Table 1.
Experimental evidence | Yeast | Mammals |
---|---|---|
AdoHcy is formed in vivo in response to elevated Hcy levels | + | + |
| ||
AdoHcy is more toxic than Hcy to cells deficient in Hcy catabolism | + | |
| ||
AdoHcy represents a better marker of cardiovascular risk than Hcy | + | |
| ||
Phospholipid methylation is quantitatively the major consumer of AdoMet | + | + |
| ||
Phospholipid methylation is inhibited in response to Hcy supplementation | + | |
| ||
Phospholipid methylation is inhibited by AdoHcy | + | + |
| ||
TAG is accumulating in response to Hcy supplementation | + | + |
| ||
TAG is accumulating in response to deficiency in AdoHcy hydrolysis | + | |
| ||
TAG is accumulating in response to deficiency in phospholipid methylation | + | + |
| ||
UPR is inducted in response to Hcy supplementation | + | + |
| ||
The de novo phospholipid methylation pathway produces phospholipids enriched in unsaturated fatty acids | + | + |
| ||
ER stress is inducted by accumulation of saturated fatty acids in membrane phospholipids | + | + |
| ||
Hcy/AdoHcy levels are inversely correlated to the levels of unsaturated fatty acids | + |
*The absence of a plus sign in some columns implies lack of data or nonapplicability.