Homocysteine as a Risk Factor for Atherosclerosis: Is Its Conversion to S-Adenosyl-L-Homocysteine the Key to Deregulated Lipid Metabolism?

Table 1

Experimental evidence on deregulation of lipid metabolism and UPR induction under elevated homocysteine levels in yeast and mammals*.

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.