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Micronutrients 1

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University of Guelph
NUTR 3210
Genevieve Newton

Summary Micronutrients 1: Vitamin A, vitamin D and iodide. Vitamin K, calium, phosphorus and fluoride (associated) Micronutrient basics -Minerals are inorganic and vitamins are organic. -When vitamins aren’t present in diet or aren’t absorbed or utilized properly, a deficiency disease will result. -Vitamins can’t be made, you need to get them from the diet. Type II SHR (steroid hormone receptors) • Present in the nucleus of the cell • Bind to both steroid hormones and non-steroid hormone ligands • Ligand/receptor complex forms a transcription factor that can up- or down-regulate the expression of genes. Most of the time it will up-regulate. • Ones of interest to us: thyroid hormone (iodine), retinoic acid (vitamin A), calcitriol (vitamin D, related to steroid hormone. The other ones are non-steroid ligands) Iodine • We call it iodide because in most food sources and in our bodies iodine is found in its ionic form (I-) • It is very poorly distributed globally so there are serious problems with deficiencies in developing countries (13% of the world’s population) •Iodine is the only micronutrient that is taken up by only one organ (thyroid gland) if it isn’t already saturated with iodine. •Iodide enters the thyroid gland via active transport and gets converted to T3 and T4 thyroid hormones (1:20) (see next point for how) T4 is the precursor to T3 (active form) so the body makes lots of precursors. • T3 & T4 is made in thyroid gland from post translational modification of thyroglobulin, involving an attack by a reactive Iodide radical. •T4 gets converted to T3 in the liver via 5’-deiodinase which is a selenoprotein. • Mostly T4 in circulation, with T3 (active) being formed in the liver • Levels of T3 are monitored by hypothalamus. When T3 levels are low, the hypothalamus sends a signal via TRH (thyrotropin releasing hormone) to the anterior pituitary which sends a signal via TSH (thyroid stimulating hormone) to the thyroid gland to make more thyroid hormones. •If iodide is not present in the thyroid gland, this cycle will become very active and TSH builds up, cells get bigger and you have major problems. • Proteins are expressed in response to T3 include growth hormone and mineral ATPases, which regulate metabolism • Iodide deficiency causes hyperplasia and hypertrophy of the thyroid gland (goiter) and mental retardation (cretinism) Vitamin A : Family of molecules. Fat soluble •Includes beta carotene, other carotene (plants) and Retinyl esters (animals) which get converted to retinol, retinyl palmitate, all-trans retinal, 11-cis retinal and retinoic acid (active forms) • Main plant provitamin (precursor to vitamin A) is beta carotene, which is the orange pigment in plants (also other carotenes, but minor importance, although they can similarly be converted to retinal). It acts as an antioxidant in the plant, but not so much in animals. • Animal forms are retinyl esters (mainly retinyl palmitate; storage form in animals). A lot is found in liver and egg yolks and milk. • Beta carotene can be clipped to 2 molecules of retinal by 15,15’dioxygenase and then oxidized to retinol BUT it can also be stored as beta carotene in adipose • Activity of 15,15’dioxygenase is down regulated when levels of retinol are high. •Retinyl esters (from meat) and beta carotene (from plants) are consumed and found in fat droplets in the stomach •Beta carotene enters directly into the intestinal mucosal cell (doesn’t get digested). Then it can either undergo cleavage to retinol (see above) or nothing happens to it and it gets incorporated into the chylomicrons. •Retinyl esters get digested to retinol via pancreatic retinyl esterase and then retinol enters the IMC. Retinol is a detergent so it has to get converted to retinyl palmitate to be stored or transported in chylomicrons. •As the chylomicron goes around the body to drop things off, beta carotene and retinyl palmitate stay on until the remnant gets to the liver. •When they arrive at the liver, the beta carotene gets incorporated into VLDL and gets distributed to the adipose tissues (mainly). If you get too much of this, you’ll turn orange. • Retinyl palmitate can be stored in the liver in stellate cells or re-converted to retinol via retinyl esterase. The retinol combines with retinol binding-protein (RBP) for transport to target tissue. This complex is not active, but it is a homeostatic set point (precursor to vitamin A). •Retinol-RBP regulates 15, 15’ dioxygenase and retinyl esterase. • Two functions of vitamin A: (1) night blindness (active form 11-cis-retinal) and (2) gene expression (retinoic acid) • In night vision: retinol RBP in bloodretinol in tissue  all-trans retinal 11-cis-retinal + opsin  rhodopsin Isomerase The light in a dim room strikes retina (where rhodopsin is) and rhodopsin snaps apart, reforming opsin and all Trans retinal. Bright light causes all rhodopsin to be destroyed to it takes a while to adjust to dark rooms because you need to reform rhodopsin. • In gene expression, retinol all-trans retinal  retinoic acid + retinoic acid receptor/retinoid X receptor (dimerizes) increased transcription of growth hormone, decreased transcription of collagenase, amongst others. •Because there are 2 types of receptors, each with several family members, a lot of different transcription factors will be able to be formed, so a lot of genes will be able to be regulated. On top of that, there is homodimerization and heterodimerization, i.e. each ligand-receptor complex will form a dimer with a different of same ligand-receptor complex. Basically, a lot of proteins are regulated by vitamin A Vitamin A deficiency •Night blindness is the first sign of vitamin D deficiency. Reversible. •Vitamin A is needed for proper epithelial cell differentiation, and impaired epithelial cell differentiation can cause blindness and life-threatening infections as consequences. If stem cells don’t differentiate, they go to default and make keratin which builds up on these undifferentiated cells and cells can’t do their job to protect body from infections. •Impaired growth and fertility. • Vitamin A deficiency is the leading cause of preventable blindness, and major cause of death in developing countries, particularly among young people. • RDA is measured in Retinol Activity Equivalents (accounts for intake of carotenoids) • UL is only concerned with intake of retinol (beta-carotene is safe) • Narrow therapeutic index (TI) Vitamin A toxic
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