2.2 Vitamin reqs during adulthood Flashcards
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?
- 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
- how is thiamin status assessed by? (3)
- ____ adjustment to estimated requirement fro men vs women –> why (2)
- 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
- [thiamin] and its phosphorylated esters in blood
- urinary thiamin excretion under basal conditions or after thiamin loading
- 10% (small) adjustment –> not the same energy utilization and not the same size
if someone’s erythrocyte transketolase activity coefficient is 1.2, does he/she have a thiamin deficiency?
- give ranges!
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)
what is the EAR/RDA/AI for thiamin?
- UL?
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
RIBOFLAVIN
- which vitamin letter?
- functions? examples!
- primary form of travel?
- 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
riboflavin is important in which antioxidant systems?
thioredoxin and glutathione/glutaredoxin!
riboflavin: EAR for adults derived from which (4)
- erythrocyte glutathione reductase activity coefficient
- RBC [riboflavin]
- urinary riboflavin excretion in relation to dietary intake –> if urine is really yellow = adequate B2
- studies of occurrence of signs of clinical deficiency (biochemical changes in riboflavin status occur before appearance of overt signs of deficiency)
if someone’s erythrocyte glutathione reductase activity coefficient is 1.2, does he/she have a riboflavin deficiency?
- give ranges!
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
EAR and RDA for riboflavin
- UL?
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
- what are the 2 forms of niacin?
- which form is used to lower blood lipid levels?
- niacin generates which 2 cofactors?
- function?
- vitamin ____?
- 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
NIACIN:
- primary criterion for RDA?
- adjustment made for bioavailability?
- can we synthesize niacin?
- which disease if deficient?
- urinary excretion for niacin metabolites
- nope! –> requirements expressed in niacin equivalents (NEs)
- yes! we can convert tryptophan (60mg) to niacin (1 mg)
- pellagra!
EAR and RDA for niacin?
- UL?
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
- name for vit B6?
- function?
- 2 circulating forms?
- primary criterion to estimate RDA?
- 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
Folate:
- coenzyme in _____-______ transfers in met of ______ and ______ _______
- synthesis of what?
- cofactor of enzymes that metabolize (4)
- cofactor form of folate = ___________
- 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
- 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
- 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
why is food folate not super bioavailable?
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
will homocysteine levels increase or decrease with B6 deficiency?
- folate deficiency will increase homocysteine levels bc folate needed to convert homocysteine to methionine
*but homocysteine levels also increase if B12 and choline deficiency
is there a UL for folate?
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
vitamin B12:
- name?
- acts as what?
- functions (2)
- RDA based on (2)
- EAR/RDA?
- UL?
- 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
- vit B12 only in which products?
- what does increase in L-methylmalonic acid in urine mean?
- what is the methyl trap?
- 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
Biotin:
- function? examples
- AI or RDA? basis?
- UL?
- risk of deficiency?
- 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
CHOLINE:
- precursor for (3)
- AI or RDA? criterion?
- 2 types of choline in diet
- 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)
what is the primary compound of VLDL?
- what happens if deficiency of choline?
- phosphatidylcholine
- if no choline –> liver cannot synthesize VLDL = it cannot export fat = leads to fatty liver
deficiency in betaine leads to increase or decrease of homocysteine levels?
betaine is needed as a methyl group donor
- if betaine deficiency, homocysteine will increase
choline requirement is influenced by (2)
- AI or RDA set for choline, but requirement could be met by what?
- UL?
- 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
pantothenic acid
- vitamin ____
- component of (2)
- present in foods?
- deficiency common? from what? (2)
- 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)
Pantothenic acid:
- primary criterion to estimate AI/RDA?
- usual intake?
- AI/RDA?
- UL?
- 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
vitamin C:
- functions (2)
- RDA based on vit C intake to (2)
- RDA?
- UL?
- 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
vitamin A;
- important for (6)
- EAR based on what?
- 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
vitamin A:
- preformed vit A (retinol) found where?
- provitamin A carotenoids found where?
- what is retinol activity equivalent? + examples
- 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
EAR and RDA for vit A
- UL?
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)
- 2 functions of vit D
- major physiologically relevant forms (2)
- found where? synthesized where?
- 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
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
- 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
EAR and RDA for vit D
- UL?
for men and women 19-70 yo
- EAR = 10 ug/day
- RDA = 15 ug/day (600 IU)
- UL = 4000 ug
vitamin E:
- other name?
- specific role in what?
- major function?
- lipid or water soluble? –> resides where?
- 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
vit E:
- RDA based on what? explain
- how are tocopherol radical converted back to tocopherols?
- 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…
what are the different forms of tocopherol (4) + toco_______ (4)
- give characteristics
- RDA based on which one?
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
which stereoisomer of a-tocopherol is metabolically active in humans?
- DRI limited to which form? –> examples?
- which stereoisomer does food contain?
- 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)
- 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?
- 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
why are only 2R-stereoisomeric forms used to estimate vit E requirements?
bc 2-S stereoisomeric forms, other tocopherols (b-y-d) and tocotrienols fail to bind with a-TTP
EAR and RDA for vit E?
- limitation?
- UL?
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
what are the 3 events for lipid peroxidation?
- what about when vit E is present?
- initiation radical oxidant + LH -> inactive oxidant + L°
- propagation: L° + O2 –> LOO° (peroxyl radical)
*more propogation - 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
- FR cause what?
- FR + Tocopherol –> __-______ ______ + ______a_____ _____a______
- ______a_____ _____a______ + what –> tocopherol
- ______a_____ _____a______ can also cause what?
- 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)
what are the 4 co-oxidants for vit E?
- ascorbate
- caffeic acid (plant foods, it’s a polyphenol)
- ubiquinols
- bilirubin
how can smoking cause oxidative stress?
smoking elicits an inflammatory response (bc of toxic compounds) –> increase neutrophils which produce lots of FR/ROS (like malondialdehyde)
what is the correlation btw RBC vit E and plasma ascorbate?
- high doses of vit E will significantly decrease plasma ascorbate!
what is the antioxidant network?
- if it’s optimized, what could be substantially decreased?
- 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
vitamin K
- coenzyme during synthesis of proteins involved in (2)
- RDA/AI? based on what?
- 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
what are the 2 forms of vit K?
- from what?
- bioavailability?
- number?
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
AI for vit K?
UL?
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
