UCI SOM Dai
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Can vitamins be synthesized in the human body | no
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Two classes of vitamins | water-soluble and fat-soluble
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Fat soluble vitamins | A,D,K,E
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Water soluble vitamin classes | b vitamins, folic acid and ascorbic acid (C)
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B vitamins | thiamine (B1), Riboflavin (B2), Niacin (B3), Pantothenic Acid (B5), Pyridoxine (B6; pyridoxal; pyridoxamine), biotin (B7), B12 (cobalamine)
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Sources of vitamins | food intake and synthesis by intestinal microorganisms
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6 ways to have vitamin deficiency | inadequate dietary intake, inadequate absorption, inadequate use (inadequate conversion), increased requirements, increased excretion, drug-associated deficiency
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thiamine cofactor/s, reaction/s, and disease/s | thiamine pyrophosphate; pyruvate DH, alpha ketoglutarate DH, branched chain alpha keto acid DH; Beriberi
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riboflavin cofactor/s, reaction/s, and disease/s | FAD, FMN;oxidation-reduction;no disease
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Niacin cofactor/s, reaction/s, and disease’s | NAD, NADP; oxidation-reduction; pellagra
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Pantothenic acid cofactor/s, reaction/s, and disease/s | Coenzyme A; acyl transfer, pyruvate DH, alpha keto glutarate DH; no disease
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What B vitamin can be made in small amounts in the body | niacin (made from tryptophan)
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Pyridoxine cofactor/s, reaction/s, and disease/s | pyridoxal phosphate; transamination, decarboxylation, dehydration; seizure in infants
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Cobalamin cofactor/s, reaction/s, and disease/s | 5’-deoxyadenosylcobalamin, methylcobolamin; methylmalonyl-CoA mutase, 5’methylTHF homocys transferase; pernicious anemia and others
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Folate cofactor/s, reaction/s, and disease/s | tetrahydrofolate; 1 C transfer, dTMP biosynthesis, purine synthesis; megaloblastic anemia and others
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Biotin cofactor/s, reaction/s, and disease/s | no cofactors; carboxylation; no disease
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Ascorbic acid cofactor/s, reaction/s, and disease/s | ascorbid acid; hydroxylation (collagen); scurvy
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Beriberi | thiamine deficiency; mostly in areas that used polished rice; lethargy, weight loss, irregular heart rate, convulsions, death
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Pellagra | niacin deficiency; dermatitis, diarrhea, dementia, death
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Most common vitamin deficiency | folic acid
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Normal folic acid requirement | 100-200 mg/day/adult (more for pregnant women)
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Causes of folic acid deficiency | inadequate intake, impaired absorption (intestinal diseases), impaired metabolism, increased demand
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Diagnosis of folic acid deficiency | ingest test dose of Histidine and test forminimoglutamate level in urine; if there is forminimoglutamate in urine, folic acid deficiency is present
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Consequences of folic acid deficiency | 7 weeks-nothing; 13 wks-formiminoglutamate in urine, altered read blood cells; 4 months-irritability, forgetfulness, anemia; upon addition of folic acid, everything normalized
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Biochemical consequences of folic acid deficiency | defective glycine cleavage (neurological problems), defective homocys (met conversion->neurological defects); defective purine/pyrimidine synthesis (DNA and hematopoietic defects)
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B12 deficiency comes from | impaired absorption
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B12 storage | up to 6 years in liver
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B12 absorption | parietal cell in stomach makes instrinsic factor (IF) which binds B12 and transports it to the ileum; transported in blood by TC (transcobalomine) which takes it to the liver
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Pernicious anemia | IF (intrinsic factor) deficiency through impaired absorption of B12
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Affects of pernicious anemia | impaired: regeneration of tetrahydrofolate pool, impaired purine/dTMP biosynthesis, hematopoietic defects, neurological defects
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Neurological defects of pernicious anemia | accumulation of methylmalonyl CoA intereferes with myelination of nervous tissue b/c methylmalonyl CoA is a competitor of malonyl CoA in FA synthesis
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Treatment for pernicious anemia | intramuscular B12 injection and folate supplement
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N metabolism consequences of THF deficiency due to B12 deficiency | defective: purine/pyrimidine synthesis, glycine cleavage
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N metabolism consequences from direct B12 difficency | defective: homocys->Met conversion, methylmalonyl CoA->succinyl CoA conversion
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B12 and THF correlation | B12 is necessary in THF regeneration
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5 groupings of biosynthesis of non-essential AA | 1)Ala, Asp, Glu, Gln, Asn 2)Arg, Pro 3)Ser, Gly 4)Tyr 5)Cys
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alanine synthesis | pyruvate transamination
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aspartate synthesis | oxaloacetate transamination
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glutamate synthesis | alpha ketoglutarate transamination
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glutamine synthesis | add ATP and NH3 to glutamate
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asparagines synthetase | add ATP and N to aspartate
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Arginine and proline synthesis | glutamate->glutamate semialdehyde->proline and arginine
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Tyrosine synthesis | phenylalanine hydroxylase; 3/4 of Phe in diet goest to Tyr
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Cystein synthesis | comes from cystathionine which comes from serine and homocysteine which comes from methionine; cystathionine goes to cysteine and alpha ketobutyrate
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Serine synthesis | 3-phosphoglycerate (phosphogylcerate) 3-phosphopyruvate (aminotransferase) 3-phosphoserine (phosphatase) serine
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Glycine synthesis | serine (serine hydroxymethyl transferase) glycine; the rxn uses N5N10methylene THF which becomes THF; THF returns to N5N10 through a rxn with another glycine
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Almost all non-essential AA’s can be synthesized from | glycolysis products
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