Table 1.
Model | Diet comparison | Dose & duration | Fatty acid oxidation | Mechanism | Refs |
---|---|---|---|---|---|
| |||||
Humans | Fructose or Glucose, 75g | A single drink, 4h metabolic monitoring | -Higher RER | N/A | Tappy, 1986 [76] |
Humans | Fructose or Glucose in a drink containing fat | A single drink containing 0.75 g sugar/kg body weight and 0.5g/kg of oil | -Higher RER -Higher 13 CO2 from labeled fructose -lower BHB |
N/A | Chong, 2007 [77] |
Humans | Fructose drink in addition to regular diet vs. regular diet alone | 25% additional calories from fructose (3.5mg/kg dose) for 6 d | -Decreased lipid oxidation mg/kg/min and -BHB only in male subjects | N/A | Couchepin, 2008 [78] |
Humans | Fructose or Glucose-drinks on ad libitum diet | 25% of energy requirement on normal diet containing 30% fat for 10-wk | -Decreased postprandial fat oxidation and -increased carbohydrate oxidation | N/A | Cox, 2012 [40] |
Perfused Rat Liver | Fructose | 25 and 45 mg fructose/100 mL of blood | Decreased 14 C incorporation into CO2 and lower ketone bodies. | N/A | Topping 1972 [81] |
Rat Liver and serum | Fructose, Glucose, Glyceraldehyde, Sorbitol injection in fasted rats | 1 mL of 30% fructose, glucose, glyceraldehyde, or sorbitol were injected intramuscular | Decreased in ketone bodies | N/A | Rawat 1975 [79] |
Rat Liver | Fructose addition to mitochondria-supernatant system | 5.56 mM fructose treatment along with 14 C labeled palmitate | Decreased conversion of 14 Cpalmitate to 14 CO2 | N/A | Prager 1976 [80] |
Rat Liver Isolated rat hepatocytes | High fructose diet 67% carbohydrate (98%fructose) | −8 wk of high fructose diet -Isolated hepatocytes in 25mM fructose | Decreased expression of FAO genes | -Reduced PPARα protein and activity -Decreased CPT1α |
Nagai 2002 [87] |
Rat Liver | Fructose drink on chow diet | 10% fructose in water for 2 wk | Decreased β-oxidation activity nmol/min/mg | Decreased PPARα and target gene CPT1α | Roglans 2002 [91] |
Rat Liver | Fructose or glucose drink on normal diet | 10% fructose or glucose in water for 14 d | Decreased β-oxidation activity nmol/min/mg | Decreased PPARα and CPT1α protein & mRNA | Roglans 2007 [88] |
Rat Liver & human hepatocytes | Sucrose in rats/fructose in hepatocytes | 40% sucrose diet for 10 wk/ 5mM fructose in vitro |
Decreased BHB | AMPD2 mediated decrease in AMPK activity | Lanaspa 2012 [132] |
Rat Liver Rat hepatoma cells | Fructose drink on of regular diet | −10% fructose drink for 14 d; | Decreased β-oxidation activity | -Decreased PPARα and Sirt1 | Rebollo 2014 [93] |
Human hepatocytes | In vitro fructose, glucose and mannitol | −25 mM fructose for in vitro experiments | nmol/min/mg | -Increased acetylation of PGC1α | |
Rat Liver | Fructose supplementation of regular diet | 20% fructose solution for 14 wk | Decreased FAO gene expression | DNA methylation at PPARa and CPT1A promoter regions | Ohashi 2015 [90] |
Mouse liver and Hepatocytes | 30% Fructose or Glucose drinks on chow and HFD | In vitro 25 mM fructose vs. glucose for 24 hr | Decreased β-oxidation (OCR pmol/min) with 25 mM fructose | Acetylation of metabolic enzymes dependent on KHK | Softic 2019 [23] |
Mouse liver | 15% or 30% fructose in water on chow diet | Wild type and KHK A/C KO mice treated for 25 wk | Decreased BHB with fructose | KHK KO restored BHB | Ishimoto 2012 [28] |