Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome.
Level 5 - mechanism / opinion, no new human data
Animal research with no human data
PubMed 24022321 · doi:10.1038/ncomms3434
What was done
Wild-type mice, mice unable to metabolize fructose, and aldose reductase-deficient mice were exposed to 10% glucose for 14 weeks. The authors assessed energy intake, body weight, visceral obesity, fatty liver, insulin levels, leptin levels, and polyol pathway activation.
What was found
The abstract reports no numerical values. Qualitatively, wild-type mice exhibited aldose reductase and polyol pathway activation in steatotic liver areas, whereas mice unable to metabolize fructose were protected from glucose-induced increases in energy intake, body weight, visceral obesity, fatty liver, elevated insulin, and hyperleptinaemia. Aldose reductase-deficient mice were protected against glucose-induced fatty liver.
Why it matters
It demonstrates in animal models that endogenous conversion of glucose to fructose via the polyol pathway in the liver contributes to the development of fatty liver and metabolic syndrome.
Limits
The study was conducted entirely in mouse models, and findings may not directly translate to human metabolic physiology. The abstract provides no sample sizes, effect sizes, or quantitative data.
Cited by
- supports The polyol pathway via aldose reductase is the only enzymatic pathway by which the body synthesizes endogenous fructose.
- supports When blood glucose levels rise above 120 mg/dL, the polyol pathway begins converting glucose into fructose.