作者: Leonie G. Mikael , Xiao-Ling Wang , Qing Wu , Hua Jiang , Kenneth N. Maclean
DOI: 10.1016/J.YMGME.2009.05.011
关键词:
摘要: Abstract Hyperhomocysteinemia (HHcy) can result from genetic or nutritional disturbances in folate metabolism. The most common cause of mild HHcy is methylenetetrahydrofolate reductase (MTHFR) deficiency. To explore interactions between and lipid metabolism atherogenesis, we measured plasma homocysteine (Hcy), triglycerides cholesterol Mthfr +/+ +/− mice on C57BL/6 BALB/c backgrounds, fed control folate-deficient diets. We also crossed ApoE C 57 - / with + mice, examined the same variables as well accumulation aortic sinus whole aorta. had significantly higher Hcy relative to mice. A significant positive correlation was observed all lower ApoA-IV protein levels which could reduce clearance triglyceride-rich lipoproteins circulation. In double mutant experiments, compared BALB c Triglycerides female were than those correlated positively Hcy. male more deposition aorta Our results suggest that associated hypertriglyceridemia MTHFR deficiency may exacerbate