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MONOGASTRIC GI > 6.7 – One Carbon Transfers > Flashcards

6.7 – One Carbon Transfers Flashcards

1
Q

What does the conversion of homocysteine (bad) to methionine (good) require?

A

-B12 (methylcobalamin) to donate a methyl group
-folate is required to ‘regenerate’ the methylcobalamin
*function of folic acid depends on VitB12
>VitB12 absorption can be a problem

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2
Q

Where can methionine be obtained from?

A

-diet
-remethylation of homocysteine (requires Vit B12)

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3
Q

Steps for methionine ‘breakdown’:

A
  1. Condenses with ATP to form SAM
    >SAM has methyl group that can be donated to several metabolic pathways
  2. SAH results from SAM losing methyl group
  3. SAH hydrolyzed to homocysteine and adenosine
  4. Homocysteine can be remethylated to methionine
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4
Q

What are the Vit B12 dependent enzymes:

A

-methylmalonyl CoA mutase
-leucine aminomutase
-methionine synthases (aka homocysteine methyltransferase)

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5
Q

What are the 2 forms of B12?

A

-methylcobalamin
-cyanocobalamin (synthetic form)

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6
Q

Folate (methyl-tetrahydrofolate) ‘regenerating’ the methylcarboalamin:

A

-donates a methyl group
>becomes tetrahydrofolate

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7
Q

Tetrahydrofolate is recycled back to 5,10-methyl tetrahydrofolate using:

A

-riboflavin (B6)
-5,10-methyl tetrahydrofolate can be used for DNA synthesis

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8
Q

What happens if there is NO VitB12?

A

-homocysteine accumulates (DECREASED methionine)
-cobalamin not formed
-tetrahydrofolate is NOT formed and folate is “trapped” as methylhydrofolate

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9
Q

When do we get a ‘folate trap’ ? Physiological conditions:

A

-very low supply of methionine
-starvation

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10
Q

What is the physiological consequence of ‘folate trap’:

A

-slow production of tetrahydrofolate for DNA synthesis
-DNA biosynthesis and cell division is reduced thus reducing competition for methionine
>methionine is reserved for production of S-adenosyl methionine (SAM)

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11
Q

What is SAM required for?

A

-myelin regeneration
-NTs
-carnitine

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12
Q

SAM dependent methyl transferases: (reactions)

A

-phosphatidylethanolamine + SAM to phosphatidyl choline + SAH
-lysine + SAM to carnitine + SAH
-NE + SAM to E + SAH

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13
Q

SAH:

A

-S-adenosylhomocysteine

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14
Q

What does VitB12 deficiency cause?

A

-pernicious anemia
>disturbs erythropoiesis
>irreversible degradation of SC

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15
Q

Why is there a degradation of the SC with pernicious anemia?

A

-disturbs erythropoiesis
>immature erythrocytes are released into circulation

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16
Q

What is the most common cause of Vit B12 deficiency?

A

-failure of absorption of it due to LACK of intrinsic factor
-not usually due to dietary deficiency

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17
Q

Deficiencies of folate, B6 and B12 can all lead to increased levels of:

A

-homocysteine

18
Q

Elevated homocysteine and CVD?

A

-vitamin B therapy to reduced homocysteine levels=may reduce risk of stroke
-shift workers have increased homocysteine=useful predictor of CVD

19
Q

Vitamins in general:

A

-most ARE synthesized in animal cells (except B12)
-most absorbed in SI via specific transporters
-most carried in blood in free form (some bound to proteins)
-excreted in urine (except B12=lost in feces)

20
Q

Water soluble vitamins ‘have little in common’ except that they are:

A

-soluble in water

21
Q

Choline:

A

-technically not a vitamin
-from meat, nuts, eggs
-also obtained via breakdown of phospholipids
-absorbed by enterocytes

22
Q

Choline is the precursor to:

A

-betaine
>involved in homocysteine to methionine

23
Q

Folates (vitamin B9): carry:

A

-one-carbon units bound to 1 or 2 N atoms

24
Q

Folate is absorbed via:

A

-H+ carrier dependent mechanism
>no Na+ required=NOT active transport

25
Q

Folate’s role:

A

-required for DNA synthesis
-works with VitB12 and B6 to maintain normal concentration of homocysteine

26
Q

Increased intake of folate from supplements results in:

A

-decreased homocysteine concentrations in blood

27
Q

Folate comes from:

A

-legumes
-green leafy veggies
-fortified breads

28
Q

What does deficiency of folate cause?

A

-megaloblastic anemia

29
Q

Vit B12 (cobalamin)

A

-complex molecule
-cobalt ion at center
-in liver=methylcobalamin
-free form is sensitive to acid

30
Q

Where does Vit B12 come from?

A

-seafood, poultry, red meat
*synthesized exclusively by microorganisms

31
Q

Vit B12 abosprtion during gastric phase:

A

-release of Vit B12 from proteins
-binds to endogenous carriers

32
Q

What are the endogenous carriers of Vit B12 in the gastric phase?

A

-primarily: haptocorrin (HC)
-intrinsic factor (IF)

33
Q

Vit B12 absorption during duodenal phase:

A

-HC-B12 is partially degraded
-IF-B12 remains intact
>primarily in ileum
*only 1% absorption without IF
*significant losses in feces

34
Q

Enterohepatic circulation of B12 is reported in:

A

-human
-pig
-rat
-baboon
-rabbit

35
Q

Intrinsic factor is produced by:

A

-gastric mucosal cells (most species)
-pancreas is major site in dogs and maybe cats

36
Q

Failure to absorb Vit B12 in dogs:

A

-absence of IF-B12 complex in lower intestine
-affects giant schnauzers, border collies, beagles
-symptoms generally appear around 6-12 weeks (Schnauzers) and 4-6months (Collies)
*presents the same as folic acid deficiency, but treatment with folate could be problematic(fatal)

37
Q

Giant schnauzers and failure to absorb VitB12:

A

-inherited simple recessive trait

38
Q

Why can giving folate cause problems if it the cause is due to Vit B12 defiecency?

A

-already have folate trapped
*would now get excessive folate

39
Q

What are the causes of B12 malabsorption?

A

-intrinsic factor deficiency
-Addison’s disease
-bariatric surgery
-pancreatic insufficiency
-IBD
-some drugs

40
Q

Addison’s disease:

A

-adrenal glands malfunction
>impaired gastric acid secretion
>malabsorption

41
Q

Bariatric surgery:

A

-impaired IF and gastric acid secretion

MONOGASTRIC GI (24 decks)

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