Table 1.

Overview of high fat/high carbohydrate consumption-induced characteristics of nonalcoholic fatty liver disease (NAFLD) in animal models.

Diet	Duration	Hepatic Steatosis	Hepatic Injury	Inflammation	Fibrosis	References
High fat (30–60% kcal)	1–30 weeks	Bioassay TG content ↑ Histological steatosis ↑	Serum ALT or AST ↑ Apoptotic markers ↑ Hepatocyte ballooning ↑ or none	Inflammatory markers ↑ No Histological inflammation	No change in fibrotic markers No histological fibrosis	[9,17,18,32,33]
	30–60 weeks	Bioassay TG content ↑ Histological steatosis ↑	Serum ALT or AST ↑ Apoptotic markers ↑ Hepatocyte ballooning ↑	Inflammatory markers ↑ Histological inflammation ↑ or none	Fibrotic markers ↑ Histological fibrosis ↑	[15,16,32]
High fructose (20–60% fructose)	Up to 25 weeks	Bioassay TG content ↑ Histological steatosis ↑	Serum ALT or AST ↑ Apoptotic markers ↑ Hepatocyte ballooning ↑	Inflammatory markers ↑ Histological inflammation ↑	No change in fibrotic markers No histological fibrosis	[7,10,13,14,33]
High fat, high fructose	12–25 weeks	Bioassay TG content ↑ Histological steatosis ↑	Serum ALT or AST ↑ Apoptotic markers ↑ Hepatocyte ballooning ↑	Inflammatory markers ↑ Histological inflammation ↑	Fibrotic markers ↑ Histological fibrosis ↑	[13,18,32,33,34,35]
High fat, high cholesterol (0.2–2% cholesterol)	12–42 weeks	Bioassay TG content ↑ Histological steatosis ↑	Serum ALT or AST ↑ Apoptotic markers ↑ Hepatocyte ballooning ↑	Inflammatory markers ↑ Histological inflammation ↑	Fibrotic markers ↑ Histological fibrosis ↑ or none	[19,20,21,22]
High fat, high fructose, high cholesterol	25–30 weeks	Bioassay TG content ↑ Histological steatosis ↑	Serum ALT or AST ↑ Apoptotic markers ↑ Hepatocyte ballooning ↑	Inflammatory markers ↑ Histological inflammation ↑	Fibrotic markers ↑ Histological fibrosis ↑	[13,32,34,36]

The data are based on studies in animal models. Histological changes are the pathological endpoint (more severe) phenotypes. Biomarkers alone (less severe) indicate the progression without the endpoint phenotypes. Hepatic steatosis is assessed by increased triglyceride (TG) content and histological steatosis. Hepatic injury is assessed by increased levels of liver enzymes alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST), apoptotic markers (increased mRNA or protein expression of caspase 3, B-cell lymphoma 2 (Bcl-2), and/or increased plasma level or clearing within ballooned cells of cytokeratin 18 (CK 18) fragment) and recognized histologically in the form of hepatocyte ballooning. Liver inflammation is assessed by inflammatory markers (increased mRNA or protein expression of tumour necrosis factor α (TNFα), interleukin 6 (IL-6) and/or inflammasome) and histologically by inflammatory cell infiltration; liver fibrosis is assessed by fibrotic markers (increased mRNA or protein expression of α-smooth muscle actin (α-SMA), transforming growth factor β (TGF-β) and/or collagen 1) and histologically by the presence of collagen fibres.