Impaired Fat Oxidation and Reduced Resting Energy Expenditure after a Fat Load in Individuals with Liver Steatosis

To date, the factors involved in the progression from simple liver steatosis to liver fibrosis have not been clarified. The postprandial phase after a high fat meal is pro-inflammatory and chronic low-grade inflammation is associated with the development of non-alcoholic fatty liver disease. The purpose of this study was to evaluate the effect of an oral fat load on fat oxidation in individuals with vs. without liver steatosis. Twelve adults without liver steatosis and seventeen with liver steatosis underwent an oral tolerance tests with 190 grams of a fresh cream (343 kcal/100 g, calories from fats 84%). Respiratory quotient and resting energy expenditure were evaluated using indirect calorimetry at 0, 90 and 120 minutes after load ingestion. In the subjects without liver steatosis, the fat load induced a reduction in the respiratory quotient (basal value=0.88 ± 0.07 vs. 90 min value=0.85 ± 0.06, p=0.020; and basal value=0.88 ± 0.07 120 min value=0.84 ± 0.06, p=0.001) with no change in resting energy expenditure. The liver steatosis led to a delayed switch to fat oxidation after the fat load (90 min value 0.88 ± 0.07 vs. 120 min value = 0.85 ± 0.06; p=0.032) with a significant reduction of the resting energy expenditure after 120 min (p=0.011). An impaired fat oxidation, suggesting a reduced metabolic flexibility, and reduced resting energy expenditure is demonstrated after a fat load in individuals with liver steatosis. These mechanisms may be involved in the progression from liver steatosis to fibrosis.