Metabolism Exam 2

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  1. What type of vitamin is Vit A
    Fat soluble
  2. Who isolated yellow-orange pigment from carrots, what did he name it?
    Wackenroder, carotene
  3. Who cured night blindness? With what?
    Snell, cod liver oil
  4. Who discovered "fat-soluble A" was needed for rat growth? Where did he find it?
    McCollum, cod liver oil and butter
  5. Who isolated retinol from liver oil? What did they win?
    Karrer, Nobel Prize
  6. Describe Vit A structure
    Long tail, hydrophobic, and H's structure is based largely on isoprenoid units.
  7. Image Upload
    Vitamin A
  8. What are retinoids?
    Vitamin A
  9. 4 forms of retinoids, what are they collectively?
    All-trans retinol, retinal, retinoic acid and retinyl ester (collectively Vitamin A)
  10. Retinol can be oxidized to what? Is it reversible or irreversible?
    Retinal, reversible
  11. Retinal can be oxidized to what? Is is reversible or irreversible?
    Retinoic Acid, irreversible
  12. What helps oxidized retinal to retinoic acid?
  13. What is 2 molecules of Vit A attached tail to tail?
  14. What gives food its orange/red color?
  15. What is the generic descriptor for compound exhibiting biological activity of retinol (and some carotenoids)
    Vitamin A
  16. Can all carotenoids be converted into Vit A?
    No, only about 60
  17. Preformed retinol-animal products include:
    liver, egg, yolk, margarine, milk (fortified), fish, and cod liver oil
  18. What is Vit A supplement form?
    Usually ester (retinyl palmitate)
  19. Most frequent Vit A food form?
    Retinyl palmitate
  20. What is retinol typically bound to?
    Fatty acid esters (palmitate)
  21. What are carotenoids and retinyl palmitate often bound to?
  22. Where are carotenoids and retinyl palmitate found?
    • Sweet potatos, carrots, spinach, cantaloupe.
    • Not much in eggs.
  23. Describe Vitamin A absorption
    Digestive enzymes break down protein and liberate carotenoids/retinyl esters. Digestive enzymes then remove palmitatic acid leaving carotenoids and free retinol. The cleaved fatty acids/phospholipids mix with bie ad are incoprated in the the micelle and are taken to the intestinal cell. Beta-carotene, retinol, and carotenoids reside in the micelle. Retinol is liberated from the micelle. Beta-carotene is split into 2 retinals. Retinol and retinal are bound by CRBPII (retinal will be reduced to retinol when it binds). LRAT then adds a fatty acid (palmitate) back to form an ester so that it can exit the cell and be packaged into the chylomicron. Once packaged in chylomicron, Vit A is secreted from the intestinal cell and enters the lymph system which drains to thorasic vein and is released directly to the blood stream. In this way, the liver is totally bypassed.
  24. What allows retinol and retinal to become soluble?
  25. What protects retinol from being oxidized?
  26. How are carotenoids absorbed?
    They are absorbed intact and are cleaved within the mucosal cell OR can be transported to portal blood circulation. They can be cleaved in the liver by 15,15-dioxygenase
  27. What does retinol bind to in order to be stored in the liver?
    CRBPI (if esterified)
  28. Where is Vit A stored in the liver?
    Stellate cells
  29. apo-RBP
    no retinol bound
  30. holo-RBP
    retinol bound
  31. Describe trimolecular complex
    Retinol binds to TTR and T4 to reduce kidney filtration. If retinol was not bound we would lose it in our urine.
  32. How do we get Vit A in our cells?
    holo-RBP binds to RBP receptor, the complex is endocytosed, retinol falls off and is released into the cell.
  33. Functions of Vitamin A
    • Vision
    • Cellular Differentiation/Gene Expression
    • Growth
    • Immune System
    • Bone Development
    • Reproduction
  34. Describe Vitamin A's role in vision
    Vitamin A as II-cis-retinal serves as functional group in protein called rhodopsin which is found in rod cells of the retina. Rhodopsin detects small amounts of light important for night vision. In night vision, cis-retinal is coverted to trans-retinal when light hits it. Trans-retinal is released from opsin to reform rhodopsin to go another cycle (trans is converted back to cis).
  35. What is the main purpose of the visual cycle?
    To regenerate II-cis-retinal
  36. What can be stored and hydrolyzed to II-cis-retinal?
    Retinyl esters. If there aren't enough of these there will not be enough II-cis-retinal
  37. What causes night blindness?
    Failure to regenerate II-cis-retinal
  38. Cellular differentiation
    Process whereby an immature cell is transformed into a specific type of mature cell
  39. What is needed for keratinocytes to mature and what are keratinocytes?
    Need Vit A in the form of retinoic acid, they are immature skin cells
  40. What happens if you don't have retinoic acid?
    You won't make mucous and secreting cells/keratinizing cells will build up and replace them - result is rough, dry skin
  41. What happens to membranes without Vitamin A?
    • They are more permeable for bacteria.
    • Cell dif is important for bronchial passages with a barrier function - deficiency will compromise this function and increase risk of infection.
  42. What is retinoic acid bound to cytosol? Where does it go/do from there?
    Does not float freely! Bound to CRABP which serves as a chaperone and transports it to the nucleus. Retinoic acid can then bind to specific receptors that form dimers and bind to DNA/affect transcription rates of specific genes and gene expression.
  43. Difference between CRBP and CRABP?
    • CRBP serves in storage and transport
    • CRABP binds to retinoic acid to bring to nucleus (Chaperone)
  44. What do CRABP- bound all-trans-retinoic acid and 9-cis-retinoic acid do?
    Translocate into nucleus and bind to specific receptors?
  45. What receptors to CRABP-bound all trans-retinoic acid and 9-cis retinoic acid bind to?
    RAR and RXR
  46. RAR is for?
    all-trans-retinoic acid
  47. RXR is for?
    9-cis-retinoic acid
  48. What do vitamin bound RXR and RAR do?
    Bind to DNA at specific sites called Retinoic acid response elements (RARE), located in the promoter region of specific genes. This binding results in increased transcription of specific genes.
  49. What do retinoids do?
    • 1) Act as nuclear hormones involved in "signalling" pathways
    • 2) Act as transcription factors that regulate the activation or repression of mRNA formation in the nuclei.
  50. What do vit A-DNA complexes affect?
    • Cell differentiation
    • Apoptosis
  51. Vitamin A and growth?
    Vit A def will impair growth which can stimulated with retinol and/or retinoic acid
  52. How does retinoic acid stimulate growth?
    Increases expression of growth receptors on cell surface
  53. What is conjunctiva?
    Thin membrane that causes your eye to keep moisturized
  54. Zeropthalmia
    Dry eyes
  55. What happens if eyes get too dry?
    Keratin deposits, conjiunctiva will wrinkle and will eventually lead to irreversible blindness
  56. Bilateral keratomalacia
    Vit A deficiency that leads to irreversible blindness
  57. Vit A Def results in?
    Multiple abnormalities in innate and adaptive immunity involving: cell differentiation, hematopoiesis, blood/lymph organ cell populations
  58. Does Vit A affect ability to respond to pathogens/antigens?
  59. Vit A increased/decreases # and function of:?
    • B cells
    • T cells
    • Natural Killer Cells
    • Antigen-presenting cells
    • Macrophages
  60. Accutane
    Synthetic retinoid - gets cells to differentiate normally, to help treat acne.

    Can increased congential defects. Malformed craniofacial with low-set, small/absent ears, malformed facial bones, cardiac/thymus/CNS defects
  61. How many worldwide child Vit A deficiencies?
    20-40 Million
  62. How many children go blind each year?
  63. Subclinical Vit A def can lead to:
    Increased risk of respiratory/diarrheal infections, decreased growth rates, slow bone development, decreased survival from serious illnesses
  64. Children with measles risk are treated with
    Vitamin A
  65. How to indicate Vitamin A status?
    • Liver biopsy
    • Plasma retinol (poor unless severe def)
    • Relative dose response test
    • Conjunctival impression cytology
  66. What's more efficient? B-carotene or retinol?
  67. 1 RAE = ? retinol = ? B-carotene = ? a-carotene
    • 1 microgram retinol
    • 12 micrograms B-carotene
    • 24 micrograms a-carotene
  68. Vitamin A RDA
    • Males - 900 RAE
    • Females - 700 RAE
    • Preg - 770 RAE
  69. Vitamin A UL
    3000 micrograms/day
  70. Vit A toxicity symptoms
    Nausea/Vomiting, headache, dizziness, blurred vision, lack of muscular coordination, abnormal liver function, pain in bones/joints <-- usually from too much supplement or liver
  71. Is beta-carotene toxic?
    No, it is non-toxic but you can turn orange in you have too much!
  72. Vitamin K is known as
  73. Who found that cabbage can prevent clotting defect?
    Hoist and Holbrook
  74. Who proposed Vit K when showing fat-soluble factor in green leaves corrects clotting defect?
  75. Who determined Vit K structure?
    Dam and Doisy (Each got nobel prize)
  76. What is Vit K made of?
    isoprenoid units
  77. Image Upload
    Vitamin K
  78. When you hear fat-soluble vitamins you should think...
  79. 4 Biologically active Vit K forms:
    • 1) Phylloquinone (found in plants)
    • 2) Menaquinone-4 (bacteria)
    • 3) Menaquinone-9 (bacteria)
    • 4) Menadione
    • (first 3 are found in foods)
  80. Vit K is found in
    Kale, Spinach, green leafy veggies, egg yolk
  81. Vit K is not found in
    Meat, Milk, Fruit
  82. How is Vit K absorbed?
    Brought into micelle which brings it to intestinal cell, incorporates it into chylomicron, enters lymph, thorasic vein and general blood circulation. ABsorption is enhanced by dietary fats, bile salts, and pancreatic juice (pretty much the same as Vit A).
  83. What would reduce Vit K absorption?
    • Pancreatic insufficiency
    • Bile insufficiency
    • Celiac Disease
  84. What happens with phylloquinone and menaquinone in hepatocyte?
    They are incorporated into LDL and transported to periphera
  85. What happens to menadione?
    It is alkalated with isoprenyl and converted to menaquinone.
  86. How much Vit K is stored and where?
    Very small amount stored in liver
  87. What is Vit K needed for?
    Posttranslational carboxylation of gluatmic acid residues in proteins to form gama-carboxyglutamic acid residuces which are needed for formation of blood clots and bone mineralization.
  88. What is required for blood clotting and bone mineralization and how does it work?
    Dihydroquinone form is needed.
  89. When you think Vit K, think..
    • blood clotting proteins!
    • Prothrombin
    • Factos VII, IX, X
    • Protein C
    • Protein S
    • Protein Z
    • (All synthesized in liver)
  90. Vit K's main role in blood clotting:
    Converts inactive clotting factors to active clotting factors
  91. Prothrombin Time Test
    measures the time it takes to form a clot. Most common test for Vit K deficiency
  92. Warfarin
    Keeps from clotting (for people with stroke or heart attack issues). Can also be used as rat poison
  93. Where did warfarin name come from?
    Wisconsion Alumni Research Foundation
  94. How does Warfarin work?
    Inhibitins quinone reductase which keeps Vit-K from being regenerated after use. (remember, quinone reductase produces dehydroquinone which is what is needed for clotting)
  95. Vitamin-K dependent bone proteins
    Osteocalant Matric Gla protein
  96. Oxteocalcin
    Holds calcium by your bones
  97. Matrix Gla Protein (MGP)
    Associated with mobilization of bone calcium
  98. Vit K deficiency markers
    PIVKA and undercarboxylaed oxteocalcin
  99. Vit K def found in
    • GI maladaptive disorders
    • newborns

  100. AI for Vit K
    • Male: 120 micrograms
    • Female/Preg/Lact: 90 micrograms
  101. UL for Vit K
  102. Phylloquinone and menaquinone..toxic or nontoxic?
  103. menadione..toxic or non-toxic?
    Can be toxic (liver damage, jaundice)
  104. Image Upload
  105. Who did phd thesis on rickets?
    Daniel Whistler
  106. Who recommended cod liver oil as rickets treatment?
  107. Who induced rickets in puppies/treated them with butter and cod liver oil/determined it was a Vit A issue?
  108. Who showed that heating cod liver oil destroyed Vit A activity but retained rachitic activity? Called heat stable factor Vit D?
  109. Who cured rickets with UV lamp?
  110. Two forms of Vit D?
    D2 and D3
  111. Heat stable fraction of Vit A is?
    Vit D
  112. Who first described Vit D2 and D3 and won a Nobel prize?
    Aldolf Windaus
  113. What is Vit D3 sturcture called and what does it consist of?
    Cholecalciferol. Has 3 steroid rings and an 8 carbon side chain
  114. What can you convert Vit D from? How does this work?
    Vitamind D can be converted from 70dehydrocholesterol. This conversion can occur in the skin, catalyzed by UV light.
  115. What is 7-dehydrocholesterol synthesized from?
    It is synthesized in the body from a molecule called squalene which is derived from isoprene units
  116. What is DBP?
    Vitamin D binding protein
  117. Cholecalciferol
    Vit D3
  118. Where is cholecalciferol found (what foods)?
    ONLY found in animals: fish liver and fish oils
  119. Ergocalciferol
    Vitamind D2
  120. Where is ergocalciferol found (What foods)?
    Plants, present in only small amounts, common supplement form, less biologically active than D3.
  121. Overall Vit D food sources
    sardines, herring liver, poultry skin. Almost exclusively in animal foods. Sun-dried shitaki mushrooms also.
  122. What foods are Vit D fortified?
    Milke, OJ, Cereal, Yogurt, Cheese, Formula
  123. Vitamin D absorption
    D2 and D3 are absorbed just like Vit K. It is incorporated into the micelle, packaged into chlomicron, and enters lymph system.
  124. Vitamin D Hepatic Metabolism (how does this work?)
    • When Vit D is taken up by the liver it is hydroxylated at the 25 position by enzyme: 25-hydroxylase. It then binds to DBP in the liver and then is secreted into the plasma which circulates/transfers Vit D to other tissues. (as 25-OH D3).
    • Most important tissue to take it up is kidney which hydrolyzes it again.
  125. What is a good indicator of Vit D status?
    25-OH D3 is a good indicator of status because this is how it circulates.
  126. Renal hydroxylation of Vit D
    Here hydroxylation happens at position 1 (not 25). 25-OH D3 is hydroxylated at position 1 and becomes 1,25(OH)2 D3 which is also known as Calcitriol.
  127. Active form of Vitamin D
    Calcitriol (1,25 OH2 D3)
  128. Overall how Vit D is absorbed
    • Sunlight/UV rays hit skin and convert 7-dehydrocholestrol to cholescalciterol
    • This is transported to the liver which makes 25-hydrooxyvitamn D3
    • This is transported to the kidney which makes 1,25-dihydroxyvitamin D3 which is what circulations
  129. One of main functions of Vit D
    Maintain calcium balance in the body
  130. More sun exposure =
    More Vit D
  131. Skin pigment and sun exposure
    Dark-skinned individuals may required 5-10x more sun exposure to generate same amount of D3 as light-skinned individuals
  132. Do elderly generate as much D3 as young?
    No. (Therefore also a function of age)
  133. What happens if you make a lot of 1,25 hydroxyviamin D3?
    24-hydroxylase converts it to 1,24,25 dihydroxyvitamin D3 which is catbaolized to become soluble and secreted in urine.
  134. What is active form of Vit D3?
    1, 25 OH2 D3
  135. What will Vitamin D3 bind to in order to facilitate its' release into tissues?
  136. If rental 1-hydroxylase is deactivated..
    25-OH D3 will increase and 1,25 OH2 D3 (the active form) decreases, leading to rickets
  137. What enzyme is very important to maintaining serum calcium levels?
  138. Two main mechanisms of functioning for 1, 25 OH2 D3
    • - Functions like a hormone because it activates a pathway
    • - Affects gene expression
  139. Resorption
    Mobilization of Ca from the bone
  140. 1, 25 OH2 D3 helps to maintain blood Ca by acting on:
    • Intestine: increases Ca absorption
    • Kidney: increases Ca resorption
    • Bone: increases Ca mobilization from bone
    • - Works with PTH
  141. Blood calcium level regulation
    Very tightly regulated. If it dips too low or too high you can die.
  142. Main purpose of 1,25 OH D3 and PTH is:
    to provide plasma Ca for neuromuscular function
  143. How does 1,25 OH2 D3 relate to Ca absorption?
    Increases absorption of Ca (and P)
  144. 1,25 OH2 Dr and Ca absorption: how does it work?
    Ca enters the intestinal cell by an unknown specialized channel, crosses apical membrane and into basal membrane.

    Vit D enters the intestinal cell and binds to VDR which travels to the nucleus and stimulates the transcription of a number of genes, one which is called calbindin which binds calcium. Calbindin protein levels will increase, go to brush border, and facilitate calcium absorption
  145. Function of Calbindin
    Binds calcium!
  146. What happens to calbindin during Vit D deficiency?
    It decreases..
  147. 1,25 OH2 D3 and gene expression: how does it work?
    Vit D3 binds to VDR which forms a dimer or heterodimer with RXR and this binds to a specific region in DNA called the vitamin D response element (VDRE). This initiates the expression of genes one of which is calbindin.
  148. What does VitD do in the kidney?
    Vit D stimulates TRPV5 which reabsorbs calcium prom pro-urine and transports it into the blood. Vit D, thus, helps to reabsorb calcium in kidney and prevent calcium loss in urine.
  149. PTH
    Helps to release calcium
  150. Bone resorption
    Process by which osteoclasts break down bone and release Ca and P
  151. Osteoclast Maturation
    Osteoclasts come from preosteoclasts which only develop into osteoclasts when they bind to osteoblasts though protein called RANKL. RANKL is formed on the surface of an osteoblast when PTH increases 1-hydroxylase in the kidney and causes formation of 1,25 dihydroxy D3. This binds to preosteoclasts leading to osteoclast, releasing ca from bond and increases ca levels. BASICALLY when you have low blood calcium, you want to increase PTH and Vit D3 because they work together.
  152. Other tissues that respond to Vit D Deficiency
    • Pancreas - increase diabetes risk
    • Brain - abnormal behavioral changes
    • Immune cells - autoimmune disease
    • Skin - abnormal cell differentiation
  153. Is there an association between VitD status and type 1 diabetes?
  154. Can Vit D be used clinically to treat autoimmune diseases?
  155. Vitamin D is useful for:
    • Psoriasis
    • Osteomalacia/Oxteoporosis prevention
    • Muscle strength- fall prevention
    • Bone Integrity
    • Cancer
    • Multiple Sclerosis
  156. Rickets
    • Failure of bones to mineralize
    • Infants and children get this from Vit D deficiency
  157. Osteomalacia
    Demineralization of bone resulting from inadequate amounts of Ca and P. Result of Adult Vit D deficiency.
  158. Vitamind D RDA
    • 0-12mo: 400 IU
    • 1-18y, 19-50y, 51-70y: 600
    • 71+y: 800
    • Preg/Lact: 600
  159. Vit D UL
    • 0-6mo: 1000 IU
    • 6-12mo: 1500 IU
    • 1-3y: 2500 IU
    • 4-8y: 3000 IU
    • 9-71+, Preg/Lact: 4000 IU
  160. Vit D Toxicity
    Can result in hypercalcemia and calcification of soft tissues but takes ALOT.
  161. Who identified factor in veg oil that was required for reproduction in female rats? What did they call it?
    Evans and Bishop. Called it Vitamin E.
  162. What is Vitamin E also known as and what is the meaning of this word?
    • tocopherol
    • tokos=childbirth
    • pherein=to bear or carry
    • (appropriate because needed for rats to reproduce)
  163. Who synthesized Vit E?
  164. Image Upload
    Vitamin E
  165. What are the different forms of Vitamin E?
    4 tocopherols and 4 tocotrienols (the enols have an unsaturated side chain)
  166. What is the only Vit E form that meets human vitamin E requirement?
  167. Major Vitamin E Food Sources
    Vegetable oils, margarine, mayonnaise, wheat germ, nuts, and seed.

    Mainly found in foods of plan origin (not really in meat or fish)
  168. Vitamin E absorption
    Same as Vitamin E
  169. Vitamin E Hepatic metabolism
    Vitamin E is taken up by chylomicron remanent receptors and released once inside the liver. Alpha-tocopherol transfer protein binds to Vit E and transfers it it VLDL. This will only work for the alpha tocopherol form. Once converted to VLDL it is transported to peripheral tissues.
  170. Are Vit E forms interconvertible?
  171. What is the main Vit E type in oils?
    gama-tocopherol which will be absorbed by the liver and the excreted.
  172. Fate of Vit E forms other than alpha-tocopherol
    They are absorbed in the liver but NOT packaged and are, thus, excreted.
  173. Does vitamin E have a specific transport protein? If so what is it?
  174. How is tocopherol delivered to tissue?
    • With different mechanisms:
    • Lipoprotein lipase-mediated lipoprotein catabolism
    • Lipoprotein receptors
    • Membrane lipid transporters
  175. Primary storage site of Vitamin E
  176. Major route of Vitamin E excretion
  177. Describe Vitamin E's role as an antioxidant
    • Functions as a lipid-soluble chain-breaking antioxidant
    • Neutralizes lipid peroxyl radicals which are involved in oxidation of lipids
    • Protects PUFA within phospholipids
  178. Vitamin E and lipid peroxyl radicals
    Vitamin E reduces lipid peroxyl radicals
  179. Explain Lipid Peroxidation
    • Chain goes on forever.
    • Unsaturated fatty acid +hydroxyl radical --> carbon-center radical --> lipid peroxyl radical (which initiates propagation, aka repeats process)
    • Vit E acts as a reducing agent by providing the H that the peroxyl radical needs and ends the free radical reactions. A Vit E radical is formed but it is still quite stable.
  180. Explain regeneration of Vitamin E
    A-tocopherol becomes radical and needs a H. It gets it from ascorbic acid which becomes dehyroascorbic acid which gets one from 2GSH which gets one from NADPH.
  181. Vitamin E Deficiency can lead to:
    • Oxidative damage of tissues, membrane damage of cells and sub-cellular organelles
    • Oxidative species damage structural and functional compounds
    • Neurological abnormalities
    • Muscular function
    • Membrane instability leading to hemolytic anemia
  182. Where is Vitamin E Def found?
    It is very rare and pretty much only found in pre-me babies, people with fat-malabsorption disorders, and ataxia.
  183. Vitamin E RDA
    15 mg/day
  184. Vitamin E UL
    1000 mg/day
  185. Why is there a Vit E UL?
    Excess Vit E can interfere with the function of vitamin K which will result in increased risk for hemorrhage.
  186. What is calcium classified as?
    Macromineral, an element
  187. What type of element is calcium?
    An alkaline earth metal
  188. What foods contain calcium?
    • Milk, Cheese, green leafy vegetables, sardines.
    • Vegans can get it from tofu, fortified OJ, and soy milk.
  189. What transporter is at specialized calcium channel and is it necessary?
    TRPV6, calcium is still absorbed when it is knocked out (also still absorbed when calbindin is knocked out)
  190. Why aren't serum levels a good calcium indicator? What should be checked instead?
    Calcium is highly regulated. Better to check intestinal absorption.
  191. What type of diffusion does calcium engage in?
    Paracellular diffusion.
  192. Calcium absorption efficiency
    • Varies.
    • Adults 25-60%
    • Infants 60%
    • Influenced by Vit D, hormonal status, and dietary clacium.  (Low Ca will increase rate of absorption, high will decrease)
  193. Calcium Absorption Enhancers
    • Vit D
    • Sugar
    • Protein
  194. Calcium Absorption Inhibitors
    • Fiber
    • Phytate
    • Oxalate
    • Excessive divalent cations (Zn, Mg)
    • Unabsorbed Fatty Acids
  195. Urinary Calcium Excretion Enhancers
    • Sodium
    • Protein
    • Caffeine
  196. Excessive Calcium Inhibits
    • Iron
    • Fatty Acids
  197. Phytate and Calcium
    Phytate is a very potent inhibitor. Reduces calciums' bioavailability
  198. Oxalate and Calcium
    Found in green leafy vegetables, fruits, nuts, tea. Reduces bioavailability of Ca.
  199. Key factor influencing urinary calcium loss
    • Sodium. 1 additional gram of sodium results in aadditional urinary loss of 26mg Ca.
    • Increased Na = decreased Ca
  200. What is the most abundant divalent cation in the human body?
    • Calcium
    • 2.2 pounds in body
    • 98% in teeth and bones
  201. In what forms is calcium transported in the blood?
    • 1) Free Ca (50%)
    • 2) Bound to protein albumin (40%)
    • 3) Complexed with citrate, phosphate, and sulfate (10%)
  202. What is calcium required for?
    • Nerve and Muscle Cells
    • Blood clotting
    • Cofactor for enzymes
  203. What regulates Ca in blood
    • PTH
    • Calcitriol
    • Calcitonin
  204. What happens when blood calcium is low?
    • Parathyroid released PTH
    • PTH increased in the blood which stimulates Ca resorption in the kidneys
    • This stimulates renal hydroxylase to convert 25-OH D3 to calcitriol which increases blood Ca and blood calcitriol.
    • Increased calcitriol stimuated Ca absorption in the intestine which, again, increased Ca in blood.
    • Increased PTH and Calcitriol in the blood travels to the bone and stimulates resorption of Ca and Phosphate. The end result of all of this is increased blood calcium.
  205. What happens in high blood calcium conditions?
    Tyroid releases hormone calcitonin which acts opposite of PTH. It inhibits osteoclasts and prevents calcium mobilization from bone which reduces Ca in blood.
  206. Calcium levels inside vs outside of cells?
    Not much inside compared to outside.
  207. Where are calcium-selective channels often found?
    Plasma membrane of presynaptic nerve terminals
  208. What does calcium activate or deactivate enzymes through?
  209. Can teeth be built back up?
  210. What initiates bone breakdown
  211. What initiates bone buildup?
  212. Resorption and redeposition relationship in youth
  213. Resorption and redeposition relationship in adults
  214. How can you measure long term calcium status?
    Bone density
  215. Calcium def is clinically seen as:
    Rickets, Tetany, Oxteoporosis
  216. Osteoporosis
    Porous bonds from reduced bone mineral density
  217. Principal sites affected by osteoporosis?
    Sites with trabecular bone, like the femur
  218. Risks for osteoporosis
    • Female
    • Caucasion
    • Small Body Size
    • Family history
    • Disease
    • Caffeine
    • Smoking
  219. To reduce osteoporosis risk
    maximize peak bone mass during growth and reduce bone loss later in life.
  220. What helps repress fracture frequency?
    Calcium and Vitamin D
  221. How do estrogens spare bone?
    Increase osteoclast apoptosis
  222. Biphosphonates
    Reduce bone resorption
  223. Hormone replacement therapy
    Decreases bone loss in post menopausal women. More affective if combined with Ca.
  224. Why should estrogen be taken at lowest possible dose?
    Can lead to other issues
  225. Calcium RDA
  226. UL for calcium
    • 19-50y/o: 2500mg
    • 50+y/o: 2000mg

    High intake side affects: constipation and kidney stones
  227. What type of element is Magnesium?
    Alkaline Earth Metal
  228. Good food sources of Mg?
    • Whole Grains
    • Legumes
    • Green leafy Vegetables
    • Tofu
    • Chocolate
    • (Meat, Fruit, Dairy = not as good)
  229. Hard water has more?
  230. Soft water has more?
  231. Where does Mg absorption occur? What methods are used?
    • Small intestine
    • Passive diffusion and active transport
  232. Mg absorption enhancers
    • Vitamin D
    • Carbohydrates: lactose & fructose
  233. Mg absorption inhibitors
    • Phytate
    • Fiber
    • Excessive Unabsorbed Fatty Acids
  234. Mg interacts with:
    • Calcium
    • Phosphorus
    • Potassium
    • Protein
  235. What carrier mediates Mg's transport?
  236. What ways are Mg transported?
    • Free Mg (55%)
    • Bound to protein-albumin(30%)
    • Complexed with citrate, phosphate or sulfate (15%)
  237. What regulates MG excretion and how?
    Kidneys regulate excretion based on intake. High excretion with high intake and low excretion with low intake.
  238. What increases urinary excretion of Mg?
  239. Total body Mg
    • ~25g
    • 50% in bone
    • 50% in soft tissue
  240. Is Mg an anion or cation?
    Important intracellular cation that stabilizes over 300 complexes because it binds so well to anions.
  241. What is Mg-ATP used for?
    • Glucose Metabolism
    • Energy Storage & Transfer
    • Signaling Pathways
    • Ion transport
    • Lipid Metabolism
  242. What nutrient is important to nucleic acid structure?
    Mg (Stabilizes RNA and DNA)
  243. Mg and hydrophillic phosphates
    Mg reacts with hydrophillic phosphates of the cell membrane which affect fluidity and permeability. This influences ion channels, transporters, and signal transducers.
  244. What stabilizes sodium postassium ATPase?
  245. What is hypokalemia and what leads to it?
    • Low potassium
    • Characteristic of Mg depletion
  246. Describe Mg's relationship with CAMP and what CAMP is used for.
    • Adenyl cyclase converts ATP to CAMP and it is a Mg-dependent enzyme. For this reason Mg is required for CAMP function.
    • CAMP is needed for PTH secretion which is needed for bone calcium mobilization and kidney calcium resorption.
  247. What happens with low Mg?
    Low Mg will inhibit PTH secretions. Osteoclasts will become unresponsive, bone remodeling will be reduced as will blood calcium.
  248. Is PTH more responsive to Ca or Mg?
  249. Is plasma mg a good indicator of nutritional status?
  250. What will lead to Mg depletion?
    A genetic defect on TRPM6 (body will hold on to Mg if you aren't eating any so usually due to this genetic defect, not lack of eating)
  251. Mg deficiency leads to:
    • Low plasma Mg
    • Hypocalcemia
    • Hypokalemia
    • Abnormal Neuromuscular function
    • Low PTH
    • Low 1,25 OH2 D3

    * All can be reversed with Mg repletion
  252. Severe Mg deficiency will lead to
    • Tetany
    • Neuromuscular tremors
    • Convulsions
    • Soft Tissue Calcification
    • Cardiac Arrhythmia
    • ECG abnormalities
  253. What clinical settings is Mg deficiency found in?
    • Surgery
    • Blood Transfusion
    • Diabetic Ketoacidosis
    • Alcoholics
    • Chronic Malabsorptive Problems
  254. Mg RDA
    • 320mg for women
    • 420mg for men
  255. Mg UL

    food form not toxic, not supplement form.
  256. What type of element is Phosphorus?
  257. Best phosphorus sources?
    • High protein:
    • Poultry
    • Fish
    • Red Meat
  258. Does dairy have more Ca or P?
  259. Other foods with phosphorus:
    Nuts, legumes, cereals, grains, chocolate, coffee, tea, and soft drinks
  260. Is P usually found free in nature?
    No, it is typically bound to proteins, lipids, and sugars.
  261. What is phosphorus most frequently found as?
    Phytate (phytic acid)
  262. What's more available? Phosphorus or phytate?
    Phosphorus because it binds to Ca, Zn, Fe, Mg making it less available for absorption
  263. Phosphorus absorption enhancers
    Vitamin D
  264. Phosphorus absorption inhibitors
    • Phytate
    • Excessive Mg, Ca, Aluminum
  265. Food processing and P
    Food processing increases phosphous (cheez wiz has more than natural cheddar)
  266. Foods high in phosphorus
    Restructured meats, processed/spraedable cheeses, instant products, refrigerator bakery products, beverages
  267. High levels of P and bones
    High levels are bad for bones
  268. How is P absorbed?
    Uses facilitated diffusion and active transport (only with low intake or increased demand)
  269. What is used for active transport of P and can it be absorbed without it?
    Uses NPT2b, and it can not be absorbed without it
  270. Where is P found in the body?
    • Bone (85%)
    • Soft Tissue (15%)
  271. Hydroxyapatite crystals, Ca/P ratio
  272. P moves in and out of bone via
    • Ionic Exchange
    • Active bone resorption (which takes minerals away from bone)
  273. P excretion
    • 90% in urine
    • 10% in feces
  274. Major regulator of blood P
    Renal excretion
  275. What's more tightly regulated? Serum P or Serum Ca?
  276. P Functions
    • Regulation of acid/base balance (Acts as buffer)
    • DNA/RNA backbone
    • Mineralization of bones and teeth
    • Phospholipid structure
    • ATP
    • Absorption and transport of nutrients
    • Regulation of enzyme activity
  277. How to asses P levels
    Serum P
  278. Hypophophatemia
    P deficiency (Rare in well-nourished but common in critically ill)
  279. P Deficiency causes
    • Low absorption
    • Increased excretion
    • Hyperparathyroidism
    • Phosphorus Imbalances
    • Maladaptive Diseases
    • Alcoholism
    • Large Doses of Antacids
    • Refeeding Syndrome
  280. P RDA
  281. P UL

    Toxicity is rare but can cause hypocalcemia and tetany
  282. 1st person to describe scurvy
  283. Who prescribed lemons and oranges as scurvy cure?
  284. Who experimentally induced scurvy in guinea pigs?
    Hoist and Frohlich
  285. Antiscorbic factor
    Vitamin C
  286. Who ided antiscorbic factor as "hexuronic acid"
  287. Does Vitamin C have an amine?
  288. Image Upload
    Vitamin C
  289. 2 forms of Vitamin C
    • Ascorbic Acid
    • Ascorbate
  290. What is the chemical, ionized form of Vit C?
    • Ascorbic Acid
    • (Ascorbic Acid has 1 additional H, this is powder that people often buy)
  291. Can Vitamin C be synthesized?
    Vit C can be synthesized from glucose in animals that have gulnolactose enzyme like dogs, cats, mice, and rats. We don't have it so we can't generate it.
  292. Foods that have Vit C
    • Fruits
    • Collard Greens
    • Brocolli.
    • Not in rice, little in meat/dairy
  293. 2 forms of Vit C in food
    • Ascorbic Acid
    • Dehyrdoascorbic Acid (Has 2 less Hs)
  294. What form is most Vit C in food found in?
    ascorbic acid
  295. What transports Ascorbic Acid?
  296. What transports dehydroascorbic acid?
  297. Converstion of ascorbic acid to dehydroascorbic acid
    1 H is lost from ascorbic acid creating a semidehyroascorbic acid radical. Another is then lost making dehydroascorbic acid. To regenerate ascorbic acid, Hs are donated from reduced glutathione which becomes oxidized glutathione. Dehydroascorbate reductase is needed for this to happen.
  298. Main circulating form of Vit C
  299. Why should people with kidney stone or risk of kidney stones avoid Vit C?
    Vit C can be oxidized to dehydroascorbic acid which can be converted to oxalic acid which is a component in kidney stones.
  300. How is vitamin C excreted?
    In the urine as DHAA or metabolites
  301. How does Vit C function enzymatically?
    As a reducing agent.
  302. Vit C used for synthesis of
    • Collagen
    • Carnitine
    • Neurotransmitters
    • Tyrosine
  303. Vit C functions nonenzymatically as a(n)
  304. What is collagen and where is it found?
    A structural protein found in skin, bones, tendons, and cartilage. 1/3 of total protein in body.
  305. What does collagen synthesis require? How does it work?
    Activity of several vitamin C-dependent enzymes: Prolyl 3-hydroxylase, prolyl-4 hydroxlase, and lysyl hydroxylase.

    Lylsal hydroxylase adds a hydroxyl group to lysine which receives an electron from Iron2+. This oxidizes Iron2+ to Iron3+. Ascorbate (Vit C) will reduce iron back to 2+ by donating an electron so it can continue to be used in the cycle.
  306. Vitamin C _______ Iron
  307. Carnitine
    Moves fatty acids from the cytosol to the mitochondria to oxidize them for energy. Vitamin C keeps iron in reduced form to aid process
  308. Vitamin C donates _____ making it a _____.
    electrons, antioxidant
  309. What is the most damaging radical?
    • Hydroxyl - will rip electron off anything in it's vicinity = free-radical damage
    • Damages lipids, proteins, DNA, leads to diseases
  310. What helps neutralize reactive oxygen species?
    Vitamin C
  311. Reactive Oxygen Species Include
    • Superoxide O-O
    • Hydrogen Peroxide HO-OH
    • Hydroxyl Radical HO
  312. How do you asses Vit C levels?
    Plasma. less than .2mg is deficient
  313. How to check Vit C tissue stores?
    check Leukocyte Vitamin C
  314. One of oldest disease in history
    • Scurvy
    • Now rare but still found in alcoholics, poor, and elderly
  315. Vit C deficiency symptoms
    • Bleeding gums
    • Petechiae
    • Easy bruising
    • Joint Pain
    • Loose/decaying teeth
  316. Vit C RDA
    • Males: 90mg/day
    • Females: 75 mg/day
    • Prep: 100mg/day
    • Lact: 120mg/day
    • Smokers: +35mg/day
  317. Vit C UL
  318. Who made Vit C famous?
    Pauling (only person with 2 Nobel prizes)
  319. If you go above UL for Vit C result is:
    abdominal pain, oxmotic diarrhea, possible kidney stones
Card Set:
Metabolism Exam 2
2013-03-19 12:09:45

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