BACKGROUND AND AIM

Vitamin B6 as cofactor of Delta6 desaturase is involved in polyunsaturated fatty acid metabolism; moreover, it is a cofactor of the trans-sulfuration pathway of homocysteine. Some studies report that low concentrations of pyridoxine, by increasing homocysteine levels, are associated with coronary artery disease, and carotid and arterial lesions. The aim of this study was to verify whether different dietary amounts of polyunsaturated fatty acids associated with low content of vitamin B6 could modulate homocysteinemia.

METHODS AND RESULTS

Thirty-two rats were divided into two groups, one fed a diet with adequate vitamin B6 content the other a diet containing low amount of the same vitamin. Within each group, rats were divided into two subgroups differing in the polyunsaturated fatty acid content of the diet (63 and 33%, respectively). The vitamin B6-deficient diet induced an increase in homocysteine concentration compared to the vitamin B6-normal diet. This increase was tenfold in the subgroup fed high polyunsaturated fatty acid levels and twofold in the other subgroup. The fatty acid composition of liver phospholipids showed a lower arachidonic acid relative molar content and a lower 20:4/18:2 ratio in vitamin B6-deficient groups compared with B6-normal groups.

CONCLUSIONS

On the basis of the different biological functions of pyridoxine and considering that some factors closely related to atherosclerosis are vitamin B(6) dependent, adequate pyridoxine availability could be necessary to assure a normal long chain fatty acid metabolism and to reduce the risk linked to hyperhomocysteinemia.