Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver

LG Sánchez-Lozada, W Mu, C Roncal… - European journal of …, 2010 - Springer
LG Sánchez-Lozada, W Mu, C Roncal, YY Sautin, M Abdelmalek, S Reungjui, MP Le…
European journal of nutrition, 2010Springer
Background There is evidence that disaccharide sucrose produce a greater increase in
serum fructose and triglycerides (TGs) than the effect produced by their equivalent
monosaccharides, suggesting that long-term exposure to sucrose or fructose+ glucose could
potentially result in different effects. Aim of the study We studied the chronic effects of a
combination of free fructose and glucose relative to sucrose on rat liver. Methods Rats were
fed either a combination of 30% fructose and 30% glucose (FG) or 60% sucrose (S). Control …
Background
There is evidence that disaccharide sucrose produce a greater increase in serum fructose and triglycerides (TGs) than the effect produced by their equivalent monosaccharides, suggesting that long-term exposure to sucrose or fructose + glucose could potentially result in different effects.
Aim of the study
We studied the chronic effects of a combination of free fructose and glucose relative to sucrose on rat liver.
Methods
Rats were fed either a combination of 30% fructose and 30% glucose (FG) or 60% sucrose (S). Control rats were fed normal rat chow (C). All rats were pair fed and were followed for 4 months. After killing, blood chemistries and liver tissue were examined.
Results
Both FG-fed- and S-fed rats developed early features of metabolic syndrome when compared with C. In addition, both diets induced hepatic alterations, including variable increases in hepatic TG accumulation and fatty liver, an increase in uric acid content in the liver, as well as an increase in hepatic levels of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) measured in liver homogenates.
Conclusions
Diets containing 30% of fructose either as free fructose and glucose, or as sucrose, induce metabolic syndrome, intrahepatic accumulation of uric acid and TGs, increased MCP-1 and TNF-α as well as fatty liver in rats. It will be relevant to determine clinically whether pharmacological reduction in uric acid levels might have a therapeutic advantage in the treatment of non-alcoholic fatty liver disease.
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