Thus, metabolic syndrome has previously been demonstrated to be detrimental to the endothelial glycocalyx, as evidenced by shedding-induced increase of glycocalyx components in the bloodstream of type 1 and type 2 diabetic patients, thereby reducing shear-induced eNOS activity and NO production (Nieuwdorp et al., 2006; Broekhuizen et al., 2010). This evidence concerns the gene NOS3 and metabolic syndrome.