Guinea pigs as models for investigating non-alcoholic fatty liver disease

Hepatic steatosis is the abnormal retention of lipids in hepatocytes, which can lead to progressive inflammation and fibrosis. Several dietary strategies including the use of low carbohydrate diets have been proposed to ameliorate the metabolic dysregulations caused by hepatic steatosis. Animal models are useful to study diet effects on hepatic lipid accumulation, inflammation and oxidative stress. Guinea pigs are an excellent animal model to study diet effects on cholesterol and lipoprotein metabolism, inflammation and atherosclerosis. The use of guinea pigs as models for hepatic steatosis has not been thoroughly discussed. The purpose of this review is to discuss the metabolic abnormalities that lead to the development of hepatic steatosis, to review some dietary treatments that can reverse these abnormalities and finally to propose the guinea pig as an animal model to study the metabolic pathways, signaling and genetic mechanisms associated with hepatic steatosis and non-alcoholic fatty liver disease. Abbreviations: 4-HNE: 4-Hidroxy-2-nonenal; ALT: Alanine Aminotransferase; ATP: Adenosine Triphosphate; ER: Endoplasmic Reticulum; HDL-C: HDL-cholesterol; LDL-C: LDL-cholesterol; MAD: Malonaldehyde; NAD: Nicotinamide Dinucleotide; NAFLD: Nonalcoholic Fatty Liver Disease; NASH: Non-alcoholic Steatohepatis; PEPCK: Phosphoenol Pyruvate Carboxylase; PPAR-α: Peroxisome proliferator Activated Receptor-α; PUFA: Polyunsaturated Fatty Acids; ROS: reactive oxygen species; SFA: Saturated Fatty Acids; TC: Total Cholesterol; TG: Triglycerides; VLDL: Very Low Density Lipoprotein