Vitamin E

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Vitamin E and Alzheimer's Disease

Evidence suggests that alpha-tocopherol is beneficial in mild to moderate Alzheimer's by slowing functional decline and decreasing caregiver burden

How is Vitamin E homeostasis assessed?

Mainly determined by blood analyses: plasma levels reflect dietary intake under deficiency and toxicity situations Normal: 5-20 ug/mL in adults Deficiency < 5 ug/mL Toxicity: > 20 ug/mL Plasma gamma-tocopherol levels generally 1/10 of alpha-tocopherol levels

Vitamin E Deficiency

Results in nerve problems due to poor conduction of electrical impulses due to changes in nerve membrane structure and function.

Vitamin E as Antioxidant

Vitamin E provides a hydrogen for the reduction of lipid carbon-centered radicals. Quenching of free radical activity.

Pathways for the preferential delivery of alpha-tocopherol to peripheral tissues

Vitamin E taken up by the liver with chylomicron remnants Some vitamin E is excreted from the liver with bile Preferential selection of 2R-alpha-tocopherol in VLDL VLDL undergoes lipolysis to LDL and HDL, which both end up with alpha-tocopherol Tissue uptake of alpha-tocopherol coccurs

What are the functions of Vitamin E in target tissues? (5 major categories)

1) Antioxidant 2) Gene expression 3) Cell signaling 4) Relationship with vitamin C 5) Plays roles in eye and neurological functions; inhibition of platelet coagulation; protection of lipids; enzymatic activity regulator for PKC; peroxyl radical scavenger

How does Vitamin E move and circulate in systemic circulation (carriers)?

After being absorbed, vitamin E is packaged in chylomicrons. LPL carries fatty acids and vitamin E to tissues. HDL carries fitamin E to tissues. Chylomicrons carry vitamin E to the liver for liver uptake. Alpha-tocopherol transport protein (alpha-TTP)

Role of alpha-TTP in vitamin E metabolism and distribution

Alpha-TTP helps release vitamin E into VLDL, HDL, and carry to target tissues Mutated or deleted liver's alpha-TTP: ataxia and vitamin E deficiency (AVED)

Vitamin E and Vitamin C Relationship

As a result of Vitamin E's free radical quenching activity, it itself becomes radicalized (alpha-tocopherol radical). The ascorbate monoanion from the vitamin C cycle regenerates alpha-tocopherol from the alpha-tocopherol radical.

Alpha-tocopherol transport protein

Cytosolic 32kDa protein; facilitates secretion of alpha-tocopherol from liver into the plasma for distribution to tissues. Tissue expression: high in liver; lower levels in brain, kidney, lung, spleen Only natural alpha-tocopherol (RRR-alpha-tocopherol) and 2R-alpha-tocopherol in synthetic all-rac-alpha-tocopherol are maintained in plasma due to the selectivity of alpha-TTP.

Vitamin E Toxicity

Generally safe even at high levels; hypervitaminosis of vitamin E along with other blood thinners may exacerbate anti-coagulation / bleeding problems.

Vitamin E and CVD

Heart Outcomes Prevention evaluation found no significant effects of vitamin E.

Vitamin E and All Mortality

Meta-analysis shows high-dosage vitamin E supplementation may increase all-cause mortality

Vitamin E and Health Benefits

Might help prevent formation of blood clots Protect cell constituents from damaging free radicals Might block formation of carcinogenic nitrosamines; enhance immune function

What are the target tissues of vitamin E?

More than 90% in adipose tissue. Vitamin E is used in virtually all tissues as a fat-soluble antioxidant.

How and where is vitamin E stored?

More than 90% of the human body pool of alpha-tocopherol is located in the adipose tissue, with more than 90% of adipose tissue alpha-tocopherol in fat droplets

"At Risk" populations for deficiency

Primary vitamin E deficiency is rare; it occurs only in premature children, genetic alterations, malabsorption, and parenteral nutrition. 1) Genetic abnormalities: - tocopherol transfer protein (AVED) - Apolipoprotein B (homozygous hypobetalipoprotenemia) - Microsomal triglyceride transfer protein (abetalipoproteinemia) 2) Fat malabsorption syndromes including chronic cholestasis; cystic fibrosis; pancreatic insufficiency; short bowel syndromes; and chronic steatorrhea 3) TPN

Vitamin E and Cancer Risk

Statistically non-significant increased risk of prostate cancer with vitamin E treatment Equivocal evidence of decreased colon cancer risk No benefit in breast cancer Possible evidence of reduced mortality from bladder cancer

How is Vitamin E metabolized and excreted?

Vitamin E first undergoes a series of oxidations. After oxidations, it encounters alpha-CEHC (2-carboxyethyl-6-hydroxychroman), which leads to vitamin E being conjugated with glucuronic acid and excretion in urine.

What forms of Vitamin E are in the diet?

Vitamin E is a family of 8 antoxidant molecules (4 tocopherols and 4 tocotrienols) What germ, almonds, spinach are especially rich in alpha-tocopherol. Soy and corn oils especially rich in gamma-tocopherol. Alpha-tocopherol is the only form of vitamin E actively maintained in the human body; found in the largest quantities in blood and tissues.

How is Vitamin E absorbed by the enterocyte?

Vitamin E is absorbed primarily in the jejunum by passive diffusion. NPC1L1 may also play a role in absorption. Bile salts are required for emulsification, solubilization, and micelle formation. Rate of absorption: highly variable (10-80%).


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