Nutritional hepatic steatosis and mortality after burn injury in rats

AIMS: To investigate the effects of diet composition and starvation on hepatic steatosis and mortality after severe burn injury in rats. METHODS: Experiment 1: rats received either normal chow (55 cent of energy carbohydrates, 14 cent fat, 31 cent protein), a high-fat (40 cent carbohydrates, 40 cent fat, 20 cent protein), or a high-carbohydrate diet (81 cent carbohydrates, 4 cent fat, 15 cent 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 cent 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 cent carbohydrates, 4 cent fat, 15 cent protein) ad libitum for 6 days. RESULTS: 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 (R2=0.72; P < 0.05) to non-protein energy intake but not to total energy intake. Burn caused 33 cent mortality in the hepatic steatosis group and no deaths in the control group (P < 0.05). CONCLUSIONS: Diet composition and preceding 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.