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Digestive Systems, Nutrition, and Metabolism > Vitamins > Flashcards

Vitamins Flashcards

1
Q

Fat soluble vitamins?

A

A (retinol, B-carotene), D (cholecalciterol), E (tocopherols), K (phylloquinones, menaquinones)

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2
Q

Water soluble vitamins from non-B complex

A

C (ascorbic acid)

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3
Q

water soluble vitamins from B complex that are energy-releasing

A

B1 (thiamine), B2 (riboflavin), B3 (niacin), biotin, pantothenic acid

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4
Q

water soluble vitamins from B complex that are hematopoetic

A

folic acid, B12

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5
Q

water soluble vitamins from B complex that are neither energy releasing nor hematopoetic

A

B6 (pyridoxine), pyrodoxial, pyridoxamine

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6
Q

Vitamins involved with blood formaiton and clotting

A

B6, B12, Folate, K

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7
Q

Vitamins involved with protein and AA metabolism

A

B6, Folate, B12, C, choline (not a true vitamin), riboflavin (indirectly)

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8
Q

Vitamins involved with antioxidant defenses

A

E, C (likely), Carotenoids, riboflavin (indirect)

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9
Q

Vitamins involved with gene expression

A

A, D

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10
Q

Vitamins involved with bone health

A

A, D, K, C

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11
Q

Vitamins involved with energy metabolism

A

thiamin, riboflavin, niacin, pantothenic acid, biotin, B12

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12
Q

bio- in terms of vitamins

A

how much of the vitamin actually gets into us and is activated?

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13
Q

Facts about many vitamins

A
  1. hydrolyzed in stomach and are released from protein complexes in food
  2. most are absorbed in upper small intestine. B12 is the only exception (absorbed in ileum)
  3. water soluble vitamins are absorbed directly into portal vein, transported to liver, and are stored (B12) or sent out in circulation
  4. Excess water soluble vitamins are excreted through kidneys in urine
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14
Q

describe absorption process of fat-soluble vitamins

A

absorbed with monoglycerides and FAs.
1. mixed micelle in the intestinal lumen, containing FA, cholesterol, D, A, E, K)
2. repackaged in chylomicrons
3. chylomicron sent to lymphatics before entering blood
Note: the fats do not go directly into portal circulation because chylomicron is too large
Note: requires bile salts

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15
Q

What are all the forms of vitamin A?

A
  1. Retinol (active form, comes from retinyl esters and animal foods)
  2. retinal (note, spelt with a, not o), which converts to retinoic acid
  3. Beta-carotene (the fused form of retinal and retinol). found in plant foods and supplements. has alternating singular and double bonds, which is why it is colored!!! IN this case, plant foods that are red, orange, and yellow
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16
Q

what is a retinol activity equivalent (Rae)?

A

Note: you can eat b-carotene and get retinol. Specifically, 12 micrograms of B-carotene will yield 1 microgram of retinol.

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17
Q

Functions of vitamin A

A
  1. Vision ( Essential for seeing black and white (“rod” cells in retina)
     Particularly important for night vision and recovery of sight after a
    flash of bright light (like snow-blindness))
  2. Cell differentiation ( Process by which a new cell turns into its “destined” form
     Important for the maturing of “epithelial cells”, such as those in the intestine and skin (in deficient state, the skin is highly effected)
     Important for the development of the embryo into a fully formed
    organism
     Important synthesis of lymphocytes and antibodies (immune
    function)
     Bone health
     Protection against cancer?)
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18
Q

how does vitamin A affect vision?

A
  1. Light shines through to retina
  2. within retina are rods and cones. the light hits the rods to affect rhodopsin (combo of opsin and cis-retinal)
  3. when light hits cis-retinal, it converts to trans-retinal, separating trans-retinal from opsin.
  4. the trans-retinal is converts to cis-retinal and retinoic acid. the opsin combines back with the cis-retinal to form og rhodopsin molecule.
    Note: the splitting step is important for brain so see.
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19
Q

how does vitamin A affect cell differentiation?

A

immature cell + vitamin A = differentiation cell –> could become any cell based on location. Really important for digestional tract, as in example it became intestinal cell.

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20
Q

What happens if you are vitamin A deficient? Who are susceptible?

A

All of these disorders are more common in developing countries
Mild deficiency: night blindness
Severe forms are xerophthalmia (damage to cornea, dry eyes, scarring, and blindness)
and hyperkeratosis (increased keratin synth in skin and nails) as well as infections.

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21
Q

What can be done to prevent Vitamin A deficiency?

A

GMOs. Example: genetically modified rice what synthesizes B-carotene.

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22
Q

What are the 2 forms of vitamin D?

A
  1. D2 (ergocalciferol) (methyl + double bond)
  2. D3 (cholecalciferol) (nothing)
    Both structures look like cholesterol
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23
Q

How do you make vitamin D?

A
  1. UV rays from sun hit skin, specifically 7-deydrocholesterol to convert it to cholecalciferol (D3).
  2. D3 (from skin, or from diet…fish + meat) along with D2 (from diet only…supplements) are sent to liver, which produces 25-hydroxyvitamin D3.
  3. 25-hydroxyvitamin D3 is sent to kidney, which makes 1,25-dihydroxyvitamin D3 (aka calcitriol). Calcitriol = active form.
    Note: 1,25-dihydroxyvitamin D3 maintains Ca balance in body
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24
Q

What factors affect D3 synth?

A 
 Overcast skies
 Smog
 Dark skin (melanin)
 Angle of sunlight (winter)
 Sunscreen
 Age
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25
Q

What are the functions of vitamin D?

A
  1. Ca homeostasis ( Increases calcium absorption and bioavailability
     Decreases calcium excretion by the kidneys (urine)
     Increased calcium release from bones)
  2. Gene expression and cell differentiation (like Vitamin A) through vitamin D receptor
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26
Q

How does vitamin D help with Ca absorption and bioavailability?

A
  1. 1,25(OH)2D3 (calcitriol) enters enterocytes and binds to vitamin D receptor (cytosol receptor).
  2. Cytosol sends calcitriol to nucleus
  3. nuc causes gene expression, which causes production of Ca Binding Protein
  4. Calcium binding protein binds Ca that was absorbed from diet.
  5. Ca binding protein + Ca from diet leave enterocyte together and travel to rest of body
    Note: consuming high levels of Ca will causes Ca to just passively enter basolateral side through paracellular pathway.
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27
Q

How does vitamin maintain Ca homeostasis?

A
  1. If Ca starts to rise, signal is sent to thyroid, which releases calcitonin, which tells kidneys to reduce Ca uptake and tells bones to deposit Ca to the bones. Homeostasis obtained.
  2. If stimulus shows a drop in Ca, signal goes to parathyroid gland and tells it to secrete PTH . PTH tells bones to release calcium, tells kidneys to recycle (reabsorb) Ca, and tells kidneys to produce more calcitriol, which goes to intestines to increase Ca uptake. Homeostasis obtained.
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28
Q

How does vitamin D affect gene expression

A

calcitriol, after full synth from liver, enters nucleus and activates vitamin D receptor, which binds to the DNA and activates transcritption. Calcitriol could also bind to vitamin D receptor on the cell membrane surface, which triggers signaling pathways that trigger transcription in the nucleus

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29
Q

What happens if you have severe vitamin D deficiency?

A
  1. Rickets (in zeh kiddies, bones are not developing and strengthening. Legs become bow-legged, bending under weight of child)
  2. osteopenia (bone density begins to dwindle) and Osteoporosis (more critical loss of bone, which can lead to fractures). between 1 and -2.5 standard deviations = osteopenia. anything less than that = osteoporosis. comparison to other bone densities on the planet
  3. 1,25 hydroxylase is found in many cells (converts inactive to active form of vitamin D). Vitamin D is found in almost every cell in the body. Realized it can lead to brain abnormalities is too low. Leads to hyperintensive signal in the periventricular white matter.
  4. can also lead to alzheimer’s and dementia. All kinds of memory (spacial, executive function, episodic, sensory) all took some kind of L if they were low in vitamin D.
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30
Q

What are the forms of vitamin K?

A
  1. K1 Phylloquinone (from plants and supplements). only has single bonds
  2. K2 menaquinone (come from bacteria in large intestin) (has alternating single and double bonds)
  3. K3 menadione (man-made, “pro-vitamin”)
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31
Q

What is vitamin K involved with?

A

Blood clotting (coagulation)
1. inactive clotting factors link with K and Ca to make active clotting factors.
2. the active clotting factors convert prothrombin to thrombin
3. Thrombin converts fibrinogen (water soluble) to fibrin (NOT water soluble), which is the clotting
Note: Warfarin (Coumadin) is a blood thinner that works by cutting out vitamin K, inhibiting clotting ability. If overused, patient will bleed out in situations of a cut. Note that warfarin is also used as rat poison, causing the rats to bleed to death.

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32
Q

How does vitamin K affect bone calcification?

A
  1. Vitamin D regulates asteocalcin transcription.
  2. K catalyzes the reaction
  3. Calcium is now allowed to bind to active osteocalcin.
  4. end result is hydroxyapatite structure
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33
Q

what happens if one is K deficient?

A

Uncontrollable Bleeding!!!
 Rare in adults
 More common in newborns
 Low vitamin K stores at birth
 Little or no bacterial production in large intestine
 Low levels of vitamin K in breast milk
 All babies given vitamin K injections at birth (to get them through 6 months until they can support their own)
 Can occur in children and adults with fat malabsorption diseases, causing deficiencies in ADEK.
 Prolonged use of antibiotics kill large intestine bacteria (this tanks K presence)

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34
Q

What are the forms of vitamin E?

A

Most biologically active form is alpha-tocopherol

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35
Q

What is the main function of Vitamin E?

A

Works as an antioxidant!
 Protects biological membranes (lipophilic regions) against free radicals
 Especially important to tissues exposed to oxygen (e.g. lungs
and red blood cells)
 Works best in conjunction with vitamin C and selenium (as in E does not work best in isolation. Needs its crew)
 Protects DNA from oxidative damage (may reduce risk of cancer)
 May protect against cataracts
 May protect against heart disease

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36
Q

How does vitamin E function?

A

Oxidant (due to stress, injury, or toxins) at phospholipid membrane interacts with the FA chain on phospholipids, causing oxidation, leading to chain reaction, killing the adjacent FA chains. When it encounters E, the chain reaction stops. This allows the cell to recover and maintain membrane integrity

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37
Q

How does Vitamin E interact with vitamin C?

A

When E takes the free-radical hit, you need to convert that E back to normal. E fixes itself by passing radical off to vitamin C. Vitamin C, through enzymes, removed the free radical.

38
Q

What happens if you are deficient in E?

A

Hemolytic anemia:
 Rare, but occurs in infants fed formula with too little vitamin E, in
cystic fibrosis (fat malabsorption disorder)
 Weakened and ruptured red blood cells (due to oxidative damage to their phospholipid membranes)…link this to biliruben! You can also think about sickle cell anemia.
 Neuromuscular problems, neuromuscular pain, loss of
coordination

39
Q

What are the forms of vitamin C (ascorbate, ascorbic acid)

A
  1. L-ascorbic acid (hydroxyls)

2. L-dehydroascorbic acid (no hydroxyls)

40
Q

What are the functions of C?

A
  1. Antioxidant
     Increases absorption and bioavailability
     Reduces superoxide (bad oxygen) to hydrogen peroxide (not
    so bad oxygen)
  2. Reduces iron (and copper, and chromium)
     Increases absorption and bioavailability
     Drink orange juice with fortified cereal
  3. Synthesis of important molecules
     Carnitine: fatty acid metabolism for energy production
     Tyrosine: amino acid
     Neurotransmitters: nervous system function
     Hormones: particularly digestive hormones
     Collagen: required for making skin, muscles, cartilage,
    tendons, and gums
41
Q

How does C work as an antioxidant?

A
  1. Superoxide anion (O2-) is linked with ascorbic acid (C). C is converts to dehydroascorbic acid and superoxide is converted H2O2.
  2. H2O2 is converted to water
42
Q

How does C reduce iron?

A

Fe3 is converted to Fe2 by using ascorbic acid and converting it to dehydroascorbic acid. This is important for Fe absorption.

43
Q

How does C help with Fe absorption?

A
  1. Heme iron is absorbed (from animals) is more readily absorbed into enterocyte
  2. If you insist in getting Fe in through plant sources, you need C, which converts Fe3 to Fe2 through oxidation. Fe2 is the only form that can be absorbed. Problem is that Fe2 is not the best for the enterocyte, so Fe2 is stored in Ferritin. If not stored, it is kicked out through transporter and converted back to Fe3, and bound to transport protein called Transferrin.
44
Q

What happens in C deficiency?

A

Scurvy!
James Lind: British Doctor discovered it.
 Cured scurvy with lemons and limes in British sailors (origin
of the nickname “limeys”)
 Bleeding gums, skin irritation, bruising, poor wound healing

45
Q

Is vitamin C good at preventing colds? When you do get the cold, does it help reduce cold duration?

A

If patients are in constant cold and stressful environments, then yes, C is effective. If the patient is in normal environments, it does not have a strong effect. Upon getting the cold, C is proven to reduce its duration (10 percent reduction…so, like a day).

46
Q

Which vitamins are involved with ATP?

A

B1, B2, B3, B5, and B7

47
Q

What are the forms of B1?

A
  1. B1 (thiamin)…supplement form

2. TPP (thiamin pyrophosphate)…this is the active cofactor form…the form with addition of 2 phosphates.

48
Q

How does B1 get absorbed and made available?

A
  1. B1 gets absorbed with vitamin C. In the presence of oxidants in foods or in the presences of OH, thiamin enterocyte absorption into duodenum or jejunum fails.
  2. Thiamin that successfully enters if activated with presence of 2 ATP molecules to become TPP. TPP then flows out to basolateral side and enters blood to get to the liver.
49
Q

What are the functions of B1?

A 
1. ATP production (energy)
 Pyruvate to acetyl CoA
 Krebs cycle
 Pentose-phosphate pathway
2. DNA/RNA synth
 Required for enzymes that synthesize DNA and RNA
3. NADPH synth
 Required for various functions, including triglyceride synthesis
4. Nerve function
 Thiamin Triphosphate (TTP)
50
Q

What enzymes in the pentose phosphase, glycolysis, and krebs cycle are B1 involved in?

A
  1. Transketolase in Pentose Phosphate Pathway
  2. Pyruvate Dehydrogenase in Glycolysis
  3. alpha-ketoglutarate dehydrogenase in
51
Q

What happens if you are deficient in B1?

A

Beriberi Disease. There are 4 forms:
1. Dry
 Severe muscle wasting, leg cramps, tenderness, decreased
feeling in feet and toes (peripheral neuropathy)
2. Wet
 Swelling (edema) of arms and legs, enlargement of heart,
breathing problems, possible heart failure
3. Infantile
 Babies breast-fed by thiamin-deficient mothers
 Heart failure
4. Cerebral (Wernicke-Korsakoff Syndrome)
 Often caused by ALCOHOLISM (low B1 intake + impaired absorption)
 Involuntary movement and paralysis of the eye, poor muscle
coordination, confusion and short-term memory loss.

52
Q

What happens if you are B1 deficcient?

A

Correlated to having heart failure.

53
Q

What are the forms of B2 (riboflavin)

A
  1. Riboflavin
  2. Flavin mononucleotide (FMN)…Active form since it has a new phosphate group
  3. Flavin adenine dinucleotide (FAD)…also Active form since it added yet another phosphate group
54
Q

In Krebs, what produced energy molecule does riboflavin help to produce? How does this affect ATP production?

A
  1. 2 FADH2’s
  2. The FADPH’s are used in ox phos to pump H’s into the mitochondrial intermembrane space, which leads to ATP production.
55
Q

What are the functions of B2?

A
  1. Redox reactions (it oxidizes NADPH to NADP+ and converting FAD to FADH2. The FADH2 the oxidizes a substrate, converting itself back to FAD)
  2. ATP Production (Energy)
     Krebs cycle
     Use of fatty acids for energy
  3. Synth or activation of Vitamins
     Vitamin A, folate, niacin, vitamin B6, vitamin K
  4. Neurotransmitter Metabolism
     Dopamine, Norepinephrine
56
Q

What happens if one is deficient in B2?

A

Ariboflavinosis
 Isolated deficiency is rare
 Generally occurs in instances of malnutrition and multiple
micronutrient deficiencies
 Muscle weakness, mouth and lip sores (cheilosis), mouth
inflammation (stomatitis), enlarged and inflamed tongue (glossitis)
 Can occur secondary to alcoholism and thyroid disease.

Can also cause glossitis t(tho other vitamin deficiencies also cause this, so this is not a determining factor), and seborrheic dermititis (screws up skin on head, nose, eyes , chest area, naval, crotch area)

57
Q

What is the relationship between B2 and BP?

A

B2 reduces BP in peoplez with genetic predisposition to high BP. Can legitimately lower it as much as 10 units of BP.

58
Q

What are the forms of B3 (niacin)

A
  1. Niacin (inactive)
  2. Nicotinamide (inactive)
  3. NAD (nicotinamide adenine dinucleotide)…active form
    4 NADP (Nicotinamide adenine dinucleotide phosphate)…active form
59
Q

What AA can be converted to niacin? what other vitamins have alternate ways to be obtained int he body?

A

tryptophan
2. D can be obtained through sunlight UV reactions on skin. A can be obtained by eating B-carotene. In all 3 cases, the alternative path is not enough to sustain health, so you need all the pathways offered.

60
Q

How does B3 help with ATP production?

A

It is a cofactor for 2 steps in glycolysis and a cofactor for one step in krebs.

61
Q

What are the functions for B3 (niacin)

A
  1. Redox reactions (it oxidizes NADPH to NADP+ and converting FAD to FADH2. The FADH2 the oxidizes a substrate, converting itself back to FAD)
  2. ATP Production (Energy)
     Krebs cycle
     Use of fatty acids for energy
  3. Synth and metabolism of many compounds.
     Fatty acids, cholesterol, steroid hormones, DNA, Vitamin C, folate
  4. Cholesterol metabolism
     Lowers LDL and raises HDL
62
Q

What happens if you are deficient in niacin?

A 
Pellagra
 Once was very common in the Southern U.S. due to corn being the
primary source of protein (corn is low in both niacin and tryptophan)
 The 4 “D’s”
 Dermatitis
 Diarrhea
 Dementia
 Death

Patients with Niacin deficiency are also present with Casal’s necklace and bilateral symmetrical rash upon sun exposure

63
Q

How does Niacin (B3) affect cholesterol and TAGs?

A

Lowers them. However, the side-effect is flushing and itching, which you would treat with aspirin or ibprofen

64
Q

What are the forms of panothenic acid (B5)…Note: pan = everywhere, which describes it’s involvement in energy production.

A
  1. Pantothenic acid
  2. 4-phosphopentethenine
  3. CoEnzyme A (CoA)
  4. Acyl carrier Protein (ACP) (carries coenzyme A)
65
Q

What are the functions of B5 (panathonic acid)?

A 
1. ATP production (energy)
 Glycolysis
 Krebs cycle
2. Synthesis of many compounds
 Heme, cholesterol, bile salts, phospholipids, fatty acids, steroid
hormones
66
Q

What is special about B5’s involvement in energy production?

A

It is is the CoA in acetyl CoA. Which means, B5 is involved in nearly every energy pathway

67
Q

Describe the Biotin (B7) cycle Where is biotin obtained?

A
  1. Biotin is obtained from diet and gut flora (like K)
  2. Biotin is involved in the activation of apocarboxylase to make holocarboxylase
  3. holocarboxylase is used in protein catabolism, Fa synth, and gluconeogenesis
68
Q

How can biotin (B7)’s bioavailability be affected?

A

Biotin is typically bound to protein in food; usually does not affect bioavailability much
Exception: avidin (found in egg whites)
 Very strong binding to biotin, inhibits absorption (the strongest binding to 2 substances in all of biology that we know of)
 Only a problem when eggs are eaten raw (uncooked). you would need to cook it.

69
Q

What are the of biotin

A 
Carboxylase reactions:
 Gluconeogenesis
 Protein catabolism
 Fatty acid synthesis
 ATP Production (acts as a cofactor in conversion of pyruvate to oxaloacetate)
70
Q

What happens if one is deficient in biotin?

A

Not common. But, can be an issue B7, more so in kiddies eating foods lacking :
 Daily consumption of a large number of raw eggs
 Intestinal diseases that block absorption (e.g. inflammatory bowel
disease)
 Depression, hallucinations, skin irritation, infections, hair loss, poor
muscle control, seizures, developmental delays

71
Q

What is one-carbon metabolism? What enzyme is the simplest to mod and convert to an entirely different enzyme, affecting the direction of the C from serine?

A
  1. Based off folate metabolism
  2. Serine IS THE SOURCE of the one carbon.
  3. This one carbson leads to synth of THF, methyleneTHF, FormylTHF, and DHF. F = folate. All the folates would be affected.
  4. That one carbon is also linked to DNA production, as well as to methionine and its pathways
  5. MTHFR is the stated enzyme.
72
Q

how do you convert folic acid to THF?

A

you reduce it 2x with NADPH

73
Q

What is B6? what does it do?

A

PLP (active form), responsible of converting serine to glycine

74
Q

What are the 4 important AA in the one-carbon metabolism?

A

serine, glycine, homocysteine (has sulfur group), and methionine

75
Q

What is transulfuration pathway?

A

serine + B6 becomes cystathionine. if you add another B6, you get cystein

76
Q

What are the 4 important AA in the one-carbon metabolism?

A

serine, glycine, homocysteine (has sulfur group), and methionine

77
Q

What are the forms of B6?

A
  1. Pyridoxine (PN)- supplement
  2. Pyridoxal 5’-phosphate (PLP) - active cofactor
  3. 4-Pyridoxic acid (found in urine)
78
Q

Describe the B6 absorption process

A
  1. Phosphorylated B6 (such as PMP or PLP) encounter hydrolase in the lumen, which dephosphorylates it.
  2. Dephosphorylated forms (PN, PNG, PM, PL) can now be absorbed in jejunum.
  3. If the enterocyte needs some of the B6, it will re-phos it with a kinase.
  4. Remaining unphos forms are sent across basolateral side into blood.
  5. Some of the B6 enters RBCs, converted to PLP in the RBC, and stays trapped there (thank the phosphorylation.)
79
Q

List some of the reactions PLP are depended on to run? Note that there are over 100.

A 
1. Transamination
 Amino acids to respective keto acids
 Ex. Glutamate to α-ketoglutarate
2. Decarboxylations
 Elimination of CO2
 Ex. L-dopa (neurotranmitter...linked to parkinson's disease when in low quantities, since you would be unable to make dopamine) to dopamine. note, L-dopa does not cross BBB. It Can't. Only dopamine can, which makes treating disease difficult. If you don't have B6, you can't make dopamine, which could lead to this disease
3. Heme synth (first step)
 Succinyl CoA + Glycine = δ-Aminolevulinate
4. One-carbon metabolism
 Serine-Glycine interconversion
 Homocysteine catabolism
5. Lipid and carb metabolism
 Sphingolipid synthesis
 Muscle glycogen phosphorylase
80
Q

Describe the B6 absorption process

A
  1. Phosphorylated B6 (such as PMP or PLP) encounter hydrolase in the lumen, which dephosphorylates it.
  2. Dephosphorylated forms (PN, PNG, PM, PL) can now be absorbed in jejunum.
  3. If the enterocyte needs some of the B6, it will re-phos it with a kinase.
  4. Remaining unphos forms are sent across basolateral side into blood.
81
Q

What is the relationship between PLP and the SChiff Base Formation?

A

PLP apparently does a shift base reaction with a side chain of an enzyme, allowing for transamination/decarboxylation reactions. PLP then comes off and does it again. Those taking High dose L-dopa for parkinsons have low B6 in circulation and are at risk for being B6 dependent because of the high dose of the drug you have to give. Reason: the L-dopa drug forms a shift base reaction with PLP, locking it up and keeping it from working on anything else. Remember that PLP = B6, and B6 does over 100 reactions in the body….

82
Q

What happens if you are deficient in B6?

A
  1. Microcytic anemia (will look SMALL and EMPTY in pics because there is NO HEME in these RBCs). Note that this is more commonly caused by Fe deficiency
     Inhibited heme synthesis
  2. Convulusions/EEG abnormalities
     Inhibited neurotransmitter synthesis (e.g. serotonin, dopamine)
     Accumulation of toxic products of tryptophan metabolism
    3 Hyperhomocysteinemia
     Inhibited homocysteine catabolism
     Increased risk of vascular disease
  3. Inflammatory disease (which may be reducing the B6 level)
     e.g. inflammatory bowel disease, rheumatoid arthritis
     Reduced plasma PLP
     Cause or effect?
    Note that as inflammation increases, B6 status decreases.
83
Q

What are the different forms of folate (folic acid aka B9)? Where does the supplemental part get acted on to become active?

A
  1. supplemental, which contains glutamic acid , para-amino-benzoic acid (PABA)..found in sunscreens and lotions, and 2,4,6-substituted pterin. Gets acted on at 5 and 10 spots to become active. Note that all the active forms are reduced. They are the following:
  2.  Tetrahydrofolate (THF)
  3.  N5-methyltetrahydrofolate (CH3-THF)
  4.  N5,10-methylenetetrahydrofolate (CH2-THF)
  5.  N5-formyltetrahydrofolate (CHO-THF)
  6.  Dihydrofolate (DHF)
  7.  Methotrexate (10-methyl-4-amino-THF)…note that this substitution as at the 4th position instead of the 5th. used for arthritis (and cancer in higher doses)…works because if you block folate, you block DNA synth, which will kill the cancer cell (along with the noncancered cells :/).
84
Q

How do you absorb folate?

A
  1. Folate is thiccc (stacked with a long chain of glutamates). This long chain prevents crossing into the jejunum enterocyte. Solution: GCP-II enzyme, which cuts off the c’s (glutamates) until there is only one glutamic acid on the end.
  2. Folate enters enterocyte, simaltaneously with H.
  3. Cell may convert it to ch3-THF for its own use. It may also sent this ch3-THF out tot eh blood.
  4. It could also just go straight through to the basolateral side if given in high enough doses, without being converted to ch3-THF
85
Q

Explain the dietary folate equivalents (DFE) pertaining to folate.

A

0.5 micrograms folic acid consumed without food. This goes does to 0.6 if eaten with food. This goes down even further if you just eat it directly (like, folate found in food instead of straight up folic acid). Lgtitmately need to eat 2x as much food folate as you would need if you just ate folate acid without food. So, to best absorb folate, you need to eat it as folic acid, and you need to eat it without any food.

86
Q

What can lead to folate malabsorption?

A 
 Small bowel disease (Crohn’s, celiac)
 Infection (HIV, tropical sprue)
 Ileal resection
 Abdominal radiation exposure
 EtOH impairment of GCP II activity
 Vitamin B12 deficiency
 Drugs (anti-convulsants)
87
Q

What are the functions of Folate?

A
  1. DNA/RNA Synth (thymidine (T), adenine (A), guanine (G))
  2. Methionines recycling (conversion of homocysteine to methionine)
  3. s-adenosylmethionine (SAM) synth (methylation reactions)
88
Q

What happens if you are deficient in folate?

A
  1. Deranged DNA synth
     Uracil misincorporation (deficiency in folates means you can’t convert the U’s to P’s. All the U’s present increase the frequency at which U misincorporation occurs. The enzymes still cut the U’s out, but now there are more U’s being cut than normal, making the DNA more susceptible to breaking during the cutting process than normal.)
     DNA strand breaks (double strand breaks fam…)
  2. Hyperhomocysteinemia (folate is needed to metabolize this H-word thing. without folate, this thing increases in concentration in the blood. high amounts of this is a risk for heart disease, vascular diseasie, stroke, alzhemer;s dementia)
     Elevated homocysteine in plasma
     Elevated SAH levels in tissues
     Decreased SAM levels in tissues
89
Q

What are the clinical manifestations of folate deficiency?

A
  1. macrocytic (megaloblastic) anemia (due to inhibited DNA synth) (smear would show enlarges RBCs and macrophages with increased number of dark lobes (8)…normal amount is 3.). the cells are macrocytic because they can’t divide while in the bone marrow like they normally would, as a result of the low folate. The anemia part is the fact that there are less rbcs as a result, even tho they are bigger. Note that B12 deficiency would also have macrocytic anemia.
  2. hyperhomocysteinemia
     Inhibited homocysteine metabolism
     Increased risk of vascular disease, dementia
  3. neural tube defects
     Spina bifida
     Anencephaly (brain exposed to amniotic fluid since skull did not close. will lead to spontaneous abortion due to failed brain formation)
90
Q

describe relationship between B12 and neural tube defects

A

increase B12 = decrease in neural tube defects. does not matter if the person was given fortified folate or supplement. if the country’s diet was already B12-Lit, then the effects seen were not as great (because they were ahead of the curve to begin with). Best effects were seen in countries which were sleepin, not realizing to put B12 in their foods and then finally seeing the light that is B12.

91
Q

link relationship between folate, homocysteine, and heart disease.

A

low folate = high homocysteine = increased heart disease risk. note that if you lower homocysteine, you do not see a particular decrease in heart disease :/ weak hypothesis. but there may still be a solid correlation according to china study, which showed increased protection against stroke when homocysteine was lowered.

92
Q

How does Folate manifest in terms of toxicity?

A

Folic acid:
 May mask B12 deficiency
 May promote cancer growth (blocking DNA synth (due to low amounts of folate) kills cancer cells, so if you give a ton of folate, the cancer cells may just grow out of control
 No real toxicity known for natural forms of folate in foods

Digestive Systems, Nutrition, and Metabolism (20 decks)

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