after starvation resulted in elevated (
P < 0.05) liver triglyceride content in the high-fat (18.8±8.3) and the high-carbohydrate group (28.7±14.4 vs control 6.7±3.7). Liver triglyceride content correlated (R
2=0.72;
P < 0.05) to non-protein energy intake but not to total energy intake. Burn caused 33% mortality in the hepatic steatosis group and no deaths in the control group (
P < 0.05).
Diet composition and preceeding starvation independently manipulate hepatic fat content in rats. Hepatic steatosis increases mortality after burn injury. Thus, nutritional interventions to reduce hepatic fat accumulation may be beneficial.