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Vitamin E absorption

The d-form of the vitamin is the most active. Any studies of vitamin supplementation, and their subsequent effects in various muscle foods, must acknowledge the form of tocopherol fed before conclusions can be drawn regarding dietary uptake and antioxidant efficiency, d-a-tocopherol or its ester is more readily assimilated into tissues than the racemic (dl) form (Hidiroglou et al., 1988). Burton et al. (1988) have demonstrated that the uptake of the free phenol and acetate forms of d-a-tocopherol are equivalent. Marusich et al. (1975) reported that dl-a-tocopherol and dl-a-tocopheryl acetate were equivalent in terms of uptake by chicken liver and breast muscle, and resulted in similar oxidative stabilities within the tissue types. [Pg.162]

There are some points regarding vitamin E supplementation of meat-producing animals that deserve special note. These include the recognition that muscle is among the slowest of tissues to accumulate tocopherol the extent to which tocopherol accumulation differs between muscles within a carcass and that incorporation within a given muscle can differ substantially even between closely related species. [Pg.162]

Species Level and form of vitamin E fed Feeding period Tissue [Vit E] Reference  [Pg.163]


Thompson JN and Scott ML (1970) Impaired lipid and vitamin E absorption related to atrophy of the pancreas in selenium-deficient chicks. Journal of Nutrition 100, 797-809. [Pg.455]

Vitamin E is absorbed as free tocopherol, along with other fat-soluble vitamins and dietary lipids. Tocopheryl acetate, the form commonly used for dietary supplementation, is hydrolyzed before absorption. Uptake requires bile salts. A selective impairment of vitamin E absorption without malabsorption of other fat-soluble vitamins has been identified it was corrected after a large oral intake of the vitamin. Patients with chronic fat malabsorption and abetalipoproteinemia (Chapter 20) may develop vitamin E deficiency. [Pg.913]

Hacquebard, M. and Carpentier, Y.A., Vitamin E absorption, plasma transport and cell uptake, Curr. Opin. Clin. Nutr. Metab. Care 8 (2), 133-138, 2005. [Pg.200]

Figure 3 Intestinal vitamin E absorption and plasma lipoprotein transport. (Adapted from Traber MG (1998) Vitamin E. In Shils ME, Olson JA, Shike M, and Ross AC (eds.) Modem Nutrition in Health and Disease, pp. 347-362. Baltimore Williams Wilkins.)... Figure 3 Intestinal vitamin E absorption and plasma lipoprotein transport. (Adapted from Traber MG (1998) Vitamin E. In Shils ME, Olson JA, Shike M, and Ross AC (eds.) Modem Nutrition in Health and Disease, pp. 347-362. Baltimore Williams Wilkins.)...
In the case of Vitamin E, absorptions at 1378 cm" (methyl groups), 1260 cm and 1209 cm (phenol C-O stretching) and 1090 cm (ether group) [60] can alternatively be used for quantifying Vitamin E. Vitamin E Index is currently [62, 66] used for measuring the unreacted vitamin E. it is defined as the ratio of two areas ... [Pg.75]

The symptoms of vitamin E deficiency in animals are numerous and vary from species to species (13). Although the deficiency of the vitamin can affect different tissue types such as reproductive, gastrointestinal, vascular, neural, hepatic, and optic in a variety of species such as pigs, rats, mice, dogs, cats, chickens, turkeys, monkeys, and sheep, it is generally found that necrotizing myopathy is relatively common to most species. In humans, vitamin E deficiency can result from poor fat absorption in adults and children. Infants, especially those with low birth weights, typically have a vitamin E deficiency which can easily be corrected by supplements. This deficiency can lead to symptoms such as hemolytic anemia, reduction in red blood cell lifetimes, retinopathy, and neuromuscular disorders. [Pg.147]

Kayden, H.J. andTraber, M.G. (1993). Absorption, lipoprotein transport and regulation of plasma concentrations of vitamin E in humans. J. Lipid Res. 34, 343-358. [Pg.35]

Esterbauer et al. (1991) have demonstrated that /3-carotene becomes an effective antioxidant after the depletion of vitamin E. Our studies of LDL isolated from matched rheumatoid serum and synovial fluid demonstrate a depletion of /8-carotene (Section 2.2.2.2). Oncley et al. (1952) stated that the progressive changes in the absorption spectra of LDL were correlated with the autooxidation of constituent fatty acids, the auto-oxidation being the most likely cause of carotenoid degradation. The observation that /3-carotene levels in synovial fluid LDL are lower than those of matched plasma LDL (Section 2.2.2) is interesting in that /3-carotene functions as the most effective antioxidant under conditions of low fOi (Burton and Traber, 1990). As discussed above (Section 2.1.3), the rheumatoid joint is both hypoxic and acidotic. We have also found that the concentration of vitamin E is markedly diminished in synovial fluid from inflamed joints when compared to matched plasma samples (Fairburn etal., 1992). This difference could not be accounted for by the lower concentrations of lipids and lipoproteins within synovial fluid. The low levels of both vitamin E and /3-carotene in rheumatoid synovial fluid are consistent with the consumption of lipid-soluble antioxidants within the arthritic joint due to their role in terminating the process of lipid peroxidation (Fairburn et al., 1992). [Pg.106]

In the stomach, carotenoids are exposed to acid environments. This can lead to carotenoid isomerization, which can change carotenoid antioxidant properties, solubility, and absorption. In humans, (3-carotene absorption is reduced when the pH of the gastric fluids is below 4.5 (Tang and others 1995). Vitamin E consumption seems to reduce carotenoid absorption in animals, presumably because vitamin E and carotenoids compete for absorption (Furr and Clark 1997). Dietary sterols, such as those in sterol-supplemented functional foods, are also known to decrease carotenoid absorption. [Pg.205]

Deficiency of vitamin E is rare it can occur from abnormalities in lipid absorption as well as dietary deficiency. Its deficiency affects the muscular system, causing dystrophy and paralysis and, if the heart is affected, death by myocardial failure. This is probably caused by demyelin-ation of axons due to oxidative damage. Vitamin E is incorporated into chylomicrons within the enterocyte, so that its uptake into cells requires the activity of lipoprotein lipase. [Pg.343]

Amprenavir may be taken with or without food however, a high-fat meal decreases the absorption of amprenavir and should be avoided. Advise adult and pediatric patients not to take supplemental vitamin E since the vitamin E content of amprenavir capsules and oral solution exceeds the Reference Daily Intake (adults, 30 units pediatrics, approximately 10 units). [Pg.1821]


See other pages where Vitamin E absorption is mentioned: [Pg.688]    [Pg.688]    [Pg.162]    [Pg.138]    [Pg.688]    [Pg.688]    [Pg.162]    [Pg.138]    [Pg.1300]    [Pg.481]    [Pg.19]    [Pg.358]    [Pg.324]    [Pg.572]    [Pg.315]    [Pg.323]    [Pg.381]    [Pg.384]    [Pg.384]    [Pg.385]    [Pg.290]    [Pg.287]    [Pg.244]    [Pg.245]    [Pg.573]    [Pg.709]    [Pg.1164]    [Pg.1616]    [Pg.434]    [Pg.338]   


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