Effects of Dietary Folate Supplementation on the Homocystine Diet-Induced Hyperhomocysteinemia and Hepatic S-Adenosylmethionine Metabolism in Rats

We investigated the effects of dietary folate supplementation on plasma homocysteine, vitamin B12 and hepatic levels of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) in diet-induced hyperhomocysteinemic rats. All animals were fed 0.3% homocysteine diet for 2 weeks, then they were placed either on a 0.3% homocystine or no homocystine with or without 8 mg/kg folate diet for 8 weeks. Homocystine diet induced hyperhomocysteinemia up to 3.5-fold at 10 weeks (28.0+/-4.8 micromol/l vs. 7.9+/-0.3 micromol/l). Dietary folate supplementation caused a significant decrease in plasma homocysteine levels which had been increased by a homocystine-diet. Also, dietary folate supplementation made them return to control levels at 4 wk when the diet was free of homocystine. Plasma folate levels were markedly decreased with homocystine diet with no folate supplementation. Plasma vitamin B12 did not differ between groups. Dietary homocystine increased hepatic levels of SAM in folate supplementation group at 10 weeks (p<0.05). Dietary folate supplementation increased hepatic levels of SAM/SAH ratios in homocystine group (p<0.05). In conclusion, dietary folate supplementation can effectively ameliorate the detrimental effects of hyperhomocysteinemia.mia.

RELATIONSHIP OF INCREASED INTRACELLULAR S-ADENOSYLHOMOCYSTEINE WITH MONOCYTE CHEMOATTRACTANT PROTEIN -1 EXPRESSION IN HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS / 营养学报

Objective To explore the molecular basis of vascular endothelial cell's injury by cellular S-adenosylhomocysteine (SAH) accumulation, and the mechanism for cardiovascular disease induced by dietary high methionine intake. Method After human umbilical vein endothelial cells (HUVEC) were treated without (normal) or with different concentrations of potent S-adenosylhomocysteine hydrolase (SAHH) inhibitor 3-deazaadenosine (DZA) for 24, 48 or 72h, the level of intracellular inflammatory monocyte chemoattractant protein-1 (MCP-1) was measured with enzyme linked immunosorbent assay (ELISA). Then, the relative expression of MCP-1 mRNA was detected with quantitative reverse transcription polymerase chain reaction (qRT-PCR). Furtheremore, the methylated state of MCP-1 gene promoter was analyzed with methylation special PCR (MSP) method. Results The level of intracellular MCP-1 was increased in HUVEC incubated with DZA than normal (P