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Retinol liver content

During the development of vitamin A deficiency in experimental animals, the plasma concentration of RBP falls, while the liver content rises. The administration of retinol to deficient animals results in a considerable release of holo-RBP from the liver. This is a rapid effect on the release of preformed apo-RBP in response to the availability of retinol, rather than an increase in the synthesis of the protein. There is no evidence that retinol controls the synthesis of RB P (Soprano et al., 1982). This provides the basis of the relative dose response (RDR) test for liver stores of vitamin A (Section 2.4.1.3) administration of a test dose of retinol gives a considerably greater increase in plasma retinol, bound to RBP, in deficient subjects than in those with adequate liver reserves, because of the accumulation of apo-RBP in the liver. [Pg.46]

Carotene (all-trans), (3-cryptoxanthin (all-trans and -cis), zeaxanthin (all-trans), luteoxanthin isomers, violaxanthin (all-trans and -cis), and neoxanthin (all-trans and -cis) were identified in several mango cultivars (Mercadante and others 1997 Ornelas-Paz and others 2007, 2008). Mango retinol was found to be highly bioavail-able by estimating vitamin A and carotene reserves in the liver and plasma of rats. Information on the tocopherol content in mango is very scarce, but it seems to be low (Burns and others 2003 Ornelas-Paz and others 2007). [Pg.27]

Vitamin A (retinol) is essential for normal growth and cell differentiation, particularly for epithelial cells. 2,3,7,8-TCDD has been shown to decrease the storage of vitamin A in rodents. Decreased ability to store vitamin A (retinol) was found in rats and guinea pigs however, partial recovery of the retinol content by week 16 postexposure was reported only in rats. A single oral dose of 2,3,7,8-TCDD caused a 70% reduction in the liver storage of retinol in rats when measured 2 months postexposure (Thunberg et al. [Pg.298]

Rats were fed a control diet (2,4 mg retinol/kg diet) or a deficient diet 0.6 mg retinol/kg diet). Following the feeding trial, the stellate cells of the liver were analyzed for their content of vitamin A and other components, as shown in Tabic 9,3, The results demonstrate that the low-vitamin A diet resulted in a decrease in vitamin A content with little effect on the contents of the other lipids. [Pg.556]

Prealbumin is the transport protein for thyroxine and a carrier for retinol-binding protein. The body s content of prealbumin is low (10 mg/kg of body weight), and it has a very short biologic half-fife (I to 2 days). Prealbiunin may be reduced in as few as 3 days after calorie and protein intake is significantly decreased, or when hypercatabolism or severe metabolic stress (tramna or bmns) is present. Because of its short half-life, it is most useful in monitoring the shortterm, acute effects of nutrition support. As with ALB and TFN, sermn prealbumin concentrations are depressed in those with liver disease due to decreased hepatic synthesis. Increased serum prealbumin concentrations have been noted in patients with renal disease due to impaired renal excretion. [Pg.2564]

When retinol-deficient rats were first treated with colchicine and then injected with retinol to stimulate RBP secretion, the RBP content of a Golgi-rich fraction from liver increased markedly, to a maximum of 34% of the total liver RBP. The level of TTR in the Golgi was not influenced by retinol injection. [Pg.67]

Fig. 5. Perinatal development of CRBP and CRABP of rat liver (top) and lung (bottom). Content of binding proteins was determined by specific binding of [ H]retinol and [ H]retinoic acid evaluated by sucrose gradient centrifugation. (From Ong and Chytil, 1976a.)... Fig. 5. Perinatal development of CRBP and CRABP of rat liver (top) and lung (bottom). Content of binding proteins was determined by specific binding of [ H]retinol and [ H]retinoic acid evaluated by sucrose gradient centrifugation. (From Ong and Chytil, 1976a.)...
Epidemiologic evidence indicates that an inverse relationship exists between cancer risk and vitamin A consumption. In most epidemiologic investigations, estimates of vitamin A intake have been based on the frequency of ingestion of foods known to have a high content of p-caiotene (e.g., green and yellow vegetables) or a few foodstuffs that contain preformed retinol (e.g., liver or whole milk). [Pg.351]

Vitamin A is a colourless substance that is present in animal fats, e.g. liver, milk, butter and eggs, although the richest sources are fish liver oils. Margarines are fortified to bring their content up to that of butter. Because of its specific effects in the visual process and the fact that it is an alcohol, the alternative name for vitamin A is retinol. [Pg.153]


See other pages where Retinol liver content is mentioned: [Pg.32]    [Pg.32]    [Pg.416]    [Pg.298]    [Pg.730]    [Pg.906]    [Pg.128]    [Pg.4898]    [Pg.239]    [Pg.299]    [Pg.16]    [Pg.32]    [Pg.26]    [Pg.489]    [Pg.203]   
See also in sourсe #XX -- [ Pg.37 ]

See also in sourсe #XX -- [ Pg.37 ]

See also in sourсe #XX -- [ Pg.37 ]




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