Term
| 1.Why is retinal called a chromophore? |
|
Definition
| Because of its ability to respond to dim light by changing from cis to trans, telling the brain there’s light, and back again. |
|
|
Term
| 2.What is the process by which retinoids are formed from -carotene conversion, and which retinoids are formed. What are the functions of retinoids and retinoic acid? |
|
Definition
| B-carotene is converted to trans-retinal by 15, 15’-carotenoids dioxygenase in the enterocyte, then can be converted to retinol by retinal reductase (requires NADH) or Retinoic acid by retinal oxidase (requires NADH or FAD). Retinoic acid is used in gene expression of growth hormone. Also retinol and RA are used in morphogenesis and embryogenesis. RA also used in oocyte maturation and skin proliferation and regeneration. |
|
|
Term
| 3.What is the role of lutein in the eye, and how might a diet low in lutein affect vision? Describe the vision cycle. |
|
Definition
| Lutein absorbs damaging blue and near-ultraviolet light, protecting the macula lutea. Retinal is bound to opsin as cis-retinal making rhodopsin. When light hits the rod cell in a dark environment, it changes the conformation of retinal to trans-retinal which then dissociates and activates neuronal signaling telling the brain there is light! It then is converted back into cis-retinal in the retina. |
|
|
Term
| 4.Define transcaltachia with respect to Vitamin D action. |
|
Definition
| The process by which vit. D rapidly initiates calcium absorption. It does this by stimulating endocytosis of Ca across brush border membrane, lysosome-mediated release of Ca within cytosol, and release of Ca across basal lateral membrane by exocytosis. |
|
|
Term
| 5.How is the active form of Vitamin D produced? |
|
Definition
| Pre-vitamin D forms are obtained from either the diet or skin due to UVB ray exposure. The pre-forms are then bound to DBP and transported to liver where 25-hydroxylase (requires niacin) converts to 25-OH D3. Then bound again to DBP and goes to kidney where 1-hydroxylase (requires niacin) converts to 1, 25-(OH)2 D3 (calcitriol) the active form! |
|
|
Term
| 6.Describe the differences and similarities in etiology and presentation between rickets and osteomalacia? |
|
Definition
| Both diseases result from vit. D deficiency. Rickets is in children, osteomalacia is in adults. Rickets presents as bowed legs, curved spine, pelvic/thoracic deformities, soft skull. Osteomalacia results in soft bones, decreased mineralization and bone growth, and variable bone mass. |
|
|
Term
| 7.Vitamin A and B-carotene metabolism and action require which water-soluble vitamins? |
|
Definition
| Niacin (B3)& riboflavin (B2)! |
|
|
Term
| 8.How can Vitamin A and D metabolism or transport be influenced by thyroid problems? |
|
Definition
| If there’s a tumor on the parathyroid gland that causes excess secretion of PTH, then excess conversion of calcidiol to calcitriol in kidney and release into blood. Retinoic acid regulates expression of growth hormone, if thyroid gland is not responsive, then excess production of growth hormone and retinoic acid? |
|
|
Term
| 9. Describe the roles of Vitamin A and Vitamin D in skin, especially as they relate to the treatment of skin conditions |
|
Definition
| Retinoic Acid (vit A) is found in skin and causes increased proliferation and regeneration of skin. Studies have shown that topical treatment of acne with vit. A led to DEATH! 7-DHC (provitamin D3) is found in sebaceous glands of skin and secreted onto skin surface where it absorbs UVB light and is converted to previtamin D3. Topical or oral vit D can be used to treat psoriasis by decreasing proliferation and increasing differentiation of the epidermis. |
|
|
Term
| 10.Describe the role of Vitamin K in bone matrix formation, including the proteins involved in the process? |
|
Definition
| The proteins bone Gla protein (BGP) and matrix Gla protein (MGP) are dependent on vitamin K and used in bone matrix formation via osteocalcin synthesis. |
|
|
Term
| 11.Why did the Vitamin D DRI increase for individuals of 71 years of age in 2010? |
|
Definition
| Decreased risk of falling in elderly by 20% when Vitamin D DRI was increased from 600 to 700 – 1000 IU. The new DRI is 800 IU |
|
|
Term
| 12.Describe hypercalcemia, its symptoms and its causes. |
|
Definition
| Vitamin D toxicity, symptoms are anorexia, nausea, hypertension, and calcification of soft tissues. |
|
|
Term
| 13. Describe how the genetic disorder abetalipoproteinemia can affect all fat-soluble vitamins? (or other genetic disorders discussed in class) |
|
Definition
Abetalipoproteinemia is an autosomal recessive disease that causes a loss of ApoB which leads to an inability to absorb fat soluble vitamins b/c can’t transport through blood (chylomicrons won’t be formed).
Vitamin E- Ataxia with Vitamin E Deficiency (AVED) – deficiency of aTTP (a-tocopherol transport protein)
Vitamin K- mutation in y-glutamyl carboxylase gene can result in loss of carboxylase function which means it cannot help in coagulation processes. Also can have epoxide reductase mutation which means that vit. K cannot be recycled and could lead to loss of clotting as well.
Vitamin D- hypophosphatasia = inherited disorder which leads to defective bone/teeth mineralization and deficiency of blood/bone alkaline phosphatase activity. Tissue Non-Specific Alkaline Phosphatase Deficiency-genetic polymorphism |
|
|
Term
| 14.How are Vitamin E and Vitamin A equivalents calculated? |
|
Definition
Vitamin A = 1 IU = 0.3 ug retinol
1 RAE = 1 ug retinol
2 ug B-carotene in oil
12 ug B-carotene in food
24 ug a-carotene
24 ug B-cryptoxanthin
Vitamin E = 1 IU = 0.67 mg a-tocopherol (natural)
0.45 mg a-tocopherol (synthetic) |
|
|
Term
| What is the active form of Vitamin E, and what are the roles of the other forms? |
|
Definition
| a-tocopherol, tocotrienols protect against neural cell death and helps brain recover after a stroke |
|
|
Term
| Describe the nutrient deficiency that is most likely to be present in both mother and baby with excessive bleeding following childbirth, the proteins and enzyme affected, and how this could be treated |
|
Definition
| Vitamin K deficiency- proteins affected are proteins II, VII, IX, and X and the enzyme affected is y-glutamyl carboxylase. Vitamin K injection could treat it along with consumption of dark leafy greens. |
|
|
Term
| 17.Which fat-soluble vitamins act as antioxidants, and how exactly (which steps) are these vitamins involved in the process? |
|
Definition
| Vitamin E- terminates free radical lipid peroxidation by donating a H, which carotenoids can do as well! |
|
|
Term
| 18.Which fat-soluble vitamins are required for bone mineralization? |
|
Definition
| Vitamins A, D & K (Retinoic Acid, Calcitriol and MK4) [& niacin] |
|
|
Term
| 19.For each fat-soluble vitamin, what are the effects of deficiency and toxicity. What are the functions of each vitamin? |
|
Definition
Vit A- deficiency = night blindness, slowed growth, increase susceptibility to infection, xerophthalmia (dryness of cornea & abnormality of conjunctive/cornea [total blindness])
Toxicity = acute – hypervitaminosis A – nausea, double vision, headache, dry skin
Chronic (3-4xRDA for months/years)– hypervitaminosis A – anorexia dry/itchy/flaky skin, alopecia (hair loss), ataxia, bone/muscle pain, conjunctivitis (pink eye)
Megadoses- birth defects
Functions- retinol- vision
Retinol/RA- gene expression (embryogenesis, reproduction, skin-differentiation, immune function)
Carotenoids- antioxidant function, cell proliferation, growth & differentiation
Vit D- deficiency = rickets and osteomalacia (decreased bone mineralization making them soft, rickets cartilage grows and is not replaced by bone matrix, causing bowed legs, curved spine, other pelvic/thoracic deformities).. people at greater risk are the elderly (less synthesis in skin), fat malabsorptive disorders, anticonvulsant drugs, breast fed infants
Toxicity = symptoms – anorexia, nausea, hypertension, & calcification of soft tissue
Functions = calcium homeostasis, cellular differentiation, proliferation & growth.
Vit. E – deficiency = rare, may occur in people with fat malabsorptive conditions, hepatobiliary system disorders, or with abetalipoproteinemia – apolipoprotein B deficiency due to mutations, leads to inability to be taken to liver.
Toxicity = not very toxic, symptoms are increased bleeding, GI distress
Functions = terminates lipid radicals (anti-oxidant), also protects against stroke, cataracts, diabetes, leprosy
Vit. K – deficiency = people at increased risk are newborns, those on prolonged antibiotics, fat malabsorptive disorders. Vitamin K Deficiency-Related Bleeding (VKDB) in neonates – leads to hemorrhage .. also Vitamin K- dependant Coagulation Factor Deficiency (VKCFD) type 1 – yglutamyl carboxylase mutation.. type 2 – epoxide reductase mutation
Toxicity = no UL, synthetic menadione may damage liver, hemolytic anemia, hyperbilirubinemia, jaundice.. treated in neonates w/synkavit
Functions = blood clotting (K1)(cofactor during synthesis of 4 blood clotting proteins & 3 anti-coagulent proteins) bone mineralization (K2) (BGP(aka osteocalcin) & MGP depend on vit. K [MK4]) |
|
|
Term
| What are chylomicrons and why are they important with respect to fat-soluble vitamins? |
|
Definition
| Chylomicrons are lipoproteins that consist of phospholipids, TG’s and chol esters. Fat-soluble vit’s are packaged into chylomicrons so they can travel from enterocyte thru lymphatic system to veins to hepatic portal vein & rest of body.. |
|
|
Term
| 21. What is Ataxia with Vitamin E Deficiency (AVED)? Identify which gene is affected and what the resulting condition is. |
|
Definition
| It is a mutation in the TTPA gene that codes for aTTP which is the transport protein for a-tocopherol.. leads to vit. E deficiency, resulting in accumulation of free radicals, which are particularly harmful to nerve cells. |
|
|
Term
| Name the sources of Vitamin K and the various isoforms from these sources. Describe the Vitamin K cycle including which enzymes and water-soluble vitamins that are required for conversion of Vitamin K quinone to KH2. |
|
Definition
Name the sources of Vitamin K and the various isoforms from these sources. Describe the Vitamin K cycle including which enzymes and water-soluble vitamins that are required for conversion of Vitamin K quinone to KH2.
Vit K cycle is the process of converting vit. K quinone (inactive form) to dihydroquinone (KH2 [active form]) using quinone reductase (requires niacin) then carboxylating clotting proteins via y-glutamyl carboxylase to vit K 2,3-epoxide then back to inactive form via epoxide reductase (requires glutathione & is target of warfarin) |
|
|
Term
| 23.Which scientists were responsible for identifying or purifying each of the fat-soluble vitamins? |
|
Definition
Vit. A & D = Elmer McCollum & Margarite Davis
Vit. E = Herbert Evans & Katherine Bishop
Vit. K = Carl Peter Henrik Dam (Dane) |
|
|
Term
| what are characteristics of fat soluble vitamins? |
|
Definition
| stored in large amounts in liver & fatty tissues, absorbed in the intestine, transported thru blood in complex carrier molecules, consumption of large amounts every once in a while prevents deficiency |
|
|
Term
| what 4 protesins required vit. K to carboxylate them in the clotting process? |
|
Definition
|
|
Term
| what vitamins are required for bone mineralization? |
|
Definition
|
|
Term
| what would be the consequence of a deletion of the aTTP protein? |
|
Definition
| apparent vit. E deficiency |
|
|
Term
| what does an anti-oxidant do? |
|
Definition
| donates free H+ (electron) to radicals, neutralizing them |
|
|
Term
| what vitamins are used in the regeneration of vit. E? |
|
Definition
| Vit. B3(niacin), vit. C, & glutathione |
|
|
Term
| Is 1 day of full body sun exposure (10,000 IU) toxic? |
|
Definition
| No, within 20mins any further previtamin D or 7-DHC are photodegreaded into lumisterol and tachysterol.. not allowing further production of vit. D |
|
|
Term
| what B vitamin is important for conversion of D3 to 1,25-(OH)2 D3? |
|
Definition
|
|
Term
| what water-soluble vitamin is used in the conversion of calcidiol to calcitriol? |
|
Definition
|
|
Term
| what would be the effect of auto-immune disease of the thyroid? |
|
Definition
| No effect on Vit. D levels, but don't want too much and could effect bone mineralization and thyroid hormone levels |
|
|
Term
| which water soluble vitamin is needed for night vision? |
|
Definition
|
|
Term
Retinoids and carotenoids
Which are active versus non-active forms? |
|
Definition
retinoids- retinal, retinol, retinoic acid
carotenoids- provitamins- B-carotene, a-carotene, B-crptoxanthin
straight up carotenoids - lycopene, canthaxanthin, lutein |
|
|
Term
| what enzymes/vitamins are involved in converting vit. A isoforms to retinyl esters to be stored in liver? |
|
Definition
LRAT & ARAT - require B5
retinol DH - niacin
retinal reductase - niacin
retinal oxidase - niacin or riboflavin
CRBP II - niacin |
|
|
Term
Vitamin A is often transported in the blood by the RBP4-TTR complex, and carotenoids by lipoproteins.
-What would the consequences be of transthyretin knockout mouse or genetic mutation or any of the carriers? |
|
Definition
| if TTR is knocked out then can't transport retinol from hepatic parenchymal cell to rest of body |
|
|
Term
Vitamin A has several major functions, including in the visual cycle and in cellular differentiation
How do the effects of Vitamin A deficiency manifest in target tissues? |
|
Definition
| result in blindness in the eye due to xerophthalmia - dryness of cornea & abnormalities of conjunctive & cornea |
|
|
Term
| What forms of Vitamin A are involved in the various processes? |
|
Definition
retinol- vision & embryogenesis & immune function
RA- embryogenesis, gamete formation, skin differentiation, keratin gene expression, bone development
carotenoids- antioxidant |
|
|
Term
| what tissues are affected by vit. A toxicity? |
|
Definition
| eye, skin, hair, brain, bone & muscle & babies |
|
|
Term
| how is vit. D synthesized in the skin? |
|
Definition
| 7-DHC is found in the skin, absorbs UVB and becomes pre-vit. D, body heat then thermoizomerizes it to vit. D3 bound to DBP and transported in blood |
|
|
Term
| activation of vit. D requires 2 hydroxylation rxns in the liver and kidney.. which water-soluble vitamin plays a role here? |
|
Definition
25-hydroxylase(in liver) - niacin
1-hydroxylase(in kidney) - niacin |
|
|
Term
vit. D functions as a steroid hormone to help maintain blood Ca levels. in this capacity it works with PTH and calcitonin
-what is the relationship between PTH calcitonin? |
|
Definition
|
|
Term
| what is the biological basis of why a-TOH has the highest biological activity of all the vitamers? |
|
Definition
| a-TTP preferentially transfers a-TOH in VLDLs to be delivered to target tissues |
|
|
Term
| vit. E is primarily located in cell membranes where it can inhibit lipid peroxidation- which step is important? |
|
Definition
| a-TOH is involved in the termination phase of lipid radicals |
|
|
Term
| how is vit E regenerated? |
|
Definition
| after vit E quenches radical, becomes oxidized needs to be reduced. glutathione, niacin, and vit C regenerate it |
|
|
Term
| what are the forms of vit K and how is vit K converted to its various forms? |
|
Definition
phylloquinone - found in green plants (from diet)
menaquinone - synthesized by bacteria
menadione - synthetic - can be synthesized to menaquinone |
|
|
Term
vit K is involved in blood clotting and bone mineralization
what enzymes and other vitamins are needed for these processes
what is the vit K cycle? |
|
Definition
blood clotting- vit. K acts on y-glutamyl carboxylase to activate protein VII, IX, X & II (prothrombin)- requires vit K to activate to thrombin which then activates fibrin
anticoagulant factors- protein C, S & Z
bone mineralization - osteocalcin/BGP & MGP require vit K- their synthesis is stimulated by vit A & D.. their functions are to bind ca to form matrix of bone
vit K cycle- vit K quinone (inactive) is activated by quinone reductase which requires niacin. then carboxylates a protein, then reduced to vit K quinones by epoxide reductase which requires glutathione |
|
|
Term
Newborns & peeps w/sever GI malabsorptive syndromes are at risk of deficiency of vit K
is there an UL? why/why not? |
|
Definition
| No UL, b/c everyone has diff amount of bacteria that synthesizes menaquinone.. although excess menadione (synthetic) can damage liver |
|
|
