2.2 Vitamin reqs during adulthood Flashcards

1
Q

Thiamin:
- vitamin ___?
- functions as _______ in the metabolism of ______ and _______
- cofactor for __________ reactions, through what form?
- cofactor for synthesis of _______ and _________
- also for ______ and _______ conduction (as a cofactor?)
- deficiency leads to which disease?

A
  • vitamin B1 (first B vit discovered)
  • as coenzyme in met of carbs and branched-chain aa
  • decarboxylation reactions (ie pyruvate dehydrogenase) as thiamin diphosphate (TDP)/thamin pyrophosphate –> primary circulating form
  • synthesis of pentoses (ie transketolase) and NADPH (as TDP)
  • membrane and nerve conduction
  • beriberi
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2
Q
  • how is thiamin status assessed by? (3)
  • ____ adjustment to estimated requirement fro men vs women –> why (2)
A
  1. erythrocyte transketolase activity: take RBC out, add thiamin, if activity levels increase, that means thiamin was deficient –> based on ratio btw this enzyme’s in vitro activity in presence of TDP to that without added TDP
  2. [thiamin] and its phosphorylated esters in blood
  3. urinary thiamin excretion under basal conditions or after thiamin loading
    - 10% (small) adjustment –> not the same energy utilization and not the same size
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3
Q

if someone’s erythrocyte transketolase activity coefficient is 1.2, does he/she have a thiamin deficiency?
- give ranges!

A

they are at low risk of thiamin deficiency
- ratio of 1.1 or equal –> adequate thiamin status
- 1.15-1.25 –> low risk of thiamin deficiency
- >1.25 –> thiamin deficiency risk (ie 1.25x more activity when thiamin is added)

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4
Q

what is the EAR/RDA/AI for thiamin?
- UL?

A

MEN above 19 yo:
- EAR: 1.0 mg/d
- RDA: 1.2 mg/d
WOMEN above 19 yo:
- EAR: 0.9 mg/d
- RDA: 1.1 mg/d

  • no UL for thiamin bc readily excretable bc water soluble
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5
Q

RIBOFLAVIN
- which vitamin letter?
- functions? examples!
- primary form of travel?

A
  • B2
  • coenzyme in numerous oxidation-reduction reactions
  • ie: TCA cycle, e- transport chain, FA oxidation, Niacin synthesis, vit B6 activation, neurotransmitter catabolism, antioxidant enzymes
  • flavin mononucleotide (FMN) and/or flavin adenine dinucleotide
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6
Q

riboflavin is important in which antioxidant systems?

A

thioredoxin and glutathione/glutaredoxin!

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7
Q

riboflavin: EAR for adults derived from which (4)

A
  1. erythrocyte glutathione reductase activity coefficient
  2. RBC [riboflavin]
  3. urinary riboflavin excretion in relation to dietary intake –> if urine is really yellow = adequate B2
  4. studies of occurrence of signs of clinical deficiency (biochemical changes in riboflavin status occur before appearance of overt signs of deficiency)
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8
Q

if someone’s erythrocyte glutathione reductase activity coefficient is 1.2, does he/she have a riboflavin deficiency?
- give ranges!

A

nope! they have adequate riboflavin status
- ratio of 1.2 or equal –> adequate riboflavin status
- 1.2-1.4 –> low risk of riboflavin deficiency
- >1.4 –> riboflavin deficiency risk –> means holoenzyme had inadequate FAD levels

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9
Q

EAR and RDA for riboflavin
- UL?

A

MEN above 19 yo:
- EAR: 1.1 mg/d
- RDA: 1.3 mg/d
WOMEN above 19 yo:
- EAR: 0.9 mg/d
- RDA: 1.1 mg/d

  • no UL for riboflavin
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10
Q
  • what are the 2 forms of niacin?
  • which form is used to lower blood lipid levels?
  • niacin generates which 2 cofactors?
  • function?
  • vitamin ____?
A
  • nicotinic acid and nicotinamide (niacinamide)
  • nicotinic acid! can lower blood lipid levels
  • cofactors = nicotinamide adenine dinucleotide (NAD) and nicotinamide adeninde dinucleotide phosphate (NADP+)
  • cosubstrate or coenzyme for H- transfer (dehydrogenases)
  • vitamin B3
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11
Q

NIACIN:
- primary criterion for RDA?
- adjustment made for bioavailability?
- can we synthesize niacin?
- which disease if deficient?

A
  • urinary excretion for niacin metabolites
  • nope! –> requirements expressed in niacin equivalents (NEs)
  • yes! we can convert tryptophan (60mg) to niacin (1 mg)
  • pellagra!
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12
Q

EAR and RDA for niacin?
- UL?

A

MEN above 19 yo:
- EAR: 12 mg/d of Niacin Equivalent
- RDA: 16 mg/d
WOMEN above 19 yo:
- EAR: 11 mg/d
- RDA: 14 mg/d

  • UL = 35 mg –> can cause skin flushing/vasodilation
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13
Q
  • name for vit B6?
  • function?
  • 2 circulating forms?
  • primary criterion to estimate RDA?
A
  • pyridoxine!
  • coenzyme in metabolism of amino acids, glycogen and sphingoid bases
  • pyridoxal 5’ phosphate (PLP) and pyridoxamine 5’ phosphate (PMP) = active coenzyme forms of vit B6
  • maintenance of adequate blood 5’-pyridoxal phosphate levels
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14
Q

Folate:
- coenzyme in _____-______ transfers in met of ______ and ______ _______
- synthesis of what?
- cofactor of enzymes that metabolize (4)
- cofactor form of folate = ___________

A
  • in single-carbon transfers in met of nucleic and amino acids
  • synthesis of DNA bases (purines and pyrimidines)
  • cofactor for enzymes that metabolize histidine, serine, glycine and methionine
  • tetrahydrofolate
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15
Q
  • primary indicator for folate RDA estimates? (2)
  • RDA expressed as what? –> adjusted for what?
  • 1ug DFE = how much food folate vs folic acid (from fortified foods) vs supplement taken on empty stomach
A
  • erythrocyte folate + blood [homocysteine] and [folate]
  • as dietary folate equivalents –> adjusted for around 50% lower bioavailability for food folate vs folic acid
  • 1 ug DFE = 1 ug food folate = 0.6 ug folic acid = 0.5 ug supplement
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16
Q

why is food folate not super bioavailable?

A

bc it’s linked to glutamic acid and enzymes are needed to break down the glutamic acid for body to be able to absorb the folate

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17
Q

will homocysteine levels increase or decrease with B6 deficiency?

A
  • folate deficiency will increase homocysteine levels bc folate needed to convert homocysteine to methionine
    *but homocysteine levels also increase if B12 and choline deficiency
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18
Q

is there a UL for folate?

A

yes! UL = 1000 ug (vs RDA = 400 ug/day of DFEs)
- based on folic acid, not on food form
- unmetabolized folic acid (not converted to dihydrofolate) –> health risk = compromised immune fct, adverse brain fct in elderly

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19
Q

vitamin B12:
- name?
- acts as what?
- functions (2)
- RDA based on (2)
- EAR/RDA?
- UL?

A
  • cobalamine
  • acts as methyl group acceptor from folate
  • coenzyme for methyl transfer rxn: homocysteine –> methionine + L-methylmalonyl-coenzyme A –> succinyl-coA
  • based on maintenance of hematological status and normal blood vit B12 values
  • EAR = 2.0 –> RDA = 2.4 ug/day
  • no UL bc readily excretable BUT can be stored in liver –> stores can last pretty long = harder to discover B12 deficiencies
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20
Q
  • vit B12 only in which products?
  • what does increase in L-methylmalonic acid in urine mean?
  • what is the methyl trap?
A
  • animal products!
  • B12 deficiency bc B12 needed to convert L-methylmalonyl-coA to succinyl coA –> if no B12, L- methylmalonyl-coA becomes L-methylmalonic acid
  • when tetrahydrofolate is trapped bc cant transfer its methyl group to B12 (deficiency) = increase homocysteine + anemia from B12 deficiency
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21
Q

Biotin:
- function? examples
- AI or RDA? basis?
- UL?
- risk of deficiency?

A
  • coenzyme in bicarbonate-dependent carboxylation reactions (ie propionyl-coA carboxylase, pyruvate carboxylase, acetyl-coA carboxylase in FA synthesis)
  • estimates of intake used to set the AI –> 30 ug/day for men and females over 19 yo
  • no UL BUT notorious for causing false readings in diagnostic tests
  • rare deficiencies bc readily bioavailable in food + low AI
22
Q

CHOLINE:
- precursor for (3)
- AI or RDA? criterion?
- 2 types of choline in diet

A
  • precursor for acetylcholine, phospholipid (ie phosphatidylcholine) and the methyl donor betaine (can donate methyl group to methionine synthase rxn)
  • primary criterion to estimate AI –> prevention of liver damage as assessed by serum alanine aminotransferase levels –> insufficient data for EAR
  • free choline (predominant in animal foods) + bound as esters (phosphocholine, glycerophosphocholine, sphingomyelin, phosphatidylcholine)
23
Q

what is the primary compound of VLDL?
- what happens if deficiency of choline?

A
  • phosphatidylcholine
  • if no choline –> liver cannot synthesize VLDL = it cannot export fat = leads to fatty liver
24
Q

deficiency in betaine leads to increase or decrease of homocysteine levels?

A

betaine is needed as a methyl group donor
- if betaine deficiency, homocysteine will increase

25
Q

choline requirement is influenced by (2)
- AI or RDA set for choline, but requirement could be met by what?
- UL?

A
  • influenced by methionine and folate availability + gender, pregnancy, lactation, stage of development
  • AI set for choline but reqs could be met by endogenous synthesis at some life stages (can synthesize choline from phosphatidylcholine
  • AI = 550 mg/day for men and 425 mg/day for women
  • UL = 3500 mg
26
Q

pantothenic acid
- vitamin ____
- component of (2)
- present in foods?
- deficiency common? from what? (2)

A
  • vitamin B5
  • component of coenzyme A and phosphopantetheine (FA metabolism)
  • widely distributed in food!
  • deficiency NOT common –> can be caused by semisynthetic diet (diets in form of powder/liquid that don’t have B5) OR antagonists fo the vitamin (ie from medication)
27
Q

Pantothenic acid:
- primary criterion to estimate AI/RDA?
- usual intake?
- AI/RDA?
- UL?

A
  • intake adequate to replace urinary excretion of pantothenic acid
  • usual intake = 4-7 mg/day –> no evidence shows that this is inadequate
  • AI for men and women >= 19 yo –> 5 mg/day (approximate midpoint)
  • no UL
28
Q

vitamin C:
- functions (2)
- RDA based on vit C intake to (2)
- RDA?
- UL?

A
  • water soluble antioxidant + cofactor for enzymes involved in biosynthesis of collagen, carnitine and neurotransmitters
  • based on vit C intake to maintain near-maximal neutrophil concentration (key immune cell to combat infection) + minimal urinary excretion of ascorbate (if you have to much, it’ll be excreted in urine)
  • Men: EAR = 75 mg RDA = 90 mg/day
  • women: EAR = 60 mg RDA = 75 mg/d
  • UL = 2000mg –> can cause misdiagnosis of some tests + interacts with meds
29
Q

vitamin A;
- important for (6)
- EAR based on what?

A
  • for normal vision, gene expression, reproduction, embryonic development, growth, immune function
  • based on assurance of adequate stores (bc fat soluble) (ie maintain given body-pool size in well-nourished subjects) –> assures vit A reserves to cover increased needs during periods of stress and low vit A intakes
30
Q

vitamin A:
- preformed vit A (retinol) found where?
- provitamin A carotenoids found where?
- what is retinol activity equivalent? + examples

A
  • found in some animal-derived foods
  • found in darkly colored fruits and veg, oily fruits and red palm oil
  • RAE => used for setting vit A reqs:
    ie retinal = 1 ug (?)
    b-carotene RAE = 12 ug
    a-carotene RAE = 24 ug
    b-cryptoxanthin RAE = 24 ug
31
Q

EAR and RDA for vit A
- UL?

A

men –> pool size reqs is bigger
- EAR = 625 ug RAE/day
- RDA = 900 ug RAE/day
women:
- EAR = 500 ug RAE/day
- RDA = 700 ug RAE/day

  • UL = 3000 ug = considerable toxicity
  • 3000 calculated from retinol VS carotenoids don’t pose toxicity risk (but could pose cancer risks)
32
Q
  • 2 functions of vit D
  • major physiologically relevant forms (2)
  • found where? synthesized where?
A
  • increase absorption efficiency of small intestine –> maintains blood [Ca] and [P]
    + potent antiproliferative and prodifferentiation effects in variety of tissue (= anticancer activity!)
  • forms = vitamin D2 (ergocalciferol, yeast and plant sterols) + vit D3 (cholecalciferol: from 7 dehydrocholestrol (from UV radiation) or from animal foods)
  • found naturally in very FEW foods but is synthesized in skin
33
Q

what is the 1st metabolite of vit D in liver?
- < 30 nmol/L = associated with what?
- VS >= 50 nmol/L = considered what?
- VS > 125 nmol/L

A
  • 25-hydroxyvitamin D[25(OH)D]
  • with vit D deficiency, leading to rickets in infants/children and osteomalacia in adults
  • generally considered adequate for bone and overall health in healthy indiviudals
  • emerging evidence linkes potential adverse effects to such high levels –> hypercalcemia
34
Q

EAR and RDA for vit D
- UL?

A

for men and women 19-70 yo
- EAR = 10 ug/day
- RDA = 15 ug/day (600 IU)

  • UL = 4000 ug
35
Q

vitamin E:
- other name?
- specific role in what?
- major function?
- lipid or water soluble? –> resides where?

A
  • tocopherol
  • in required metabolic function (there “??” in the notes…)
  • non-specific chain-breaking antioxidant preventing propagation of lipid peroxidation
  • lipid soluble –>resides in lipid membrane
36
Q

vit E:
- RDA based on what? explain
- how are tocopherol radical converted back to tocopherols?

A
  • based on induced vit E deficiency in humans (take out RBCs, add H2O2 –> if enough vit E: no hemolysis) –> correlation between H2O2-induced erythrocyte lysis and blood [a-tocopherol] (H2O2 produces FR that attack the lipid membrane = lysis)
  • converted back using vit C, caffeic acid…
37
Q

what are the different forms of tocopherol (4) + toco_______ (4)
- give characteristics
- RDA based on which one?

A

TOCOPHEROLS: saturated phytyl tail
- a-tocopherol –> 3 methylated
- b-tocopherol, y-tocopherol, d-tocopherol –> only 1 or 2 methyl groups –> don’t contribute to vit E reqs –> can acts as antioxidants too but not enough data
TOCOTRIENOL: unsaturated tail
- from nuts and seeds
- a, b, y, d-tocotrienol
- don’t contribute to vit E reqs
- might have fct in chronic disease risks but not enough data

38
Q

which stereoisomer of a-tocopherol is metabolically active in humans?
- DRI limited to which form? –> examples?
- which stereoisomer does food contain?

A
  • 2R stereoisomers are maintained by humans, not the 2S
  • limited to 2R-steroisomers: RRR, RSR, RRS, RSS (VS SRR, SSR, SRS, SSS are not maintained by humans)
  • foods = all racemic tocopheral –> 1/2 activit of RRR-a-tocopherol + 1/2 activity of other 2R forms (ie SRR: don’t contribute to RDA)
39
Q
  • are vit E forms interconvertible in humans?
  • plasma [vit E] forms: dependent on affinity to what?
  • [_ _ _-a-tocopherol] are maintained in human plasma
  • synthetic _ _ _-a-tocopherol and natural _-tocopherol are not maintained in human plasma –> _________ absorbed (through what?) to which organ? but what?
A
  • nope!
  • dependent on affinity of hepatic a-tocopherol transfer protein (a-TTP) –> transfers vit E to general circulation
  • RRR-a-tocopherol maintained
  • synthetic SRR and natural y-tocopherol NOT maintained: efficiently absorbed (chylomicrons) to liver –> BUT poorly packaged into lipoproteins for delivery to peripheral tissues to provide antiox activity
40
Q

why are only 2R-stereoisomeric forms used to estimate vit E requirements?

A

bc 2-S stereoisomeric forms, other tocopherols (b-y-d) and tocotrienols fail to bind with a-TTP

41
Q

EAR and RDA for vit E?
- limitation?
- UL?

A

for men and women >= 19 yo:
- EAR = 12 mg/d of a-tocopherol
- RDA = 15 mg/d of a-tocopherol = 15 mg/d of RRR-a-tocopherol = 15 mg/day of 2R-stereoisomeric = 30 mg/day of all racemic-a-tocopherol
- UL = 1000 mg –> vit C can get depleted if too much vit E (bc vit C used to convert TO radical to normal TO) + potential effects in not having enough coantioxidant (ie vit C) –> can cause tocopherol mediated peroxidation

42
Q

what are the 3 events for lipid peroxidation?
- what about when vit E is present?

A
  1. initiation radical oxidant + LH -> inactive oxidant + L°
  2. propagation: L° + O2 –> LOO° (peroxyl radical)
    *more propogation
  3. termination: LOO° + LOO°/L° –> nonradical products
    - vit E resides in lipid membranes –> prevents cascade of membrane breakdown: reacts with LOO° or with radical oxidant and becomes a tocopherol radical
43
Q
  • FR cause what?
  • FR + Tocopherol –> __-______ ______ + ______a_____ _____a______
  • ______a_____ _____a______ + what –> tocopherol
  • ______a_____ _____a______ can also cause what?
A
  • FR cause oxidative stress –> excessive FR exposure leading to cell damage
  • FR + TO –> non-radical species (detoxified form of FR generated via antioxidative action) + tocopheroxyl radical (a stable tocopheral FR formed from antioxidative action of tocopherol)
  • TO° + vit C –> tocopherol
  • tocopheroxyl radical can also cause oxidative stress (occurs when tissue buildup of TO° due to high intake of tocopherol supplements)
44
Q

what are the 4 co-oxidants for vit E?

A
  • ascorbate
  • caffeic acid (plant foods, it’s a polyphenol)
  • ubiquinols
  • bilirubin
45
Q

how can smoking cause oxidative stress?

A

smoking elicits an inflammatory response (bc of toxic compounds) –> increase neutrophils which produce lots of FR/ROS (like malondialdehyde)

46
Q

what is the correlation btw RBC vit E and plasma ascorbate?

A
  • high doses of vit E will significantly decrease plasma ascorbate!
47
Q

what is the antioxidant network?
- if it’s optimized, what could be substantially decreased?

A
  • the concept of “network” of antioxidants in the body (GSH, vit C, vit E), acting synergistically and regenerating each other
    *you can’t rely on only 1 antioxidant
  • disease burden could be substantially decreased
48
Q

vitamin K
- coenzyme during synthesis of proteins involved in (2)
- RDA/AI? based on what?

A
  • coenzyme during synthesis of biologically active form of a number of proteins involved in blood coagulation (vit K = carboxylase cofactor) and bone metabolism (osteocalcium requires vit K)
  • AI! based on representative dietary intake data from healthy individuals
49
Q

what are the 2 forms of vit K?
- from what?
- bioavailability?
- number?

A

PHYLLOQUINONE:
- major form of vit K in the diet
- mostly from plant foods –> badly absorbed, better absorbed if taken with fat source
- vit K1
MENAQUINONES:
- produced by bacteria in the lower bowel
- more bioavailable + stays in blood longer than vit K1
- from probiotic foods, yogurt, fermented soy…
- vit K2

50
Q

AI for vit K?
UL?

A

AI = 90 ug/day for women, 120 ug/day for men
- no UL! except if on anticoagulant therapy! if taking coumadin/warfarin, don’t increase plant foods bc vit K will override meds

51
Q
A