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Vitamin A binding proteins

Foster I don t know the mechanism whereby chromophore is retained. The bottom line is that we know chromophore is only depleted in flies and mice, and that most of the retinoid will be part of the visual system anyway. There must be some other way of retaining vitamin A. In fact in mammals, there are a whole range of potential vitamin A binding proteins, hke IRBP in the pigmented epithelium, that could serve to mop-up and act as a chromophore sink. [Pg.30]

Li E and Norris AW (1996) Structure/function of cytoplasmic vitamin A-binding proteins. Annual Reviews of Nutrition 16,205-34. [Pg.437]

Wolf, G. and Phil, D. (1991). The intracellular vitamin A binding proteins an overview of their function, Nutr. Rev., 49, 1. [Pg.138]

Fluorination of the vitamin D3 side chain was anticipated to have an impact on its metabolism pathway. 26,27-Hexafluorocalcitriol, faiecaicitrioi, was found to be several times more potent than caicitrioi in the regulation of Ca metabolism and of the immune system. The reason for this higher biological activity has been attributed to several mechanisms a higher activity of its 23(5)-hydroxylated metabolite [26,27-hexafluoro-l,23(5),25(OH)3D3], a lower affinity of faiecaicitrioi for the vitamin D binding protein and a higher affinity of falecalcitriol-... [Pg.106]

A few substances are so large or impermeant that they can enter cells only by endocytosis, the process by which the substance is bound at a cell-surface receptor, engulfed by the cell membrane, and carried into the cell by pinching off of the newly formed vesicle inside the membrane. The substance can then be released inside the cytosol by breakdown of the vesicle membrane. Figure 1-5D. This process is responsible for the transport of vitamin B12, complexed with a binding protein (intrinsic factor) across the wall of the gut into the blood. Similarly, iron is transported into hemoglobin-synthesizing red blood cell precursors in association with the protein transferrin. Specific receptors for the transport proteins must be present for this process to work. [Pg.23]

Vitamin D and its metabolites circulate in plasma tightly bound to a carrier protein, the vitamin D-binding protein. This .-globulin binds 25(OH)D and 24,25(OH)2D with comparable high affinity and vitamin D and l,25(OH)2D with lower affinity. [Pg.959]

The liver appears to be the principal organ for clearance. Excess vitamin D is stored in adipose tissue. The metabolic clearance of calcitriol in humans indicates a rapid turnover, with a terminal half-life measured in hours. Several of the l,25(OH)2D analogs are bound poorly by the vitamin D-binding protein. As a result, their clearance is very rapid, with a... [Pg.959]

Janmey, P.A., T.P. Stossel, and S.E. Lind. 1986. Sequential binding of actin monomers to plasma gelsolin and its inhibition by vitamin D-binding protein. Biochem Biophys Res Commun. 136 72—9. [Pg.66]

Adebanjo OA, Moonga BS, Haddad JG, Huang CL-H, Zaidi, M. 1998b.. A possible new role for vitamin D-binding protein in osteoclast control. Inhibition of Ca2+ sensing at low physiological concentrations. Biochem Biophys Res Commun249 668-671. [Pg.553]

Vitamin D regulates calcium and phosphorus absorption and deposition and serum alkaline phosphatase levels. The recommended daily allowance is 5 /xg, increasing to 10 to 15 /xg in older age.109 Vitamin D3 is synthesized under UVB irradiation in the skin where it is stored and released into the circulation in a complex with the vitamin D binding protein. In liver it is hydroxylated to 25(OH)-cholecalciferol, the hormonal precursor, followed by another hydroxylation step in the... [Pg.381]

Vitamin B12 depletion could be expected in chronic alcoholics since their diet is often low in animal protein, and, although many alcoholic beverages are the result of bacterial fermentation, they have nevertheless been found to be essentially free of vitamin B12 (L9). Reduced levels of serum vitamin B12 have been reported in alcoholics by some workers (H16.L9) while others have found the concentration to be normal or elevated (Dll). Because of the liver damage often associated with alcoholism, serum levels of the vitamin may be normal or elevated even though liver stores of the vitamin are reduced (RIO, S15). An elevated level of serum vitamin B12 binding protein may also serve to increase the vitamin B12 level. The interpretation of serum vitamin B12 levels in alcoholics is of very limited importance since a clinically significant deficiency of the vitamin very rarely occurs. [Pg.184]

There are three classes of vitamin B12 binding proteins intrinsic factor, which facilitates absorption of the vitamin from the ileum R-proteins, which include TC I and TC III (the function of these proteins is not clear, but they probably act as mobile storage forms) and TC II, which is the transport protein responsible for carrying the vitamin to the tissues. Abnormalities of intrinsic factor or TC II could be expected to have serious consequences for the patient, and in recent years a number of such abnormalities have been reported. [Pg.196]

An unusual vitamin B12 binding protein has been described by Jacob et al. (J7). The patient was a 59-year-old black male with widely metastasized carcinoma of the lung. The tumor produced a protein that complexed with R-protein, forming a macromolecular complex which was distinct from TC I, II, or III, and 90% of the endogenous vitamin B12 was held in this complex. [Pg.198]

Previtamin D3 is thermodynamically unstable and rearranges its double bonds to form the more thermodynamically stable vitamin D3. After synthesis, vitamin D3 is transported to the liver by a vitamin D-binding protein, which is an a-globulin. [Pg.328]

Transport of vitamin D3 away from the dermal junction of skin is accomplished by a 52 kDa serum vitamin D-binding protein (DBP). Serum DBP is a member of the a-fetoprotein-albumin super family [36], DBP has high affinity for vitamin D3, but does not bind to its precursors or the products of previtamin D3 side-reactions, lumisterol and tachysterol [37], Accumulation of 7-dehydrocholesterol in skin occurs in sebaceous glands at the malpighian layer of the epidermis, mostly in the stratum spinosum and stratum basal... [Pg.6]


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See also in sourсe #XX -- [ Pg.144 , Pg.145 ]




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