Micro - Exam 3 Flashcards
B12 absorption
Gastric acid removes B12 from food protein»_space; gets bound to R-binder to protect from acid»_space; in duodenum, B12 gets bound to intrinsic factor which allows it to be transported into enterocyte
Manifestations of B12 deficiency
B12:
methylmalonyl CoA -> succinyl CoA
No B12:
methylmalonyl CoA -> methylmalonyl acid
- High MMA
- High homocysteine
- RBC macrocytosis
- Neurological problems
B12 functions (two)
- Coenzyme to convert homocysteine to methionine (and SAM) – methylation
- involved in degradation of FA and amino acids for energy – necessary for enzyme methylmalonyl-Coa mutase
Cons of folic acid fortification
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
Dietary sources of folate vs folic acid
Folate: widespread, naturally
Folic acid: fortified foods, cereals, supplements
Effects of Thiamine deficiency (two names of diseases)
Cellular energy failure
Not making ATP
Reduced neurotransmitter synthesis
Beriberi – impaired sensory, motor functions; tachycardia, heart failure
Wernicke-Korsakoff syndrome
Folate deficiency (biochemical and physical manifestations)
Decrease in methylation, DNA repair, nucleic acid synthesis
Neural tube defect
Manifestations of B12 deficiency (three)
Low biomolecule methylation
Low RBC proliferation
Low catabolism of FA and AA
Folate MTHFR 677C->R polymorphism
Polymorphism impairs folate metabolism –> high homocysteine concentration –> lowers SAM concentration –> 50% reduction in DNA methylation –> increased risk for CHD
Pros of folic acid fortification
Increased concentration of plasma folate, lower rates of neural tube defects.
Riboflavin function (three main)
Precursor for FAD
Used in TCA cycle: succinate -> fumerate
Used in Beta-oxidation of FA
Used in ETC (complex II)
Thiamine deficiency risk factors
Inadequate intake
Alcohol abuse (reduced THTR-1 and -2 expression; liver damage impairs storage)
Bariatric surgery
Mutation in THTR-1
Thiamine function
Enzyme cofactor for NADPH biosynthesis, AA catabolism
Niacin function
Precursor to NAD
Non-consumptive: energy metabolism in TCA and ETC
Consumptive: DNA repair, gene expression
Folate and cancer
Too much or too little disrupts homeostatic methylation pathways
Also may exacerbate cancer by allowing nucleic acid synthesis