NUTR 3210 Study Guide - Final Guide: Retinoic Acid Receptor, Basal Metabolic Rate, Vitamin K

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Micronutrients 1
What are characteristics for classification as a vitamin?
- Exogenous supply is required b/c body can’t produce it (or produce quickly)
- Needed in the amounts
- Distinct from sugars, fats, and proteins in regard to structure + function
- Performs at least 1 essential biochemical function in the body
- When lacking in diet, a characteristic deficiency disease develops
- Vitamins are organic
primary distinction from minerals
minerals = inorganic
What are the functional groupings of micronutrients?
- Group 1: Micronutrients that control type II steroid hormone receptors ( TF) and
have major global health implications
Iodine Vit.A Vit.D Calcium Vit.K Phosphorus Fluoride
- Group 2: Micronutrients that work together in oxidant defense
Vit.E Selenium Vit.C Niacin Riboflavin Copper Zinc Manganese
- Group 3: Micronutrients that act as enzyme cofactors
Thiamin Niacin Riboflavin Vit.B6 Folate Vit.B12 Biotin
Pantothenic acid
- Group 4: Iron Copper Zinc-related divalent cations
What’s up with Group 1?
- They are ligand-activated, something has to bind them
- Not all act directly on steroid hormone receptors (only vit.A, vit.D, and iodine)
vit.D = calcium = phosphorus = vit.K (involved bone metabolism)
- Vit.A consumed as retinol (animal based source) or beta carotene (plant), which
is eventually converted into retinoic acid = bioactive form that activates TF = the
ligand
- Vit.D precursors converted to calcitriol, which regulates calcium levels in the
body
- Iodine used to make T3 hormone = regulates synthesis of proteins that control
basal metabolic rate
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What are the 2 types of steriod hormone receptors?
- SHRs are intracellular protein receptors that bind ligands and become active
transcription factors
1) Receptors Cytosolic:
Respond to steroid hormones like estrogen, testosterone, glucocorticoids
2) Receptors Nuclear:
Respond to steroid and non-steroid ligands, like thyroid hormone, retinoic acid,
and calcitriol.
- TF in cytosol in inactive activates when ligand binds
- Not all ligands and derived from steroids
- SH transported bound to plasma carrier protein lipophilic move across
plasma membrane binds to cell cytoplasm receptor translocates as a
complex to nucleus binds to DNA (acts as a TF) stimulates gene
transcription protein produced response
How is Iodine absorbed?
- Iodine is very H2O soluble
- Seafood has high concentrations
- Salt fortified with potassium iodide
- Typically found in the body in ionic form (I-); 70-80% located in thyroid gland.
- Dietary I can be bound to AA or found free
bound = rapidly convert to I- and absorb
most absorption in stomach
- In blood, free I- is found and can enter all tissues
most accumulate in thyroid gland, specially thyroid follicles
- Uptake in thyroid meditated by an active transport system known as (Na+/I-)
symporter (NIS) = allows uptake into follicles
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How iodide is transported and its functions?
- All tissues depend on THs T3+T4 rather than iodide (lipophilic)
- Once T3 + T4 made, they are secreted into blood and transported by specific
carrier proteins (albumin)
- 50x more T4 in plasma compared to T3, BUT T3 100x more potent b/c bioactive
T3 half-life < T4 ∴ more T4 b/c lasts longer
- T3 interacts with THR (thyroid hormone receptor)
- T3 + T4 production regulated by TSH (thyroid stimulating hormone)
- Dietary iodide GIT (I-) blood I- through NIS to thyroid to make T3 + T4
(storage + secretion) T4 to liver to convert to T3 by 5’ deiodinase enzyme
T3 in blood to regulate metabolic rate & growth by THR interaction brain
hypothalamus sense low levels of T3 signals to pituitary to release TSH.
How does iodide make thyroid hormones?
- Follicles take up iodide from blood
- In the colloid, iodide is oxidized to from a free radical,
TPO helps attach it to a tyrosine residue in thyroglobulin
- THG peptide is made up the follicle cells with lots of Tyr chains on it (found in
colloid)
- Iodide is brought from the blood into follicular cell by NIS transporter. Then into
the colloid by a transporter called Pendrin
- Iodine Iodide by TPO and added to THG
- Iodide radical attacks Tyr residues in THG via 2 ways:
1 iodine on Tyr ring = monoiodotyrosine
2 iodines on Tyr ring = diiodotyrosine
- Tyrosine molecules joined = THs
T3 : MIT+DIT
T4 : DIT+DIT
- T3+T4 still attached to the THG, THG taken up by follicular cells, thyroid cell
proteases hydrolyze THG releasing (mostly) T4 and T3
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Document Summary

Exogenous supply is required b/c body can"t produce it (or produce quickly) Distinct from sugars, fats, and proteins in regard to structure + function. Performs at least 1 essential biochemical function in the body. When lacking in diet, a characteristic deficiency disease develops. Group 1: micronutrients that control type ii steroid hormone receptors ( tf) and have major global health implications. Iodine vit. a vit. d calcium vit. k phosphorus fluoride. Group 2: micronutrients that work together in oxidant defense. Vit. e selenium vit. c niacin riboflavin copper zinc manganese. Group 3: micronutrients that act as enzyme cofactors. Thiamin niacin riboflavin vit. b6 folate vit. b12 biotin . They are ligand-activated, something has to bind them. Not all act directly on steroid hormone receptors (only vit. a, vit. d, and iodine) Vit. d = calcium = phosphorus = vit. k (involved bone metabolism) Vit. a consumed as retinol (animal based source) or beta carotene (plant), which is eventually converted into retinoic acid = bioactive form that activates tf = the ligand.

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