Michelle A.J. van Oeteren1,2, Jean L.J.M. Scheijen1,2, N. Simons1,2, Petra M. Niessen1,2, Marjo P.H. van de Waarenburg1,2, Alfons J.H.M. Houben1,2, Martijn C.G.J. Brouwers2,3, Casper G. Schalkwijk1,2
1. Laboratory for Metabolism and Vascular Medicine, Division of General Internal Medicine, Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands. 2. Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands. 3. Division of Endocrinology and Metabolic Diseases, Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands.
michelle.vanoeteren@maastrichtuniversity.nl
Excessive fructose consumption can lead to several complications, including liver damage, insulin resistance, and cardiovascular disease. Fructose-induced formation of advanced glycation endproducts (AGEs) might mediate these negative health effects. Fructose can form AGEs either via a direct interaction with lysine residues resulting in fructose-specific glucoselysine production, or via generation of methylglyoxal (MGO), the major precursor in the formation of AGEs. However, it is unknown whether dietary fructose effectively augments systemic glucoselysine and MGO levels.
We measured serum glucoselysine and MGO levels in individuals with a BMI >28 kg/m2 who received 45 grams daily fructose (n=19) or glucose supplementation (n=16) at the background of a fructose-restricted diet. In addition, we examined the effect of an acute 20 grams fructose challenge on serum MGO levels in healthy individuals (n=11). Glucoselysine and MGO were quantified with ultra-performance liquid chromatography tandem mass spectrometry.
Serum glucoselysine levels were significantly reduced after a six-week fructose-restricted diet (median difference -8.0 nmol/L, 95%CI: -12.0; -4.5). No differences were observed in serum MGO after six weeks of fructose or glucose supplementation (median difference between change from baseline -15.5 nmol/L, 95%CI: -111.0; 90.0). In the acute 20 grams fructose challenge, serum MGO did not significantly differ from baseline (p>0.05 for all comparisons).
In summary, dietary fructose induces the formation of fructose-specific AGEs and this is independent of MGO. Future research is warranted to study the role of AGEs in fructose consumption-induced complications.