week 2, lecture 2 Flashcards

(72 cards)

1
Q

vitamins get metabolized into larger ______?

A

coenzymes

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2
Q

B2 is aka

A

ribofalvin

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3
Q

what are the B2 coenzymes

A

FAD and FMN

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4
Q

FAD –> FADH2 is oxidation or reduction

A

reduction

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5
Q

what 3 reactions are vitamin B2 (FAD) needed for

A
  1. beta oxidation of fatty acids
  2. ETC: FADH2 –> FAD to give electrons and make ATP
  3. CAC for succinate –> fumarate via succinate dehydrogenase (reduce FAD to FADH2)
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6
Q

what is vitamin B3 AKA

A

niacin

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7
Q

what are the coenzynmes of vitamin B3/niacin

A

NADH and NADP+

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8
Q

what 3 reactions need vitamin B3/ coenzymes NAD+ and NADP+

A
  1. glycolysis and CAC (glucose and pyruvate) [NAD+]
  2. lipid and amino acid metabolism [NAD+ and NADP+]
  3. ETC: give ATP via NADH oxidized to NAD+
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9
Q

Based on size, which is more likely to diffuse across cell membranes: vitamins or coenzymes?

A

vitamins (smaller)

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10
Q

Can a Co-enzyme turn back into a Vitamin?

A

no (its unidirectional)
- i.e phosphorylation alters its structure
-i.e. vitamins only from diet

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11
Q

b vitamin defifiencies

A

stress, alcohol, IBS< meds, autoimmune, inadequate intake, malabsorption, pregnancy

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12
Q

B1 is AKA

A

thiamin

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13
Q

B1 pathways

A
  1. CAC: pyruvate dehydrogenase complex and the alpha- ketoglutarate dehydrogenase complex
  2. pentose phosphate shunt: for transketolase enzyme (connect to glycolysis)
  3. succinyl coa (from CAC) is substrate for heme synthesis –> oxygen –> ATP
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14
Q

what is the coenzyme of vitamin B1/thaimin

A

TDP/ TPP
(thiamine diphosphate/pyrophosphate)

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15
Q

what type of enzyme takes the TDP from food and turns it into thiamin (vitamin B1)for absorption?

A

phosphatase

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16
Q

What type of enzyme takes absorbed thiamin and metabolizes it to make the TDP coenzyme?

A

thiamine pyrophosphokinase (TPK)

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17
Q

what does pyruvate dehydrogenase complex and alpha ketoglutarate complex in the CAC produce

A

NADH

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18
Q

how does B1 contribute to energy via succinyl coA being a substrate for the synthesis of what?

A

heme synthesis
heme –> hemoglobin –> oxygen to tissues –> oxygen for glucose and other nutrients into ATP

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19
Q

what are anti thiamine factors that can cause deficiency

A
  1. sulphur dioxide (dried fruti and veg, alcohol)
  2. thiaminases (raw fish- inactivated by heat)
  3. polyphenols (tea and coffee–> join 2 thiamines together and make too big for absorption)
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19
Q

what pharmaceuticals contribute to B1 deficiency and how

A

5-fluorouracil (chemo) and diuretics

inhibit thiamine phosphorylation so it cannot be converted to its active form, TDP

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20
Q

how does B1 affect energy dependent tissues like heart and brain

A

no thaimine to turn pyruvate to acetyl coa in the CAC so it reduces ATP production

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21
Q

B1 deficiency and nerve conduction issues? which neurotransmitter?

A

myelin sheath integrity not maintained

cant make acetyl coa which is a precursor for synthesis of acetylcholine (needed for brain function and muscles)

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22
Q

which b vitamin deficiency leads to beriberi

A

b1/ thaimine

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23
Q

which b vitamin deficiency leads to wenicke-korsakoff syndrome

A

b1/ thaimine

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24
wenicke-korsakoff syndrome effects which system
CNS- memory and confsuion seen in alcholism
25
wet and dry beriberi - which system effected?
wet beriberi- cardiovascular system dry beri beri- CNS and motor
26
what enzyme is tested for B1/thiamine levels
transketolase enzyme activity --> Add TDP and measure activity --> if B1 deficient then addition of TDP shows increase in activity
27
main sources of riboflavin/ vitamin B2
Meats (especially liver and organ meats), milk products, brewer’s yeast, legumes, eggs, almonds, leafy greens
28
which riboflavin/ B2 coenzymes are required for metabolism and absorption?
metabolism: FAD synthetase absorption: FMN phosphatase and FAD pyrophosphates
29
which coenzyme of riboflavin/ vitamin B2 can cause bright yellow urine
FMN
30
b2 and energy: Which pathways make FADH2 for energy?
beta oxidation CAC
31
What same type of enzyme produces FADH2 (and/or NADH) for energy in catabolic pathways?
dehydrogenase
32
b2 and energy: In addition to being part of the CAC, succinyl CoA can also feed into heme synthesis?
oxygen transport in blood for aerobic respiration and dingy metabolism
33
how does FADH2 provide energy
CAC and beta oxidation --> donates electrons in ETC in mitochondria --> ATP
34
FMN/FMNH2 role in energy production (vitamin B2)
part of dehydrogenase complex in ETC --> inner mitochondria membrane gradient which drives ATP synthesis
35
which vitamins help regenerate glutathione antioxidant
b2 and b3
36
b2: how do FMN and FADH2 relate to ETC
1) FADH2 supplies electrons to the ETC, leading to ultimate production of ATP 2) FMN acts as an electron carrier in the ETC
37
which neurotransmitters does FAD (from vitamin B2) help metabolize (so we dont get too much)
dopamine, epinephrine, norepinephrine --> monoamine oxidase uses FAD to degrade the amines
38
b2 prevent migraines and cataracts
Migraines * Migraines may be due to decreased mitochondria energy production in the brain ▪ Cataracts * Cataracts may be caused by UV damaged
39
testing for B2 deficiency via which enzyme
glutathione reductase
40
If you had a B2 deficiency, would glutathione reductase activity go up or down if additional FAD were added to the test tube?
up
41
other names for vitamin B3/ niacin
nicotinic acid or nicotinamide
42
is nicotinic acid or nicotinamide more found in supplements?
nicotinamide --> fewer side effects (nicotinic acid can cause flashing) -->nicotinamide is more direct in synthesis of NAD+
43
what amino acid can make NAD+ (from vit B3)
tryptophan Unique to B3: RDA for niacin includes 1/60mg tryptophan, as can also make NAD+ from tryptophan
44
which vitamin and form can cause flushing
vitamin b3- nicotinic acid
45
which vitamin does corn contain? and how does this reduce bioavailability?
Corn contains niacin bound to carbohydrates (niacytin) and small peptides (niacinogen) -->makes it too big for absorption so reduces bioavailability
46
b3 and energy: Which catabolic pathways produce NADH for energy?
glycolysis, beta oxidation, CAC, anaerobic respiration
47
which enzyme in glycolysis makes NADH (b3)
glyceraldehyde phosphate dehydrogenase
48
from glycolysis where can NADH go to make energy in anaerobic and aerobic conditions
aerobic- ETC anaerobic- cori cycle
49
which enzyme in the cori cycle (anaerobic) makes B3/NADH
lactate dehydrogenase Muscle: Produces NAD+ to keep glycolysis running * Liver: Uses NADH to make glucose for muscles for glycolysis -->glycolysis produces ATP for energy
50
all CAC dehydrogenases make NADH (B3) except for which one? hint: this one makes FADH2
succinate dehydrogenase
51
how does B3/ NADH help to make heme
succinyl coa (made by alpha ketoglutarate dehydrogenase)
52
how does beta oxidation make NADH/B3
via dehydrogenase
53
how does NAD+ help metabolize alcohol
via dehydrogenases
54
nicotinic acid physiological effects
1. vasodilatory prostaglandin release (niacin flush) 2. enhanced fibrinolysis (clot dissolution, helps blood flow) 3. improves lipids: decerase VLDL/LDL and increases HDL 4. increased histamine release 5. potential for hyperglycemia
55
what enzyme helps produce prostaglandins (vasodilatory effect of nicotinic acid
cylcooxygenase therefore COX inhibitor like aspirin/NSAIDs reduce prostaglandins and can reduce the niacin flush
56
how does nicotinic acid enhance fibrinolysis?
increase plasmin and decrease fibrinogen --> dissolve clots
57
how does nicotinic acid improve lipid profiles
decrease circulating VLDL/LDL and increase HDL decrease VLDL/LDL by blocking lipolysis in adipose tissue increase HDL by downregulation of HDL receptors that internalize and catabolize HDL
58
effect of nicotinic acid on lipolysis
can bock it
59
what is Raynaud's phenomenon?
Condition characterized by spasm of digital arteries, especially in response to cold or stress, causing numbness and tingling in fingers/toes
60
how can nicotinic acid help raynauds phenomenon?
vasodilator (via cyclooxygenases helping with vasodilatory prostaglandins)
61
how can nicotinic acid help with atherosclerosis
improve blood flow by enhancing fibrinolysis and decreasing clot formation increases plasmin and decrsases fibrinogen
62
how does nicotinic acid increase histamine release
can make peptic ulcer disease worse Histamine binds to H2 receptors in the stomach lining, promoting gastric acid secretion. In patients with peptic ulcer disease, excessive gastric acid can worsen the condition by irritating the ulcerated mucosa and increasing ulcer pain or bleeding.
63
how can nicotinic acid cause hyperglycemia
partially due to decreased glucokinase phosphorylation of glucose --> increasing blood sugar if glucokinase decreased then in liver glucose is trapped and cant be converted to metabolic intermediates or glycogen (storage) higher free glucose in blood less glucose uptake and storage in liver
64
nicotinamide use in diabetes??
can protect insulin-secreting pancreatic beta cells from damage * Does not necessarily protect against development of diabetes
65
symptoms of niacin/B3 deficiency
Pellagra: dementia, dermatitis, diarrhea, death
66
causes of niacin deficiency
▪ Corn-based diet * B3 in niacytin or niacinogen form * Low in tryptophan * Why is pellagra is not common in Mexico and Central America, which have largely corn-based diets? bc soak it in lime to release it ▪ Carcinoid syndrome * Condition of increased secretion of serotonin (and other catecholamines)
67
vitamin B5 is aka
pantothenic acid
68
structure of coA/ vitamin B5
has S to carry acyl group
69
b5/ CoA and the energy pathways (match the coA to the path) CAC (2) beta oxidation (2) ketolysis (1) heme synthesis (1)
▪ CAC: Acetyl CoA, succinyl CoA (substrates) ▪ Beta oxidation: Fatty acyl CoA (substrate), acetyl CoA (product) ▪ Ketolysis: Acetyl CoA (product) ▪ Heme synthesis: Succinyl CoA (substrate)
70
b5/ coa and synthesis fatty acids phospholipids and triglucerides cholesterol and ketones
Fatty acids: * CoA: makes acetyl CoA and malonyl CoA substrates * Also: Part of fatty acid synthetase complex ▪ Phospholipids and triglycerides * Fatty acyl CoA substrates ▪ Cholesterol and ketones * Acetyl CoA = substrate to make HMG-CoA
71
b5 deficiency
burning food syndrome fatigue and listlessness