Micro - Exam 3 Flashcards

1
Q

B12 absorption

A

Gastric acid removes B12 from food protein&raquo_space; gets bound to R-binder to protect from acid&raquo_space; in duodenum, B12 gets bound to intrinsic factor which allows it to be transported into enterocyte

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2
Q

Manifestations of B12 deficiency

A

B12:
methylmalonyl CoA -> succinyl CoA

No B12:
methylmalonyl CoA -> methylmalonyl acid

  • High MMA
  • High homocysteine
  • RBC macrocytosis
  • Neurological problems
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3
Q

B12 functions (two)

A
  1. Coenzyme to convert homocysteine to methionine (and SAM) – methylation
  2. involved in degradation of FA and amino acids for energy – necessary for enzyme methylmalonyl-Coa mutase
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4
Q

Cons of folic acid fortification

A

May increase risk of cancer (cancer cells need folate for nucleic acid synthesis/proliferation)

High maternal folate may lead to allergy/respiratory problems

Mask B12 deficiency, exacerbate problems
Folate enters folate cycle after the blocked step of B12 deficiency, so nucleic acids can still be produced and macrocytosis does not occur

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5
Q

Dietary sources of folate vs folic acid

A

Folate: widespread, naturally

Folic acid: fortified foods, cereals, supplements

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6
Q

Effects of Thiamine deficiency (two names of diseases)

A

Cellular energy failure
Not making ATP
Reduced neurotransmitter synthesis

Beriberi – impaired sensory, motor functions; tachycardia, heart failure
Wernicke-Korsakoff syndrome

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7
Q

Folate deficiency (biochemical and physical manifestations)

A

Decrease in methylation, DNA repair, nucleic acid synthesis

Neural tube defect

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8
Q

Manifestations of B12 deficiency (three)

A

Low biomolecule methylation

Low RBC proliferation

Low catabolism of FA and AA

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9
Q

Folate MTHFR 677C->R polymorphism

A

Polymorphism impairs folate metabolism –> high homocysteine concentration –> lowers SAM concentration –> 50% reduction in DNA methylation –> increased risk for CHD

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10
Q

Pros of folic acid fortification

A

Increased concentration of plasma folate, lower rates of neural tube defects.

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11
Q

Riboflavin function (three main)

A

Precursor for FAD

Used in TCA cycle: succinate -> fumerate

Used in Beta-oxidation of FA

Used in ETC (complex II)

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12
Q

Thiamine deficiency risk factors

A

Inadequate intake
Alcohol abuse (reduced THTR-1 and -2 expression; liver damage impairs storage)
Bariatric surgery
Mutation in THTR-1

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13
Q

Thiamine function

A

Enzyme cofactor for NADPH biosynthesis, AA catabolism

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14
Q

Niacin function

A

Precursor to NAD

Non-consumptive: energy metabolism in TCA and ETC
Consumptive: DNA repair, gene expression

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15
Q

Folate and cancer

A

Too much or too little disrupts homeostatic methylation pathways

Also may exacerbate cancer by allowing nucleic acid synthesis

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16
Q

Folate functions

A

Folate coenzyme is required for synthesis of methionine from homocysteine

Involved in nucleic acid synthesis, methylation

17
Q

Biomarker of folate

A

Plasma, serum, urine folate levels

Homocysteine accumulates with low folate status

18
Q

Niacin salvage pathway

A

Allows for constant supply of NAD from NA, NAM, and NR

Allows body to contain regenerating NAD even when niacin intake decreases for a while

19
Q

Pantothenic acid

A

Component of Coenzyme A

Participates in a number of metabolic reactions

CHO, Protein, and FA metabolism
Acetylation

20
Q

Biotin

A

Lysine binding
Biotinylation of carboxylases
Gene expression

21
Q

Vitamin B6 function and connection with inflammation

A

Coenzyme of over 100 enzymes
Protein metabolism, hemoglobin synthesis
Inflammation may impair status