Diet and liver apoptosis in rats: a particular metabolic pathway

Various studies have indicated an association between modifi cation in dietary macronutrient composition and liver apoptosis.

To explain how changes in metabolic pathways associated with a high-protein, high-fat, and low-carbohydrate diet causes liver apoptosis.

Two groups of rats were compared. An experimental diet group (n = 8) using a high-protein (59.46%), high-fat (31.77%), and low-carbohydrate (8.77%) diet versus a control one (n = 9) with American Institute of Nutrition (AIN)-93-M diet. Animals were sacrificed after eight weeks, the adipose tissue weighed, the liver removed for flow cytometry analysis, and blood collected to measure glucose, insulin, glucagon, IL-6, TNF, triglycerides, malondialdehyde, and β-hydroxybutyrate. Statistical analysis was carried out using the unpaired and parametric Student's t-test and Pearson's correlation coeffi ents. Significance was set at p < 0.05.

Animals from the experimental group presented less adipose tissue than dose of the control group. Percentage of nonviable hepatocytes in the experimental group was 2.18 times larger than the control group (p = 0.001). No statistically significant differences were found in capillary glucose, insulin, glucagon, IL-6, or TNF-α between two groups. Plasmatic β-hydroxybutyrate and malondialdehyde of the experimental group expressed higher levels and triglycerides lower levels compared with the control group. The results show a positive and significant correlation between the percentage of nonviable hepatocytes and malondialdehyde levels (p = 0.0217) and a statistically significant negative correlation with triglycerides levels (p = 0.006).

Results suggest that plasmatic malondialdehyde and triglyceride levels are probably good predictors of liver damage associated with an experimental low-carbohydrate diet in rats.