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Metabolism > Vitamin B12 > Flashcards

Vitamin B12 Flashcards

1
Q

Thomas Addison

A

English Physician. Describes a group of patients with a “remarkable form of anemia”.

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2
Q

Biermer

A

Named Pernicious anemia (fatal anemia)

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3
Q

Whipple

A

Describes treating experimental anemia in dogs by feeding raw liver.

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4
Q

Minot and Murphy

A

Successfully treat pernicious anemia in humans by feeding cooked liver (120 to 240 g/d)

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5
Q

1934 Noble Prize in Physiology or Medicine

A

Whipple, Minot and Murphy. “for their discoveries concerning liver therapy in cases of anemia”

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6
Q

Vitamin B12

A

the generic descriptor for corrinoid compounds exhibiting the biological activity for B12.

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7
Q

Cyanocobalamin

A

-CN

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8
Q

Hydroxocobalamin

A

-OH

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9
Q

Aquocobalamin

A

-H2O

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10
Q

Nitritocobalamin

A

-NO2

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11
Q

5’-deoxyadenosylcobalamin

A

5’-deoxyadenosyl

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12
Q

Methylcobalamin

A

-CH3

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13
Q

Food sources

A
  • Synthesized solely by bacteria

- Only dietary sources are animal products, which have derived their B12 from bacteria

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14
Q

Why animal tissues?

A
  • Animal tissues accumulate B12 (liver)

- Ruminant animals obtain B12 from gut bacteria

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15
Q

What does not contain B12?

A
  • Plants do not synthesize B12

- Fruits, vegetables, and grains contain no B12 (unless contaminated by bacteria).

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16
Q

Most amount of B12

A
  • Beef liver
  • clams
  • oysters
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17
Q

Vegan friendly sources of VitB12

A

Silk, cereal, tofu

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18
Q

Naturally occurring B12 in food

A
  • Bound to protein
  • Must be released for absorption
    - Gastric acid is essential
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19
Q

Synthetic B12 in fortified foods

A

Not bound to protein

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20
Q

Vitamin B12-binding/ transport proteins

A

R-Protein
Intrinsic Factor
Transcobalamin II

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21
Q

R-Protein

A
  • Also called haptocorrin or transcobalamin I)
  • Glycoproteins secreted by salivary glands
  • Binds to B12 and protects it from stomach acid
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22
Q

Intrinsic Factor

A
  • Glycoproteins secreted by gastric parietal cells

- Binds to B12 in intestine and transport it to IF receptor

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23
Q

Transcobalamin II

A

Main transport protein for B12 in plasma

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24
Q

Vitamin B12: Active Absorption

A

Stomach, Duodenum, Ileum

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25
Q

Stomach

A

Food B12 is released from proteins by pepsin and HCl

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26
Q

Duodenum

A
  • B12-R is acted upon by pancreatic protease, releasing free B12
  • Free B12 binds to intrinsic factor, forming B12-IF complex
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27
Q

Ileum

A
  • B12-IF binds to B12-IF receptor (cubilin) on intestinal cell
  • B12-IF-cubilin complex is internalized by endocytosis
  • B12 is released from IF-cubilin
  • Free B12 binds to transcobalamin II in portal bloodstream.
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28
Q

Passive Absorption

A
  • Simple diffusion
  • Occurs throughout the small intestine
  • Inefficient (~1% absorbed)
  • Used in therapy (>500 ug/day)
  • Usually given per os
  • Can be given intranasally
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29
Q

Atrophic Gastritis

A
  • Chronic inflammation of gastric mucosa with loss of parietal cell function
  • Autoimmune disorder in which antibodies destroy parietal cells
  • Results in loss of intrinsic factor
  • MOST COMMON CAUSE OF PERNICIOUS ANEMIA
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30
Q

Dr. William B Caste

A

Found the IF. Ate raw beef. Added HCl, let simmer for 6 hours put back into a container and given to patient. RBC count increases

31
Q

Vitamin B12 Transport

A

TCI, TCII, TCIII

-B12 in plasma is bound to transcobalamin (TC) proteins

32
Q

TCI

A
  • ~80%
  • Also known as haptocorrin (see absorption)
  • Circulating storage form
33
Q

TCII

A
  • (10-25%)
  • MAIN TRANSPORT PROTEIN
  • delivers B12 to all cells
34
Q

TCIII

A

Function unknown

35
Q

B12 Storage

A
  • 2-4 mg store in body, mainly (~50%) in liver

- 70% stored as adenosylcobalamin

36
Q

B12 Excretion

A
  • Bile (~1.5 ug/day)
  • about 70% reabsorbed
  • Patients with pernicious anemia do not reabsorb b/c they lack intrinsic factor
37
Q

Vitamin B12 Function

A

2 Types of Reactions

  • methyl group transfer reactions
  • mutases
    - exchange a hydrogen and some other groups between 2 adjacent carbons atoms
38
Q

Methionine Synthase (MS)

A
  • Uses methylcobalamin as an intermediate methyl carrier at one active site of MS enzyme
  • Transfers methyl group from cobalamin to homocysteine at another site
39
Q

Methylmalonyl CoA Mutase (MCM)

A
  • Located in mitochondria
  • Enzyme that catalyzes the isomerization of methylmalonyl-CoA to succinyl-CoA
  • Uses adenosylcobalamin in active site
40
Q

Adenosylcobalamin

A

The Co-CH2 bond is relatively weak and can therefore be easily broken, forming a free radical that can abstact a hydrogen (from methylmalonyl)

41
Q

Vitamin B12 Function

A

Two Primary enzymatic pathways

42
Q

B12 Function #1

A

Remethylation of homocysteine

  • methylcobalamin
  • occurs in cytoplasm
43
Q

B12 Function #2

A

L-methylmalonyl CoA –> Succinyl CoA

  • Adenosylcobalamin
  • Occurs in Mitochondria
44
Q

Methyl Trap Hypothesis

A

In a vitamin B12 deficiency

  • Methyl group is “trapped” in the N-5 methyl form
  • MTHFR reaction is irreversible
45
Q

When B12 is low. What is high?

A
  • Homocysteine

- 5-CH3THF

46
Q

When B12 is low… What else is?

A

EVERYTHING

47
Q

Megaloblastic Anemia

A
  • DNA synthesis is needed for early erythroblasts to divide and mature.
  • In folate/b12 deficiency DNA synthesis is impaired; early erythroblasts cannot divide and escape into bloodstream
  • Early erythroblasts cannot divide and escape into bloodstream
  • Early erythroblasts are large (megalo) and do not contain much hemoglobin
  • clinically known as megaloblastic anemia
48
Q

B12 Deficiency and MMA

A

B12 is required for conversion of methylmalonyl CoA to succiny CoA

  • In B12 deficiency, methylmalonyl-CoA accumulates and is hydrolyzed to CoA and Methylmalonic acid (MMA)
  • MMA is associated with neurodegeneration
49
Q

Masking of B12 deficiency by folic acid

A
  • B12 deficiency is often identified by megaloblastic anemia
  • folic acid can correct megaloblastic anemia due to B12 defiency– but cannot correct the other effects of B12 deficiency (neurologic effects)
  • Thus, folic acid can “mask” or hide B12 defiency
50
Q

How does folic acid mask B12 deficiency?

A

Folic acid treatment reverses anemia because B12 deficiency causes “secondary folate deficiency” because it reduces THF and thus 5,10methyleneTHF for DNA

51
Q

If anemia due to B12 deficiency:

A
  • degeneration of the spinal cord
  • difficult to diagnose early stages
  • worsens without B12 therapy
  • cells view folate/ b12 deficiency the same way
52
Q

Vitamin B12 Deficiency

A

Status Assessment
Causes
Clinical Significance

53
Q

B12 Status Indicators

A
  • Diet and supplement history & medical history
  • Serum vitamin B12
  • Homocysteine increases: NOT specific but functional
  • METHYL MALONIC ACID INCREASES: SPECIFIC INDICATOR, FUNCTIONAL
  • Holotranscobalamin (
54
Q

Serum deficiencies

A

-

55
Q

Monitoring Vit. B-12 in the U.S.

A

uses plasma methylmalonic acid & serum Vit. B12

56
Q

Vit B12 deficiency causes

A 
-malabsorption
     Pernicious anemia
     Food Bound
-Nitrous oxide
-Dietary Inadequacy
57
Q

Pernicious Anemia

A
  • usually caused by lack of functional IF in stomach
    - autoimmune destruction of the gastic parietal cells
  • prevalence 2-3% of the populations >65 years
    - rarely occurs in younger individuals
  • gastrectomy
    - surgical removal of stomach
58
Q

Treatment for pernicious anemia

A
  • IM b12 injections (100-1000ug cyanocobalamin)
    • injections at monthly intervals
  • Oral b12 supplement (> or + to 1000ug)
    • daily dosing recommended
59
Q

Gastric Atrophy

A
  • Loss of stomach acid for extraction of B12 from food
  • Can absorb crystalline normally (have intrinsic factor)
  • May affect >30% of elderly
  • H. pylori is a cause of gastric atrophy
60
Q

Elderly B12 status in the US

A
  • Elderly have lower serum vitamin B12 than younger individuals
    - related to food-bound malabsorption
  • elevated serum methylmalonic acid concentrations common in elderly
    - population-based data
61
Q

Nitrous oxide

A
  • laughing gas, anesthesia
  • oxidizes cobalt in B12
  • results in B12 deficiency and spinal cord degeneration as seen in classical B12 deficiency
  • seen in dentists, dental assistants, individuals who use nitrous oxide as recreational drug
62
Q

Lacto-ovo vegetarians

A

excludes all meat except dairy and eggs

63
Q

Lacto-vegetarians

A

excludes all meat except dairy

64
Q

Vegans

A

Exludes all meat and products

65
Q

Deficiency and vegetarianism

A
  • Reported in all who do not take supplements or eat B12-fortified foods
  • the more restricted the diet, the more likely a deficiency may occur
66
Q

Infants on Macrobiotic diets

A

Research study
-41 infants (10-20mo) fed a macrobiotic diet
-50 controls (omnivorous)
Mothers of macrobiotic infants consumed macrobiotic diet for ~3 years
-Breast fed infants from birth with complementary macrobiotic foods

67
Q

Macrobiotic B12 deficient diet

A

Diet consists of:

  • grain cereals
    • mainly rice
  • veggies
  • pulses
    • mainly soy
  • sea vegetables
  • small amount of fruit
68
Q

Infants whose mothers ate macrobiotic vegetarian diets

A
  • High in methylmalonic acid, homocysteine.

- Low in cobalamin

69
Q

Clinical significance

A
  • Impaired neurological function
  • megaloblastic anemia
  • neural tube defect increased risk
70
Q

Neurological Abnormalities

A
  • Neurological degeneration of peripheral nerves
    - impaired touch and pain sensation
  • Ataxia - unsteady gait
  • Degeneration of spinal nerves
71
Q

Other neurological abnormalities

A
  • -Physical reflexes and stamina
  • mental attributes including memory loss
  • behavioral changes
    - altered mood and reaction to stress
72
Q

Demylination of nervous system: proposed mechanisms

A
  • Decreased synthesis of S-adenosylmethionine
    • methylation reactions
      - neurotransmitters
      - membrane phospholipids in myelin
  • Disrupted odd chain fatty acid metabolism related to the accumulation of methylmalonic acid and its precursos (proprionic acid)
73
Q

EAR

A

2 ug/day

74
Q

RDA

A

2.4 ug/day

Metabolism (8 decks)

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