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IHN: Biochemistry 2 > Thiamin: Vitamin B1 > Flashcards

Thiamin: Vitamin B1 Flashcards

1
Q

thiamin rich foods

A

grains, proteins, legumes, fruits

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2
Q

active form of thiamin

A

thiamin pyrophosphate (diphosphate, TPP) or TDP

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3
Q

thiamin has __ activity

A

thiamin has co-factor activity

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4
Q

thiamin is very stable in __
unstable in __ and __

A

thiamin is very stable in acid
unstable in base and UV light

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5
Q

thiamin binds __ and converts to __ form

A

thiamin binds keto-sugar and converts to CoA form

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6
Q

most important biological form of thiamin:

A

TPP or TDP bc of its co-factor activity

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7
Q

thiamin is destroyed by __ and __

A

thiamin is destroyed by alkali (pH > 8) and by prolonged heat

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8
Q

__, __, and __ consumption can decrease thiamin availability

A

raw fish, heme-containing meats, and coffee/tea consumption can decrease thiamin availability

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9
Q

thiaminases exist in __ and function to __

A

thiaminases exist in 2 isoforms and function to cleave thiamin at methylene bridge

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10
Q

thiaminases are __ and inactivated with __

A

thiaminases are thermolabile and inactivated with cooking

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11
Q

which thiaminase is more common?

A

thiaminase 1

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12
Q

thiaminase 1 is mainly present in

A

freshwater fish and shellfish

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13
Q

thiaminase II is present in

A

some bacteria and yeast

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14
Q

raw fish contains __ that destroy __

A

raw fish contains thiaminases that destroy thiamin

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15
Q

OCT aka

A

organic cation transporter

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16
Q

absorption of thiamin at physiological concentrations: __
inhibited by __

A

absorption of thiamin at physiological concentrations: Th-Tr mediated
inhibited by alcohol

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17
Q

absorption of thiamin at high concentrations:

A

passive diffusion

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18
Q

2 main thiamin transporters:

A

ThTr1 and ThTr2

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19
Q

ThTr1 and ThTr2 are __
they exchange thiamin for __
greatest activity in __

A

ThTr1 and ThTr2 are antiporters
they exchange thiamin for H+ ions
greatest activity in upper jejunum

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20
Q

ThTr1 expression and capacity

A

highly expressed in all cells
high capacity

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21
Q

ThTr2 expression and capacity

A

low capacity, high specificty for thiamin
expression increases in response to LOW thiamin intake

22
Q

main form of thiamin in portal circulation

A

free thiamin

23
Q

thiamin release into circulation

A
  1. ThTr2 on basal side of enterocyte pushes thiamin to basal side
  2. free thiamin goes into portal circulation
24
Q

thiamin absorption

A
  1. TMP, TDP to free thiamin (alkaline phosphatase)
  2. ThTr1 and 2 on apical surface of enterocyte absorb thiamin
25
Q

organic cation transporters (OCT) may transport __ thiamin in __

A

organic cation transporters (OCT) may transport free thiamin in intestine

26
Q

Defects in __ gene which encodes ThTr1 causes a thiamin responseive deficiency disorder, known as __

A

Defects in SLC19A2 gene which encodes ThTr1 causes a thiamin responseive deficiency disorder, known as Rogers syndrome

27
Q

Rogers syndrome, what transporter still works? is it enough?

A

ThTr2
but it is not enough to do the work of both

28
Q

~90% thiamin in circulation is in __ as __

A

~90% thiamin in circulation is in blood cells as TDP

29
Q

thiamin enters red blood cells by

A

facilitated diffusion

30
Q

in peripheral tissues, transport into cells mediated by __ (__) and __ (__)

A

in peripheral tissues, transport into cells mediated by ThTr1 (free thiamin) and RFC-1 (uptakes TMP, also reduced folate carriers)

31
Q

mutations in ThTr1 (Rogers syndrome) is characterized by __, __, and __
repsonsive to __

A

mutations in ThTr1 (Rogers syndrome) is characterized by megaloblastic anemia, sensorineural deafness, and diabetes
repsonsive to thiamin treatment

32
Q

thiamin is stored mostly in (5)

A
  1. liver
  2. skeletal muscle
  3. heart
  4. kidney
  5. brain

these are high energy tissues, thiamin deficiency = low energy

33
Q

50% of body’s thiamin is in

A

muscle

34
Q

is we consume no thiamin, we notice in __

A

is we consume no thiamin, we notice in a few weeks

35
Q

2 types of TDP dependent rxns

A
  1. decarboxylation of alpha-ketoacids to acyl-CoA
  2. interconversion of sugar phosphates
36
Q

3 decarboxylation rxns requiring TDP

A
  1. pyruvate dehydrogenase (TCA)
  2. alpha-KG dehydrogenase (TCA)
  3. branched-chain amino acid dehydrogenase
37
Q

1 interconversion of sugar phosphates rxn

A
  1. transketolase (PPP)
38
Q

TDP-depdendent rxns create __ and __ equivalents for macromolecule synthesis

A

TDP-depdendent rxns create energy: ATP and reducing equivalents for macromolecule synthesis

39
Q

inhibition of the TDP requiring rxns leads to accumulation of pyruvate, lactate, and alpha-KG, leading to __

A

inhibition of the TDP requiring rxns leads to accumulation of pyruvate, lactate, and alpha-KG, leading to acidosis

40
Q

determining thiamin status

A

measure RBC transketolase

41
Q

excess __ causes thiamin deficiency

A

excess glucose causes thiamin deficiency

42
Q

why does excess glucose cause thiamin deficiency?

A

thiamin follows glucose
SO, we supplement thiamin with IV glucose

43
Q

__ inhibits both thiamin transporters

A

alcohol

44
Q

groups at risk for thiamin deficiency

A
  1. elderly
  2. malabsorption
  3. alcohol (Wernicke-Korsakoff syndrome)
  4. cancer patients undergoing chemo
  5. excess glucose infusion
  6. congestive heart failure
45
Q

why does excess glucose infusion put you at risk for low thiamin?

A

thiamin follows glucose
thiamin is involved in rxns that produce glucose

46
Q

thiamian deficiency

A
  1. beri beri
  2. Wernicke-Korsakoff
47
Q

dry beri beri

A

chronic
neuropathies caused by inactivity + calorie restriction + not enough thiamin

48
Q

wet beri beri

A

cardiovascular, rapidly fatal (bc cardiac component)
severe physical effort + high carb intake = edema

49
Q

acute beri beri

A

infants
anorexia, vomiting
lactic acidosis
heart failure

50
Q

Wernicke-Korsakoff syndrome
alcohol addiction promotes low __ and __ damage

A

Wernicke-Korsakoff syndrome
alcohol addiction promotes low thiamin intake and liver damage

51
Q

Wernicke encephalopahty

A

ataxia, abnormal motor function, paralysis of eye movements, amnesia, apathy

52
Q

wernicke-korsakoff treatment?

A

thiamin supplementation usually helps, but some damage is irreversible

IHN: Biochemistry 2 (38 decks)

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