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The atherogenic effect of excess methionine intake
Aron M Troen1, Esther Lutgens, Donald E Smith
1Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, 711 Washington Street, Boston, MA 02111, USA. aron.troen@tufts.edu
Summary
High methionine intake, not high homocysteine, caused vascular disease in mice. This suggests excess methionine metabolism products, not homocysteine itself, may link to vascular issues.
Area of Science:
- Cardiovascular Science
- Nutritional Science
- Metabolic Pathways
Background:
- Elevated plasma homocysteine (hyperhomocysteinemia) is linked to occlusive vascular disease.
- The exact cause of vascular disease in hyperhomocysteinemia remains unclear.
- Previous studies could not differentiate effects of dietary methionine from hyperhomocysteinemia.
Purpose of the Study:
- To investigate whether high methionine intake or hyperhomocysteinemia causes atheromatous pathology.
- To determine the independent atherogenic potential of high plasma homocysteine.
- To explore the role of methionine metabolism in vascular disease.
Main Methods:
- Apolipoprotein E-deficient mice were fed experimental diets.
- Diets were designed to achieve: high methionine/normal homocysteine, high methionine/hyperhomocysteinemia, or normal methionine/hyperhomocysteinemia.
- Vascular pathology in the aortic arch was assessed.
Main Results:
- Mice fed methionine-rich diets showed significant atheromatous pathology, even with normal homocysteine levels.
- Mice with B vitamin deficiency developed severe hyperhomocysteinemia but no increased vascular pathology.
- High plasma homocysteine was not independently atherogenic in this model.
Conclusions:
- Moderate increases in methionine intake are atherogenic in susceptible mice.
- Products of excess methionine metabolism, rather than high homocysteine, may underlie the association with vascular disease.
- Further research is needed to identify specific atherogenic metabolites of methionine.