Vitamin E is a generic term for a group of fat-soluble compounds and consists of eight chemical forms. Foods rich in this vitamin include nuts, cereals, broccoli, and green leafy vegetables like spinach.
CYP4F2 produces the only known enzyme to metabolise vitamin E in humans and the change in enzyme activity associated with these two variants may explain individual variation in vitamin E levels, and response to supplements.
The study led by Dr Robert Parker, an associate professor of nutritional sciences at Cornell University, looked at CYP4F2-dependent metabolism of six of the most commonly occurring forms of the compound in the human diet.
The researchers found that the W12G variant showed more enzyme activity and the V33M variant less activity, than a normal copy of the gene. The two genetic variants were both the result of a single DNA base change.
The US study found that the variants commonly occur in many populations, with the W12G variant present in 21 percent of African Americans and the V33M variant present in 17 percent of European Americans.
Given the frequency at which these variants occur, and the health problems associated with vitamin E deficiency, the investigators suggest that the clinical implications of CYP4F2-dependent activity should be studied further.
Although it is known that decreased CYP4F2 activity affects vitamin E levels in humans, this study investigated the gene by inserting it into insect cells; therefore the researchers do not know what impact the two SNPs (single nucleotide polymorphisms) have in the human body.
This study was published in the November issue of The Journal of Nutrition.