Nutrition Fat Soluble Vitamins (9)

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mse263
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Nutrition Fat Soluble Vitamins (9)
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2013-12-10 23:08:07
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Nutrition
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Final Exam
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  1. 9 - Fat Soluble Vitamins
  2. vitamers
    • the different families/forms of fat soluble vitamins
    • eg. vitamin A has at least six vitamer chemicals that all qualify as "vitamin A", each with slightly different property
    • e/a set of vitamers has some forms that are active & some forms that contribute to toxicity
  3. Short-chain Fatty Acids
    • a sub-group of fatty acids with aliphatic tails of 2-6 carbons
    • they are produced in small amounts when dietary fiber is fermented in the colon
    • they are primarily absorbed through the portal vein during lipid digestion (while long-chain fatty acids are packed into chylomicrons & enter lymphatic capillaries)
    • eg. Formic acid. Acetic acid, Butyric acid, Propionic acid
  4. Medium-chain Triacylglycerides (MCTs)
    • medium-chain (8-10 carbons) fatty acid esters of glycerol
    • they passively diffuse from the GI tract to the portal system (longer fatty acids are absorbed into the lymphatic system)
    • they don't require modification like long-chain fatty acids or very-long-chain fatty acids nor do they require bile salts for digestion
    • *malnutrition patients are treated with MCTs because they do not require energy for absorption, utilization, or storage
    • are found in palm kernel oil, coconut oil, & camphor tree drupes
  5. Where does ALL absorption of fat soluble vitamins occur?
    • the small intestine
    • except for some forms of vitamin K (menaquinones) produced by bacteria & absorbed in the COLON
    • digestion + absorption of fat soluble vitamins requires normal digestion of fat by pancreatic enzymes & micelle formation by bile acids
    • fat soluble vitamins in vegetables or fruit eaten without fat have REDUCED bioavailability
  6. Vitamin A
    • family = retinoids, which refers to retinol, metabolites in the body, & synthetic analogs
    • it plays a role in reproduction & bone growth
  7. What role does vitamin A play in vision?
    • the retina requires retinal to adapt to dim light because 11-cis-retinal is a critical part of the rhodopsin molecule of the rods
    • also retinoic acid is required for normal corneal differentiation
  8. How does a vitamin A deficiency affect eyesight?
    • it can cause diminished night vision
    • dryness (xeropthalmia)
    • Bitot’s spots (accumulation of keratinized tissue on the cornea) which if left untreated will lead to blindness
  9. What role does vitamin A play in cell division & differentiation?
    retinoic acid is required for gene expression of enzymes & structural proteins
  10. What effect does Vitamin A deficiency have on the immune system?
    vitamin A DEFICIENCY increases the risk of viral ailments such as measles or respiratory infections
  11. How do carotenoids acts as antioxidants?
    • an example would be the role of leutine in retina: it scavenges free radicals generated during phototransduction
    • *age related Macular Degeneration is more likely to occur in people deficient in leutine & other pigments in the retina
  12. What are the two dietary sources of vitamin A?
    • 1. Vitamin A: a family of compounds related to Retinol (retinol itself = pre-formed vitamin A)
    • 2. Provitamin A Carotenoids: precursors that can be converted to vitamin A in the intestine + elsewhere
  13. Out of the 600 carotenoids identified, what three are provitamin A carotenoids that are cleaved to form retinol?
    • 1. α-carotene
    • 2. β-carotene
    • 3. β-cryptoxanthin
    • aka out of all the carotenoids only 3 form vitamin A
  14. What are the biological properties of non-provitamin A carotenoids?
    • they protect against cancer
    • there's no vitamin A activity involved
    • eg. lutein, lycopene, & zeaxanthin
  15. provitamin A carotenoid cleavage
    • central cleavage --> creates vitamin A
    • eccentric cleavage --> creates 2 molecules that don't have vitamin A activity
    • this process is regulated by vitamin A stores THEMSELVES
    • ingesting retinol/pre-formed vitamin A is more efficient than central cleavage of carotenoids
  16. What food sources contain pre-formed vitamin A?
    • animal foods: [polar bear] liver, meat, poultry, fish, dairy, eggs, animal oils, & fortified foods such as cereals
    • this pre-formed vitamin A exists as retinyl esters or retinol
    • it naturally occurs in milk but removing fat (making skim milk) takes out the vitamin A --> it is later fortified in skin milk
    • is not added back in whole milk because it's already present
  17. What food sources contain provitamin A carotenoids?
    • brightly colored fruits, green leafy vegetables, vegetable oils, eggs, & fortified foods such as cereals
    • carotenoids are why egg yolks are yellow
  18. How is Retinol absorbed?
    • retinol absorption is carrier mediated & facilitated by pancreatic lipase + bile
    • transport from the intestine to the liver occurs in chylomicrons
    • about 70-90% of pre-formed vitamin is absorbed
  19. How is β-carotene absorbed?
    • passively in micelles
    • it has poor average absorption of ~10-20%
    • however depleted vitamin A stores may up-regulate absorption & central cleavage to vitamin A in enterocytes or other tissues
  20. Which is more readily converted to retinol, β-carotene in supplements or food?
    β-carotene in supplements is converted to retinol more effectively than β-carotene in food due to reduced bioavailability in food
  21. Where are approximately 50-80% of body stores of vitamin A?
    • the liver
    • retinol is released from liver stores bound to retinol binding protein (RBP) or in lipoproteins & secreted into circulation
    • retinol binding protein (RBP) is cleared by the kidney
    • once in a cell, retinol is converted to its active form retinoic acid
    • retinoic acid acts on nuclear receptors
    • vitamin A metabolites are excreted in urine & bile if liver stores are high
  22. Why do obese people have LOWER concentrations of carotenoids?
    • because it gets sequestered in their large fat stores & can't get out into the circulation
    • obese males can also have low sperm levels & vitamin A deficiency can lead to decreased spermatogenesis
  23. Vitamin A Deficiency
    • primary deficiency: accompanies protein energy malnutrition (PEM) & zinc deficiency
    • secondary deficiency: low fat diets, disorders of fat digestion/absorption such as pancreatic insufficiency, low bile production, SI diseases
    • generally occurs with poor diet, malabsorptive disorders, or parasite infestation
    • mild deficiency treatment: oral supplements + correcting dietary or other reasons for deficiency
    • moderate to severe deficiency treatment: parenteral vitamin A
  24. Who would be a good candidate for intermittent parenteral vitamin A?
    patients with fat malabsorption syndromes
  25. Vitamin A Deficiency Chart


    • stunting: kids that have an abnormally low height for weight at a certain age
    • wasting: low weight for a height at a certain age
  26. Vitamin A Toxicity
    • occurs with excess ingestion of pre-formed vitamin A OR w/ impaired excretion of vitamin metabolites
    • is almost always due to supplement use, but CAN occur with very high intake of vitamin A containing foods
    • is mostly due to chronic excess but acute toxicity can be caused by supplement overdoses
    • • Headache, dizziness, loss of muscle coordination, & eventual coma
    • • Liver damage -> eventual cirrhosis
    • • Teratogenicity
    • • Osteoporosis
  27. What is a condition where vitamin A excretion may be impaired?
    • Chronic Kidney Disease - RBP is not well cleared by dialysis machines
    • this predisposes a person to vitamin A toxicity so supplementation with pre-formed Vitamin A aren't recommended long-term
  28. Why don't provitamin A carotenoids result in vitamin A toxicity?
    • because their cleavage to vitamin A can be down-regulated when the body detects enough vitamin A already present
    • excess provitamin A carotenoids instead results only in hypercarotenemia (excess pigmentation of skin)
    • unlike jaundice, this orange discoloration of the skin doesn't affect the sclerae of the eye - they remain white
  29. What is the relationship between β-carotene supplementation in smokers & lung cancer?
    • smokers who take β-carotene supplements have an INCREASED risk of lung cancer
    • therefore in general routine supplementation β-carotene is not recommended
    • *one condition in which carotenoid supplements might IMPROVE outcome is age related macular degeneration*
  30. Vitamin A Recommendations
    • its RDA is based on intake necessary to maintain adequate liver stores of vitamin A
    • its UL is based on risk of liver disease & in women of childbearing age the risk of teratogenicity
    • there are NO DRI for carotenoids
  31. Vitamin D2
    • ERGOcalciferol
    • it can be found in plants, fungi, invertebrates, & supplements
    • if you irradiate mushrooms (fungi) them with UV light [aka give them a tan] they produce Vitamin D2
    • this form isn't endogenously synthesized
  32. Vitamin D3
    • CHOLEcalciferol
    • it comes from SYNTHESIS IN THE SKIN, animal foods (fatty fish, liver, whole milk, other dairy products), fortified foods (eg. skim milk, orange juice, cereal), & supplements
  33. How is Vitamin D synthesized if not derived from dietary D2 or D3?
    • it's made in the skin from 7-dehydrocholesterol (which is the last intermediate before cholesterol is formed) when 7-DCH is hit by solar UVB radiation (UV light)
    • this process is regulated BY the amount of vitamin D already stored in the body (in the liver); if a lot is already present 7-DHC isn't converted
  34. 25-hydroxyvitamin D [25(OH)D]
    • a pre-hormone produced in the liver by hydroxylation of vitamin D3 by cholecalciferol 25-hydroxylase
    • *its levels are used to determine a patient's vitamin D status because it is a stable form that can exist for weeks in the body
    • it has a half-life of 15 days
  35. 1,25(OH)2D [1,25-dihydroxyvitamin D]
    • the ACTIVE form of vitamin D made in the kidneys by hydroxylating 25-hydroxyvitamin D
    • this active form moves to the intestine & increases absorption of calcium (+ phosphate & vitamin D)
    • it's not a good indication of vitamin D status b/c a person will have normal levels until SEVERE deficiency
    • half-life = 4-6 hours
  36. Vitamin D Form Order
    • Vitamin D2, Vitamin D3, or 7-dehydrocholesterol
    •                              ↓
    • 25(OH)D 25-hydroxyvitamin D (form in the liver)
    •                              ↓
    • 1,25(OH)2D *ACTIVE FORM
    • 1,25-dihydroxyvitamin D
    • (formed in the kidney)
  37. What stimulates the hydroxylation of 25-hydroxyvitamin D to the active form of vitamin D, 1,25(OH)2D?
    • Parathyroid Hormone
    • which itself is secreted from the parathyroid when blood calcium levels are LOW
  38. parathyroid hormone (PTH)
    • hormone made by parathyroid gland chief cells that INCREASES blood calcium (opposes the action of calcitonin)
    • increases osteoclast activity - bone breakdown & liberation of calcium
    • stimulates vitamin D activation in kidney, which stimulates calcium resorption in GI tract & kidney)
    • *is a vital hormone
  39. How are vitamin D metabolites excreted?
    primarily in bile into the feces, but some metabolites are excreted in urine
  40. Roles of Vitamin D
    • the traditional roles include calcium (& phosphorous) homeostasis, bone health, & muscle function [which is heavily dependent on normal intracellular calcium levels]
    • vitamin D is also thought to influence cancer (colon, prostate, breast), diabetes type 2, cardiovascular disease (blood pressure), immune function, & depression
    • however the dietary recommendations of vitamin D (20 ng/mL) are still based only on its effect on bone health, not on any of its emerging roles
  41. What role does vitamin D play in immune function? Cancer? Diabetes?
    • in macrophages, vitamin D stimulates the release of a compound that kills bacteria (eg. tuberculosis)
    • vitamin D inhibits angiogenisis in tumors cells & may also regulate apoptosis & cell death
    • it may regulate insulin secretion from pancreas or induce insulin sensitivity
  42. What are risk factors for deficiency of vitamin D derived from 7-dehydrocholesterol?
    • anything that decreases the skin's ability to synthesize vitamin D:
    • 1. aging (impaired synthesis)
    • 2. limited sun exposure (no UV rays to convert)
    • 3. dark skin (UV rays are less well absorbed)
  43. What are risk factors for dietary vitamin D deficiency?
    • Infants who are exclusively breastfed
    • Lactose intolerance
    • Fat malabsorption
    • Obesity (D is also stored in but possibly not release from adipose as well as the liver)
    • End stage liver or kidney disease
    • Medications such as corticosteroids & anticonvulsants
  44. What is the relationship between body fat & vitamin D levels?
    • as body fat decreases, SO does vitamin D
    • low vitamin D levels translate to low Calcium levels as a result of poor Calcium absorption
    • active vitamin D is what goes to the intestine & increases absorption of Calcium - no Vit D, no Ca2+
    • this can lead to secondary hyperparathyroidism, when excessive PTH is secreted to try to compensate for low Calcium levels
  45. What does Vitamin D deficiency cause?
    • poor Calcium absorption & therefore low Ca2+ levels
    • the PTH secreted to activate vitamin D only functions to increase osteoclast activity & facilitate bone demineralization to maintain Ca2+ levels
    • in children this leads to Rickets, & in adults this leads to Osteomalacia
  46. Rickets
    • softening of bones in immature mammals due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium
    • can lead to fractures & deformity
    • is characterized by growth retardation + bowing of lower extremities
  47. Osteomalacia
    • softening of the bones caused by defective bone mineralization secondary to low levels of phosphorus & calcium
    • is characterized by diffuse bone & muscle pain, muscle weakness, & frailty
    • long term osteomalacia increases the risk of osteoporosis
    • is caused by vitamin D deficiency which can lead to overactive resorption of calcium from the bone as a result of hyperparathyroidism
  48. What do supplements containing calcium & vitamin D protect against?
    • bone mineral loss & bone fracture
    • they should be considered for those who don't meet dietary goals
  49. How are vitamin D deficiencies treated?
    • oral supplementation w/ the doses dependent on severity of deficiency
    • hydroxylated forms of vitamin D (at the 1, the 25, or both sites) are prescription medications that can be used for patients w/ parathyroid, liver, or renal disease
  50. What are symptoms of excess vitamin D?
    • Hypercalcemia
    • Calciuria & kidney stones
    • Arrhythmia
    • Confusion
    • Lethargy
    • Soft Tissue Calcification
    • Impaired GI Motility
    • Polyuria (excessive urination)
    • Polydipsia (excessive thirst)
    • this CAN'T be caused from UV exposure - it's caused by supplements or medications
  51. How can vitamin D status be assessed besides by measuring 25-OH vitamin D?
    • Calcium levels
    • Parathyroid hormone levels
    • giving a DEXA scan to check bone mineral density
  52. Vitamin E - BioChem definition
    • terminates free radical oxidation of unsaturated fatty acids
    • double bonds in PUFAs (poly-unsaturated fatty acids) are good at stabilizing free radicals, meaning they SPOIL quickly
    • vitamin E can take up free radicals & prevents PUFAs from spoiling
    • the reduced form of vitamin E is regenerated in a reaction using vitamin C & glutathione
  53. Vitamin E
    • a family of compounds that exhibit the antioxidant activity of α-tocopherol & tocotrienol derivatives
    • alpha, beta, gamma & delta forms exist based on different side chain stereoisomers
  54. What type of vitamin E occurs naturally?
    • RRR α-tocopherol
    • it's the only biologically active form & the only one that contributes to the vitamin E RDA
    • ALL α-tocopherol forms contribute to toxicity risk defined by the UL
    • other forms are may be present in food to a lesser extent or can be synthesized for use in supplements
  55. What foods contain vitamin E?
    • wheat germ, vegetable oils, nuts, seeds, green leafy vegetables, olives, fortified foods (cereal), & supplements
    • it is added to some foods to function as an antioxidant
  56. Vitamin E Absorption, Trnsprt, Metabolism
    • it is absorbed as part of micelles in the small intestine
    • it is secreted from enterocytes as part of chylomicrons, where it can be transferred to other lipoproteins, enter cell membranes, or be taken up by the liver
    • from the liver vitamin E can be secreted straight into the plasma or as part of VLDL (lipoproteins)
    • in addition to liver, it can also be stored in adipose tissue
  57. α-tocopherol transfer protein (TTP)
    • a liver protein that facilitates transfer of α-tocopherol from the liver into the plasma
    • genetic abnormalities of TTP result in an inability to export vitamin E from the liver & therefore systemic deficiency of vitamin E even though adequate stores may be present
  58. What are the biological roles of vitamin E?
    • 1. Antioxidant - it prevents RBC hemolysis & lipid peroxidation (is reduced by vitamin C)
    • 2. Immune Function
    • 3. DNA Repair
  59. What is the RDA for vitamin E based on?
    the amount necessary to prevent hemolysis of red blood cells in response to oxidative stress
  60. What puts someone at RISK for vitamin E deficiency?
    • Dietary insufficiency
    • Premature infants w/ very low birth weight
    • Fat malabsorption
    • α-tocopherol transfer protein (TTP) defects
    • Abetalipoproteinemia
  61. Abetalipoproteinemia
    • a rare autosomal recessive disorder that interferes with the normal absorption of fat + fat-soluble vitamins from food
    • it is caused by a mutation in microsomal triglyceride transfer protein resulting in deficiencies in the apolipoproteins B-48 and B-100 used in the synthesis and exportation of chylomicrons & VLDL (respectively)
  62. What are SYMPTOMS of vitamin E deficiency?
    • 1. Peripheral neuropathy
    • 2. Spinocerebellar Ataxia with vitamin E deficiency (AVED) due to TTP mutations
    • 3. Myopathy
    • 4. Retinopathy
    • 5. Immune dysfunction
    • 5. RBC hemolysis
  63. Vitamin E Excess
    • caused by: OVER-SUPPLEMENTATION
    • results in: bleeding (hemorrhage due to a possible interaction w/ vitamin K - mainly an issue in surgery), worsened risk or outcome for some cancers, & an increased risk of mortality if levels go above 400 IU/day
  64. How is vitamin E excreted?
    • in bile and subsequently in feces
    • some is also lost in urine & through sebaceous gland secretions
  65. Vitamin K - BioChem definition
    • a cofactor in γ-carboxylation required for prothrombin & other blood clotting factors to function
    • is PRO BLOOD CLOTTING
    • is given to premie babies who lack it to prevent hemorrhaging disease
  66. What are the 2 forms of Vitamin K?
    • 1. Phylloquinone (K1): common US form from plants
    • 2. Menaquinones (K2, MK): come from fermented foods, animal feeds
    • *side chains are what distinguishe the two forms
  67. What foods are good sources of phylloquinone (K1)?
    • Green leafy vegetables (kale)
    • Green vegetables (broccoli)
    • Vegetable oils (eg. soy bean but not olive oil)
    • Soybeans
    • Fortified foods (breakfast cereal = main source for kids)
  68. What foods are good sources of menaquinones (K2)?
    • Some fermented foods
    • Animal foods
    • Dairy
    • Intestinal bacteria ("we" can make it, just like we can synthesize D3)
  69. Vitamin K is absorbed from the intestinal lumen in ________, secreted from enterocytes with dietary fat in ___________, transported in the serum in __________, stored in the ________, & its metabolites are excreted primarily in ____.
    • absorbed from intestine lumen in: micelles
    • secreted from enterocytes as: chylomicrons
    • serum transported in: lipoproteins
    • stored in: the liver
    • excreted in: bile
  70. What reaction is vitamin K a cofactor for?
    • the γ-carboxylation of glutamic acid to form carboxyglutamic acid (Gla)
    • the carboxylation allows calcium to bind to vitamin K dependent blood coagulation factors (II, IV, VII, X, Protein C, & Protein S) & clot blood
    • after acting as a cofactor vitamin K exists in epoxide form
    • warfarin blocks the regeneration of active vitamin K through the vitamin K cycle, lengthening the time it takes for a blood clot to form
  71. Warfarin
    • an anti-coagulant given to people who get blood clots easily
    • consistent intake of vitamin K is recommended when on the drug
    • a person's vitamin K cycle polymorphisms predict dosage & response to warfarin
  72. How are Vitamin K levels measured?
    • using prothrombin time: a measure of the extrinsic pathway of coagulation
    • the body regulates the production of clotting factors, therefore excess vitamin K doesn't result in excessive clotting
    • blood levels reflect recent intake not stores, which is why such info is rarely used to assess vitamin K levels
  73. Risk Factors for Vitamin K Deficiency
    • Birth
    • Liver disease (difficulty absorbing/storing the vitamin)
    • Alcoholism
    • Fat malabsorption
    • Malabsorptive disorders
    • Poor intake
    • Surgical resection of the small intestine
  74. Symptoms of Vitamin K Deficiency
    • Bleeding abnormally
    • Embryopathy caused by warfarin (a teratogen) use or severe deficiency in mothers
    • Disorders of soft tissue and bone calcification (caused by warfarin)
    • *people at greatest risk are babies born in home births
  75. Warfarin Embryopathy
    • caused by warfarin use & severe vitamin K deficiency
    • Chondrodysplasia punctata (bony deformities with excess calcification
    • Nasal hypoplasia (depressed nose bridge)
    • Mental retardation
  76. What is the UL of vitamin K?
    • it has NO UL & no toxicity
    • high intake of vitamin K does NOT promote abnormal coagulation

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