The impact of B vitamins on the functioning of methylation cycle in the liver and the kidneys of hyper- and hypothyroid rats

Abstract

Hyperhomocysteinemia is a risk factor for endothelial dysfunction and, consequently, for cardiovascular disease and multiple other conditions. Impairment of homocysteine metabolism is known to occur in thyroid dysfunction. In particular, patients with hypothyroidism have significantly higher homocysteine levels than healthy people. Metabolism of homocysteine occurs in methylation cycle (whose normal functioning is dependent on tissue pools of vitamins B9, B12 and betaine), and also in reactions of trans-sulfonation, where pyridoxal phosphate (a pyridoxine derivative) acts as a coenzyme