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BMS200 > week 2, lecture 2 > Flashcards

week 2, lecture 2 Flashcards

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
Q

wenicke-korsakoff syndrome effects which system

A

CNS- memory and confsuion

seen in alcholism

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25
Q

wet and dry beriberi - which system effected?

A

wet beriberi- cardiovascular system
dry beri beri- CNS and motor

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26
Q

what enzyme is tested for B1/thiamine levels

A

transketolase enzyme activity

–> Add TDP and measure activity
–> if B1 deficient then addition of TDP shows increase in activity

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27
Q

main sources of riboflavin/ vitamin B2

A

Meats (especially liver and organ meats), milk products, brewer’s yeast, legumes, eggs, almonds, leafy greens

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28
Q

which riboflavin/ B2 coenzymes are required for metabolism and absorption?

A

metabolism: FAD synthetase
absorption: FMN phosphatase and FAD pyrophosphates

29
Q

which coenzyme of riboflavin/ vitamin B2 can cause bright yellow urine

A

FMN

30
Q

b2 and energy: Which pathways make FADH2 for
energy?

A

beta oxidation
CAC

31
Q

What same type of enzyme produces FADH2 (and/or NADH) for energy in catabolic pathways?

A

dehydrogenase

32
Q

b2 and energy: In addition to being part of the CAC, succinyl CoA can also feed into heme synthesis?

A

oxygen transport in blood for aerobic respiration and dingy metabolism

33
Q

how does FADH2 provide energy

A

CAC and beta oxidation –> donates electrons in ETC in mitochondria –> ATP

34
Q

FMN/FMNH2 role in energy production (vitamin B2)

A

part of dehydrogenase complex in ETC –> inner mitochondria membrane gradient which drives ATP synthesis

35
Q

which vitamins help regenerate glutathione antioxidant

A

b2 and b3

36
Q

b2: how do FMN and FADH2 relate to ETC

A

1) FADH2 supplies electrons to the ETC, leading to ultimate production of ATP
2) FMN acts as an electron carrier in the ETC

37
Q

which neurotransmitters does FAD (from vitamin B2) help metabolize (so we dont get too much)

A

dopamine, epinephrine, norepinephrine

–> monoamine oxidase uses FAD to degrade the amines

38
Q

b2 prevent migraines and cataracts

A

Migraines
* Migraines may be due to decreased mitochondria energy production in the brain

▪ Cataracts
* Cataracts may be caused by UV damaged

39
Q

testing for B2 deficiency via which enzyme

A

glutathione reductase

40
Q

If you had a B2 deficiency, would glutathione reductase activity go up or down if additional FAD were added to the test tube?

A

up

41
Q

other names for vitamin B3/ niacin

A

nicotinic acid or nicotinamide

42
Q

is nicotinic acid or nicotinamide more found in supplements?

A

nicotinamide
–> fewer side effects (nicotinic acid can cause flashing)
–>nicotinamide is more direct in synthesis of NAD+

43
Q

what amino acid can make NAD+ (from vit B3)

A

tryptophan

Unique to B3: RDA for niacin includes 1/60mg tryptophan, as can also make NAD+ from tryptophan

44
Q

which vitamin and form can cause flushing

A

vitamin b3- nicotinic acid

45
Q

which vitamin does corn contain? and how does this reduce bioavailability?

A

Corn contains niacin bound to carbohydrates (niacytin) and small peptides (niacinogen)
–>makes it too big for absorption so reduces bioavailability

46
Q

b3 and energy: Which catabolic pathways produce NADH for energy?

A

glycolysis, beta oxidation, CAC, anaerobic respiration

47
Q

which enzyme in glycolysis makes NADH (b3)

A

glyceraldehyde phosphate dehydrogenase

48
Q

from glycolysis where can NADH go to make energy in anaerobic and aerobic conditions

A

aerobic- ETC
anaerobic- cori cycle

49
Q

which enzyme in the cori cycle (anaerobic) makes B3/NADH

A

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
Q

all CAC dehydrogenases make NADH (B3) except for which one? hint: this one makes FADH2

A

succinate dehydrogenase

51
Q

how does B3/ NADH help to make heme

A

succinyl coa (made by alpha ketoglutarate dehydrogenase)

52
Q

how does beta oxidation make NADH/B3

A

via dehydrogenase

53
Q

how does NAD+ help metabolize alcohol

A

via dehydrogenases

54
Q

nicotinic acid physiological effects

A
  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
Q

what enzyme helps produce prostaglandins (vasodilatory effect of nicotinic acid

A

cylcooxygenase

therefore COX inhibitor like aspirin/NSAIDs reduce prostaglandins and can reduce the niacin flush

56
Q

how does nicotinic acid enhance fibrinolysis?

A

increase plasmin and decrease fibrinogen –> dissolve clots

57
Q

how does nicotinic acid improve lipid profiles

A

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
Q

effect of nicotinic acid on lipolysis

A

can bock it

59
Q

what is Raynaud’s phenomenon?

A

Condition characterized by spasm of digital arteries, especially in response to cold or stress, causing numbness and tingling in fingers/toes

60
Q

how can nicotinic acid help raynauds phenomenon?

A

vasodilator (via cyclooxygenases helping with vasodilatory prostaglandins)

61
Q

how can nicotinic acid help with atherosclerosis

A

improve blood flow by enhancing fibrinolysis and decreasing clot formation

increases plasmin and decrsases fibrinogen

62
Q

how does nicotinic acid increase histamine release

A

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
Q

how can nicotinic acid cause hyperglycemia

A

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
Q

nicotinamide use in diabetes??

A

can protect insulin-secreting pancreatic beta cells from damage
* Does not necessarily protect against development of diabetes

65
Q

symptoms of niacin/B3 deficiency

A

Pellagra: dementia, dermatitis, diarrhea, death

66
Q

causes of niacin deficiency

A

▪ 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
Q

vitamin B5 is aka

A

pantothenic acid

68
Q

structure of coA/ vitamin B5

A

has S to carry acyl group

69
Q

b5/ CoA and the energy pathways (match the coA to the path)

CAC (2)
beta oxidation (2)
ketolysis (1)
heme synthesis (1)

A

▪ 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
Q

b5/ coa and synthesis

fatty acids
phospholipids and triglucerides
cholesterol and ketones

A

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
Q

b5 deficiency

A

burning food syndrome
fatigue and listlessness

BMS200 (19 decks)

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