chapter 12: fat soluble vitamins

  1. What are retinoids? 3 forms?
    • biologically active form
    • preformed vitamin A
    • 1. retinol
    • 2. retinal
    • 3. retinoic acid
  2. what are carotenoids?
    provitamins that can be converted to vitamin A
  3. where are carotenoids converted into retinal and retinoid acid?
    intestinal cells
  4. which 3 provitamin A carotenoids can be converted into active forms of vitamin A
    • beta-carotene
    • alpha carotene
    • beta-cryptoxanthin
  5. 6 functions of retinoids
    • cell growth and development
    • cell differentiation
    • production of epithelial cells
    • vision
    • immune function
    • dermatological treatments for skin
  6. 4 functions of carotenoids
    • prevention of CVD
    • antioxidant capabilities
    • cancer prevention
    • helps with age-related macular degeneration/cataracts
  7. sources of retinoids vs carotenoids
    • retinoids - beef liver, fish, fortified milk
    • carotenoids - dark greens, yellow-orange fruits
  8. what are RAE and IU?
    • IU = international unit (crude method of measurement)
    • RAE = retinol activity equivalent (more precise method)
    • *this is for vitamin A
  9. 1 RAE = ____ ug retinol
  10. 1 IU vitamin A = _____ ug retinol
  11. how are retinoids and carotenoids absorbed and how much?
    • 90% absorbed
    • packaged in chylomicrons and transported from intestinal cells to liver via lymphatic system
    • retinoids - retinyl esters are broken down to free retinol in the SI with help of bile + pancreatic lipase to be absorbed. after that, they can reform retinyl esters in intestinal cells
    • carotenoids - absorbed intact but at a lower rate
  12. how are retinoids vs carotenoids transported in the body?
    • retinoids - transported from liver to target tissue while bound to retinol binding protein -> which is bound to transthyretin
    • carotenoids - carried by VLDL
  13. where is vitamin A stored and how much?
    • liver stores 90%
    • reserve is enough for several moths
  14. populations susceptible for vitamin A deficiency
    more common in developing countries
  15. how does vitamin A deficiency result in night blindness
    not enough retinol to replace retinol lost in visual cycle -> rods in retinal regenerate rhodopsin more slowly
  16. what are bitot’s spots
    • foamy gray spots on eye made of hard epithelial cells
    • due to vitamin A deficiency
  17. what is xerophthalmia
    • dryness of eye bc less mucus production
    • due to vitamin A deficiency
  18. what is follicular hyperkeratosis
    • keratinizes cells replace mucous forming epithelial cells underlying the skin -> leads to rough, sandy texture to skin
    • due to vitamin A deficiency
  19. what is hypervitaminosis A
    • excessive vitamin A
    • comes from long term supplement sues of 5-10x of RDA
  20. 3 forms of toxicity of vitamin A
    • acute - short term megadose, symptoms disappear when intake stops (GI effects, HA, blurred vision, poor muscle contraction)
    • chronic - long term megadose, possible permanent damage (bone and muscle pain, skin disorders, increased liver size)
    • teratogenic - causes birth defects (spontaneous abortion)
  21. toxicity of carotenoids
    not likely bc the rate of conversion of carotenoids to retinoid acid by liver is slow and absorption decreases as intake increases
  22. hypercarotenemia
    • high amounts of carotenoids in the bloodstream
    • excessive consumption of carrots/squash/beta-carotene supplements
    • skin turns a yellow-orange color
  23. why is vitamin D a conditional vitamin/prohormone
    • UV light can convert a form of cholesterol into vitamin D
    • if production is adequate, intake isn’t necessary
  24. what are the 3 forms of vitamin D
    • D2 = ergocalciferol - naturally found in foods
    • D3 = cholecalciferol - created by UV light
    • Dihydroxy vitamin D3 = calcitrol - converted form in liver
  25. functions of vitamin D
    • calcium and phosphorous homeostasis
    • regulates blood calcium level
    • cell differentiation
    • immune function
  26. how does UV light form vitamin D
    • UV light changes form of cholesterol to cholecalciferol (D3)
    • provitamin D3 -> provitamin D3 in skin -> vitamin D3 released into bloodstream
    • travels to liver and kidney and converted to bio active form of calcitrol
  27. dietary sources of vitamin D
    • fatty fish
    • cod liver oil (2 tsp = 680% of DV)
    • some fortified breakfast cereals
    • supplements and fortified foods are in the form of D2, which provides less activity than vitamin D3
  28. 1 IU = _____ micrograms of vitamin D
    .025 ug
  29. 1 microgram calciferol = ____ IU vitamin D
    40 IU
  30. how is vitamin D absorbed and transported
    • ~80% is absorbed via micelles
    • transported with chylomicrons in the lymphatic system
    • this is why fat malabsorption can impair vitamin D absorption
  31. what regulates synthesis of vitamin D
    parathyroid gland and kidneys
  32. deficiencies of vitamin D in adults and kids
    • kids - rickets (bow legs, protruding belly, weak brittle bones)
    • adults - osteomalacia (soft bones)
  33. vitamin D toxicities
    • doesnt occur from sunlight or dietary sources bc excess previtamin D3 is rapidly degraded
    • occurs with supplements
  34. 8 forms of vitamin E
    • 4 tocopherols - alpha, beta, gamma, delta
    • 4 tocotrienols - alpha, beta, gamma, delta
  35. what is the most active form of vitamin E
    alpha tocopherol
  36. main function of vitamin E
    antioxidant - protects cell from free radicals -> reduces oxidative stress
  37. sources of vitamin E
    • best source is plant oils and plants in general
    • animals and dairy have very little
    • easily lost in presence of oxygen, light, metals, high heat
  38. 1 mg alpha-tocopherol = ___ IU synthetic
    0.45 IU
  39. 1 mg alpha-tocopherol = _____ IU natural
    0.67 IU
  40. absorption, transportation, and storage of vitamin E
    • 20-70% of intake is absorbed
    • transported by chylomicrons into the liver -> incorporated into lipoproteins
    • absorption is dependent on the absorption of dietary fat
    • stored in adipose tissue, very little in liver and muscle
  41. vitamin E deficiencies
    • rare
    • hemolytic anemia -> RBCs break down faster than they can be replaced
    • nervous system damage
  42. ppl susceptible to vitamin E deficiencies
    • premature infants (born with limited stores of vitamin E)
    • ppl with fat malabsorption (Crohns disease, celiac disease, IBS)
    • ppl on low-fat diets
    • smokers (destruction of vitamin E in lungs due to oxidative stress)
  43. two form of vitamin K
    • phylloquinones (K1) - most biologically active form, predominant form of vitamin K
    • menaquinones (K2) - made by probiotic bacteria in digestive tract of animals
  44. functions of vitamin K
    • blood clotting factors
    • bone health
    • support brain and nervous system structure
    • protects against inflammation, CVD, and osteoporosis
  45. food sources of vitamin K
    green leafy veggies
  46. where is vitamin K stored
    • liver is main storage site but vitamin K also found in extra hepatic tissues
    • body recycles it through vitamin K cycle
    • allows vitamin K to function in g-carboxylation of proteins over and over
  47. how is vitamin K excreted
    • mainly bile
    • small amount through urine
  48. how is vitamin K absorbed and transported
    • absorbed in SI via chylomicrons in lymphatic system
    • transported via lipoproteins in the liver
    • or carried by LDL and HDL to cells throughout body
  49. deficiency of vitamin K
    • antibiotics -> destroy intestinal bacteria, inhibit vitamin K synthesis and absorption
    • excess vitamin A and E interferes with vitamin K
    • newborns have very little bc placenta transfer is poor and human milk has little -> they are injected with it
  50. how can vitamin K become toxic
    • through injections of synthetic vitamin K (menadione)
    • causes hemolytic anemia, excess bilirubin in blood (jaundice), and death in newborns
Card Set
chapter 12: fat soluble vitamins
ch 12