Our Brains Need Vitamin E!

by Biotics Research

Researchers from the Linus Pauling Science Center at Oregon State conducted a study using zebrafish to elucidate the molecular consequences of vitamin E deficiency on brain lipids. Zebrafish express the α-tocopherol transfer protein (α-TTP), which facilitates hepatic α-tocopherol secretion into the circulation in humans. The fish were fed defined diets for nine months; one group without vitamin E, and one group supplemented with α-tocopherol acetate. They discovered that low brain α-tocopherol concentrations are associated with a nearly 60% depletion of a total of 19 brain lysophospholipids (lysoPLs), suggesting the entire lysoPL populations are affected. DHA-containing lysoPLs were present at significantly lower levels in the vitamin E deficient brains. LysoPLs are required for PL remodeling during membrane synthesis, repair and replacement. Their findings suggest that increased lipid peroxidation due to inadequate α-tocopherol leads to the depletion of 1 hexadeconoyl-2-docosahexaenoyl-sn-glycero-3-phosphocholine (DHA-PC), as well as other PLs containing both DHA and oleic acid, and that inadequate α-tocopherol concentrations allow lipid peroxidation to deplete not only brain DHA-PC, but DHA throughout the body, thereby limiting DHA delivery to the brain. Their data clearly indicates that critical lipids are protected by α-tocopherol, and that α-tocopherol is needed as a vitamin.

J Choi, et al. Novel function of vitamin in in regulation of zebrafish (Danio rerio) brain lysophospholipids discovered using lipidomics. Journal of Lipid Research, doi: 10.1194/jlr.M058041

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Vitamin D for Diabetes and Clogged Arteries?

by Biotics Research

Because low vitamin D levels are associated with diabetes and heart disease, researchers at the Washington University School of Medicine looked at the associations between vitamin D, immune function, and these two diseases, the combination of which are the most common cause of illness and death in Western populations. They found that in mice engineered to lack expression of the vitamin D receptor in monocytes and macrophages, the animals accumulated atherosclerotic plaques in the blood vessels and developed insulin resistance. Bone marrow transplantation of cells that expressed the vitamin D receptor into the mice improved their insulin sensitivity, suppressed atherosclerosis, and decreased the formation of fat-laden macrophages that accumulate along blood vessel walls. According to Dr. Bernal-Mizrachi, the lead investigator, “The finding that vitamin D helps regulate glucose metabolism may explain previous epidemiological studies identifying and increased risk of diabetes in patients with vitamin D deficiency.” This research was supported by NIH, the Children’s Discovery Institute, and the American Diabetes Association.

J. Oh, et al. Deletion of Macrophage Vitamin D Receptor Promotes Insulin Resistance and Monocyte Cholesterol Transport to Accelerate Atherosclerosis in Mice. Cell Reports, June 19, 2015

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