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1. Are there UIs or RDAs for ultratrace minerals?
2. Where does absorption of most micronutrients occur?
1. Sources of iodine? (8)
2. Do processed foods or sea salt have iodized salt?
3. Which soils have more iodine? Iodine deficiency?
4. ^ Unless? (2)
1. SEAWEED, iodized food products (in US, bread, milk, iodized salt) & meat, fish eggs, breast milk!!!
3. Coastal. Iodine deficiency occurs in inland areas
4. Unless (1) There is iodine added into the food chain (i.e., iodized salt) or (2) diversification of diet, where foods for iodine-rich soil areas are brought in.
1. What is RDA for iodine?
2. How is dietary iodine found?
3. How is its absorption rate?
4. What blocks uptake in thyroid? Describie mechanism. What contains this? (4)
6. For the above, how can you get around this?
- 1. 90-290 micrograms
- 2. Either free or bound to amino acids
- 3. Well-absorbed during deficiency. In times of sufficiency, iodine absorption is <10% of intake.
- 4. linamarin. Linamarin is hydrolyzed by gut bacteria to form HCN --> thiocyanate. This is found in sweet potato, beans, cruciferous veggies, and millet.
5. By soaking/cooking the food to get rid of linamarin
1. What is the most preventable cause of mental retardation and endocrinopathy?
2. What is thyroglobulin? Where is it present?
3. What allows uptake of iodine in the cell? What else is imported?
4. What concentrates iodine in the thyroid?
5. Describe mechanism of thyroid hormone synthesis in the thyroid
1. Iodine deficiency
2. Thyroglobulin is the iodine carrier in the thyroid. It is present in the follicular lumen called the colloid
3. NIS (sodium-iodide symporter) - it imports both sodium & iodide in the same direction
5. (1) Follicular cell synthesizes enzymes & thyroglobulin for colloid (2) I- is co-transported into the cell w/ Na+ and is transported into the colloid (3) Enzymes (thyroperoxidase) add iodine to tyrosine --> added to thyroglobulin.
(4) Thyroglobulin - T3/T4 complex enters follicular cell from colloid
(5) Enzymes in follicular cell dissociate thyroglobulin from T3 and T4 and they're free to go into circulation.
1. What are the real names for T3 and T4?
2. How do T3 and T4 travel in blood? (3)
3. What is the ratio of T4 to T3 in the blood? Why? How are amounts regulated?
4. What transporters take up T3 and T4 into cell?
5. What happens first after T3 and T4 are taken up into target tissue?
6. What is the active form
1. T3 = triiodothyronine. T4 = thyroxine
2. Bound to carrier proteins (thyroxine-binding globulin or transthyretin (TTR seen in retiniol + RBP) or albumin
3. [T4] >> [T3] b/c T3 is very potent. The amounts are regulated by deiodinases
4. not known, just some random transporters
5. T4 is catalyzed by iodothyronine deiodinases into T3.
1. How does T3 act?
2. What does it bind to? What doe this require? What does the complex bind to? Then what?
3. How does T3 affect gene transcription?
1. As steroid hormone
2. Binds to thyroid hormone receptors in the nucleus, which require Zn fingers for structural complex. T3-thyroid hormone receptor complex heterodimerizes with RXR. They then bind to TRE (T3 response element)
3. In the presence of T3, corepressors fall off and HAT activates transcription.
Describe how stress/cold activate T3 or T4
Stress and cold act as signal inputs into hypothalamus which releases TRH --> anterior pituitary ---> releases TSH --> thyroid gland producing T3 and T4.
T3 and T4 come back as feedback inhibition to inhibit hypothalamus and anterior pituitary.
What are actions of thyroid hormone overall (5)
1. Increases basal metabolic rate:
- Affects lipid metabolism (increases lipolysis/oxidation, lowers cholesterol & triglycerides)
- Carb metabolism (stimulates all aspects of carb metabolism, esp GNG and glycogenolysis to generate free glucose)
- 2. Affects growth (def = growth retaration, works with GH)
- 3. CV system (increases heart rate, contractility, output, vasodilation, etc)
- 4. CNS (too little T3/T4 -> sluggishness. Too much = anxiety)
5. Reproductive system (hypothyroidism --> infertility)
1. What causes a goiter?
2. What does iodine deficiency lead to overall?
3. How much of global population has mild-severe iodine def? severe def?
4. What happened w/ the chernobyl nuclear reactor?
5. What was used in poland? How did it help?
- 1. I def or toxicity
- 2. Growth impairment, cognitive impairment
- 3. 30%. Rare
- 4. Iodine-131 was released, penetrated thyroid gland causing mutation --> thyroid cancer.
- 5. SSKI (saturated solution of potassium iodide) as prophylactic measure. Prevented risk of developing thyroid cancer by preventing the amount of iodine-131 absorbed by thyroid
1. How does iodine deficiency lead to neurocognitive impairment?
2. What else does it do to prenatal child? 3
3. Is I toxicity common? why or why not?
4. What are symptoms of acute poisoning? (4)
5. What does excess I in the system do? Which leads to? Which also leads to? 1
1. B/c it has something to do with neuronal migration and myelination
2. Stillborn births, abortions, congenital defects
3. No, b/c most people have a high tolerance for I.
4. GI irritation, coma, cyanosis, CV symptoms
5. Stops production of T3 and T4 --> increased TSH stimulates thyroid --> goiter
1. What are clinical applications of iodine? 1
1. Radioactive iodine (I-131) absorbs iodine which destroys thyroid gland (including cancer cells) that take up iodine w/ little effect on the rest of the body.
1. What are the functions of fluorine? (4)
2. What has high affinity for fluoride?
3. What contains calcium fluoride? Where is this found? (2)
1. (1) Protects against dental cavities - pathological demineralization of calcified tissues (2) Not an essential function, but a pharmacological one (3) Stimulates mineral deposition and new bone formation (4) Decrease acid prodouction by oral plaque-producing bacteria.
3. Hydroxyapatite (bone & teeth)
1. Describe absorption/bioavailability of fluoride? What limits bioavailability
2. Where is it stored? (2) What does this account for F in body?
3. What are the two types of pool storing fluoride?
4. What else can be mineralized
5. What happens to excess fluorine?
6. Is toxicity possible? What is it called? What does this cause? Is it lethal?
1. Very bioavailable, absorbed via passive diffusion. Absorption decreases to 50-80% when consumed w/ solid foods or calcium.
2. Stored in bone and teeth (99%)
3. Amorphous state (rapidly exchanging pool) and crystalline state (slowly exchanging pool)
5. Peed out
6. Yes. its called fluorosis and can lead to bone, kidney, nerve, and brain damage --> GI symptoms/cardiac arrythmias --> DEATH HAS BEEN REPORTED
1. What is chromium transported with?
2. What are Cr's valence states? Which is most stable? Which is found in food? Is it well-absorbed?
3. What is special about this?
- 1. Transferrin
- 2. 3+ and 6+ (3+, 3+) NO
3. It can improve glucose tolerance by potentiating insulin action. Works best in those w/ some kind of impaired glucose tolerance.
1. What is the main function of Mb? (2)
2. Where is it found?
3. How often is def seen? Usually in what type of people?
4. What is the main Mb containing co factor?
- 1. Redox rxns and cofactors
- 2. Meats
- 3. Not very often, usually seen in people on TPN for more than 18 months
- 4. Molybdopterin
1. What is the main purpose of Mn?
2. What are the two special enzymes associated with Mn? Where is the second one found?
3. What happens with As deficiency? Is it essential? What is it categorized as?
1. Activates enzymes in almost every class.
2. PEPCK and Mn-SOD (mitochondria)
3. Lower reproductive success. No. It's classified as a human carcinogen
1. Which ultratrace min has role in embryogenesis?
2. Which one is 2nd to O in earth-wide abundance? What is it important for?
3. What inhibits Na/K+ ATPase?
4. What mimics action of insulin?
5. What's the other one?
5. Nickel - can substitute for Mg