ABSTRACT
The "fructose hypothesis," based on numerous publications, alleges that dietary fructose plays a unique and causative role at the root of modern health problems with a detrimental impact on humans. Detrimental impact of fructose is assumed to be mediated and amplified by advanced glycation end products (AGEs) that are produced in the late stages of fructation and are able to generate additional reactive species forming a vicious cycle of chronic/severe carbonyl/oxidative stress. Fructose also forms both pyranose and furanose structures but exists to a greater extent in the open-chain active form than glucose does. The initial step of fructation is the covalent interaction between free carbonyl group of open-chain fructose and amino group of any biomolecule, resulting in the Schiff base formation. Being a more potent glycation agent than glucose, fructose nonenzymatically produces a higher level of reactive species, which during long-term excessive fructose consumption leads to chronic/severe carbonyl/oxidative stress and AGEs-mediated adverse effects on human health.
