Vitamin A
Vitamin A is an essential micronutrient because it cannot be biogenerated de novo by animals. It must be obtained from plants in the form of provitamin-A carotenoids: α-, β-, and γ-carotenes and β-cryptoxanthin. These substances can be converted to vitamin A compounds in the body. The term vitamin A refers to all-trans-retinol, the alcohol form of the vitamin. The storage form of vitamin A is retinyl palmitate. The aldehyde form of vitamin A is retinal and functions in vision. The physiologically most important vitamin A metabolite is the acid derivative, retinoic acid. Retinoic acid functions at the gene level as a ligand for specific nuclear transcription factors that regulate many genes involved in fundamental biologic activities of the cell. The term retinoids includes both natural and synthetic compounds with vitamin A activity and is most often used in the context of vitamin A action at the gene level.Absorption, Transport, Metabolism, Storage
The body acquires vitamin A either as preformed vitamin A (usually as esters) or as provitamin-A carotenoids. In the USA, grains and vegetables supply approximately 55% and dairy and meat products supply approximately 30% of vitamin A intake from food. Vitamin A and the provitamins-A are fat-soluble, and their absorption depends on the presence of adequate lipid and protein within the meal. Chronic intestinal disorders or lipid malabsorption syndromes can result in vitamin A deficiency. Ingested and absorbed provitamins-A are bioconverted to vitamin A molecules in the small intestine by the carotene cleavage enzyme dioxygenase; β-carotene provides twice the vitamin A activity of the other provitamins-A. Further processing in the enterocyte involves the esterification of vitamin A to retinyl palmitate for incorporation into chylomicrons, which are released into lymph and transported via the circulation to the liver for storage or to other tissues. The vitamin A content in the liver is low at birth, but it increases 60-fold during the first 6 mo of life. If the growing child has a well-balanced diet and obtains vitamin A from foods that are rich in vitamin A or provitamin-A the risk of vitamin A deficiency is small. However, even subclinical vitamin A deficiency can have serious consequences. Stored vitamin A is released from the liver into the circulation as retinol bound to its specific transport protein, retinol-binding protein (RBP), which binds to the thyroid hormone transport protein, transthyretin; this complex delivers retinol (as well as the thyroid hormone) to tissues. Normal plasma levels of retinol are 20-50 mug/dL in infants and 30-225 mug/dL in older children and adults. Uncleaved provitamin-A carotenoids in the intestine are also incorporated into chylomicrons and delivered to various tissues. Malnutrition, particularly protein deficiency, can cause vitamin A deficiency by the impaired synthesis of retinol transport protein. However, if dietary vitamin A is provided in the absence of RBP, vitamin A is transported to the tissues via chylomicrons and almost completely alleviates the symptoms of vitamin A deficiency. In developing countries, subclinical or clinical zinc deficiency can increase the risk of vitamin A deficiency. There is also some evidence of marginal zinc intakes in children in the USA.Function and Mechanism of Action
Vitamin A is required throughout the life cycle, beginning with embryogenesis. Except for its role in vision, the pleiotropic actions of this micronutrient include many systemic functions that are mediated at the gene level by all-trans-retinoic acid (RA), which is a ligand for specific nuclear transcription factors, the retinoid receptors: RARs and RXRs. When an RAR is activated by the presence of RA, it combines with an RXR, and the resulting heterodimer binds to target genes that have specific recognition sites. Thus, vitamin A, via its active form, retinoic acid, regulates many genes that are involved in the fundamental biologic activities of cells, such as cell division, cell death, and cell differentiation. Retinoic acid is among the most important signaling molecules in vertebrate ontogenesis. It affects many physiologic processes, including reproduction, growth, embryonic and fetal development, and bone development, in addition to respiratory, gastrointestinal, hematopoietic, and immune functions. The role of vitamin A in immune function and host defense is particularly important in developing countries, where vitamin A supplementation or therapy reduces the morbidity and mortality rates of various diseases, such as measles The best understood function of vitamin A is its nongenomic role in vision. The human retina has two distinct photoreceptor systems: the rods, containing rhodopsin, which can detect low-intensity light, and the cones, containing iodopsin, which can detect different colors. The aldehyde form of vitamin A, retinal, is the prosthetic group on both visual proteins. The mechanism of vitamin A action in vision is based on the ability of the vitamin A molecule to photoisomerize (change shape when exposed to light). Thus, in the dark, low-intensity light isomerizes the rhodopsin prosthetic group, 11-cis retinal, to all-trans-retinal, generating an electrical signal that is transmitted via the optic nerve to the brain and results in visual sensation.
Vitamin A is an essential micronutrient because it cannot be biogenerated de novo by animals. It must be obtained from plants in the form of provitamin-A carotenoids: α-, β-, and γ-carotenes and β-cryptoxanthin. These substances can be converted to vitamin A compounds in the body. The term vitamin A refers to all-trans-retinol, the alcohol form of the vitamin. The storage form of vitamin A is retinyl palmitate. The aldehyde form of vitamin A is retinal and functions in vision. The physiologically most important vitamin A metabolite is the acid derivative, retinoic acid. Retinoic acid functions at the gene level as a ligand for specific nuclear transcription factors that regulate many genes involved in fundamental biologic activities of the cell. The term retinoids includes both natural and synthetic compounds with vitamin A activity and is most often used in the context of vitamin A action at the gene level.Absorption, Transport, Metabolism, Storage
The body acquires vitamin A either as preformed vitamin A (usually as esters) or as provitamin-A carotenoids. In the USA, grains and vegetables supply approximately 55% and dairy and meat products supply approximately 30% of vitamin A intake from food. Vitamin A and the provitamins-A are fat-soluble, and their absorption depends on the presence of adequate lipid and protein within the meal. Chronic intestinal disorders or lipid malabsorption syndromes can result in vitamin A deficiency. Ingested and absorbed provitamins-A are bioconverted to vitamin A molecules in the small intestine by the carotene cleavage enzyme dioxygenase; β-carotene provides twice the vitamin A activity of the other provitamins-A. Further processing in the enterocyte involves the esterification of vitamin A to retinyl palmitate for incorporation into chylomicrons, which are released into lymph and transported via the circulation to the liver for storage or to other tissues. The vitamin A content in the liver is low at birth, but it increases 60-fold during the first 6 mo of life. If the growing child has a well-balanced diet and obtains vitamin A from foods that are rich in vitamin A or provitamin-A the risk of vitamin A deficiency is small. However, even subclinical vitamin A deficiency can have serious consequences. Stored vitamin A is released from the liver into the circulation as retinol bound to its specific transport protein, retinol-binding protein (RBP), which binds to the thyroid hormone transport protein, transthyretin; this complex delivers retinol (as well as the thyroid hormone) to tissues. Normal plasma levels of retinol are 20-50 mug/dL in infants and 30-225 mug/dL in older children and adults. Uncleaved provitamin-A carotenoids in the intestine are also incorporated into chylomicrons and delivered to various tissues. Malnutrition, particularly protein deficiency, can cause vitamin A deficiency by the impaired synthesis of retinol transport protein. However, if dietary vitamin A is provided in the absence of RBP, vitamin A is transported to the tissues via chylomicrons and almost completely alleviates the symptoms of vitamin A deficiency. In developing countries, subclinical or clinical zinc deficiency can increase the risk of vitamin A deficiency. There is also some evidence of marginal zinc intakes in children in the USA.Function and Mechanism of Action
Vitamin A is required throughout the life cycle, beginning with embryogenesis. Except for its role in vision, the pleiotropic actions of this micronutrient include many systemic functions that are mediated at the gene level by all-trans-retinoic acid (RA), which is a ligand for specific nuclear transcription factors, the retinoid receptors: RARs and RXRs. When an RAR is activated by the presence of RA, it combines with an RXR, and the resulting heterodimer binds to target genes that have specific recognition sites. Thus, vitamin A, via its active form, retinoic acid, regulates many genes that are involved in the fundamental biologic activities of cells, such as cell division, cell death, and cell differentiation. Retinoic acid is among the most important signaling molecules in vertebrate ontogenesis. It affects many physiologic processes, including reproduction, growth, embryonic and fetal development, and bone development, in addition to respiratory, gastrointestinal, hematopoietic, and immune functions. The role of vitamin A in immune function and host defense is particularly important in developing countries, where vitamin A supplementation or therapy reduces the morbidity and mortality rates of various diseases, such as measles The best understood function of vitamin A is its nongenomic role in vision. The human retina has two distinct photoreceptor systems: the rods, containing rhodopsin, which can detect low-intensity light, and the cones, containing iodopsin, which can detect different colors. The aldehyde form of vitamin A, retinal, is the prosthetic group on both visual proteins. The mechanism of vitamin A action in vision is based on the ability of the vitamin A molecule to photoisomerize (change shape when exposed to light). Thus, in the dark, low-intensity light isomerizes the rhodopsin prosthetic group, 11-cis retinal, to all-trans-retinal, generating an electrical signal that is transmitted via the optic nerve to the brain and results in visual sensation.
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