TY - GEN A1 - Kotula-Horowitz, Katarzyna N2 - PPARα activation increases the rate of transmethylation processes that provide the cells with essential metabolites (creatine, N1-methylnicotinamide; MNA), and a by-product, i.e. homocysteine. The main adverse effect of fibrate therapy consists in the incidence of mild hyperhomocysteinemia. The principal aim of the present study therefore consisted in assessing the effect of fenofibrate therapy on the brachial artery diastolic response, homocysteine, and MNA levels in the patients with dyslipidemia. The study involved 50 men (31-58 years) with dyslipidemia and 50 healthy controls. Biochemical tests, homocysteine, MNA, and FMD measurements were pursued at baseline, after 6, and 12 months of fenofibrate treatment. Following the treatment, improvement in endothelial function was associated with the reduction of triglycerides, and an increase in MNA, unlike in homocysteine. The reduction of systemic oxidative stress and proinflammatory status was observed, which may also have contributed to the improvement of FMD. In clinical terms, fenofibrate therapy, apart from improving the serum lipid profile, also brings about numerous pleiotropic effects, whereas its introduction within the reversible period of impairment of endothelial function associated with hypertriglyceridemia, is believed to be essentially instrumental in vascular protection. CY - Kraków L2 - http://dl.cm-uj.krakow.pl:8080/Content/4464 PY - 2019 KW - fenofibrate KW - homocysteine KW - N1-metylonikotynamide KW - FMD KW - F2-isoprostanes T1 - Effect of fenofibrate therapy on brachial artery diastolic response, and plasma N1-methylnicotinamide, and homocysteine concentrations in the subjects with dyslipidemia UR - http://dl.cm-uj.krakow.pl:8080/dlibra/publication/edition/4464 ER -