Vitamins Flashcards
what are vitamins
- chemically unrelated compounds
- cannot be synthesised by human body
- required in diet
fat soluble vitamins
- A, D, E, K.
- released, transported and absorbed in chylomicrons with dietary fat
- not readily excreted
- sig. qts in liver and adipose tissue
good source of folic acid
- leafy, dark green veggies
- wholegrains
- beans
function of folic acid
- tetrahydrofolate is the reduced coenzyme form of folate
- receives 1C fragments from donors
- synthesis of AA, purine nucleotides, thymidine monophosphate (pyrimidine nucleotide incorporated into DNA)
- deficiency = cant make DNA = can’t divide
cause of inadequate serum levels of folate
- increased demand (pregnancy, breastfeeding)
- poor absorption
- alcoholism
- treatment with drugs
- folate-free diet
how long does folate free diet take to cause deficiency
few weeks
what are common neural tube defects
- spina bifida
- anencephaly
how are common NTDs prevented
- adequate nutrition at time of conception as critical folate-dependent development occurs in 1st weeks
biomedical functions of vitamin B12
- remethylation of Hcy to methionine
- isommerisation of methylmalonyl CoA
one cause of neurological manifestations of B12 deficiency?
- methylmalonyl cOa produced during degradation of fatty acids
- if left un-isomerised, unusual branched FA accumulate + become incorporated into cell membrane, including those of CNS
sources of B12
- only micro-organisms, not made in plants
- liver
- red meat
- fish
- eggs
- dairy products
- fortified cereal
Explain the folate trap hypothesis
- methionine synthase uses B12 as coenzyme when converting 5-methylTHF into other forms of THF
- deficiency = folate cant be converted and is trapped = decrease in other forms of THF
- other forms required for purine and TMP synthesis = symptoms of megaloblastic anaemia
which cells are effects of cobalamin deficiency most pronounced?
- rapidly dividing cells:
- erythropoietic tissue
- mucosal cells
how long does cobalamin deficiency symptoms take to show
- several years as significant amounts stored in body IF due to intake
- more quickly if due to absorption
which test evaluates b12 absorption
schilling test
increased levels of what in blood indicate b12 deficiency
methylmalonic acid
How is cobalamin absorbed by the body?
- released from food in acidic environment of stomach
- free b12 binds to glycoprotein, transp to intestine
- pancreatic enzyme releases from R-protein, b12 binds to IF
- b12-IF complex travels through intestine, binds to cubulin receptor on surface of mucosal cells in ileum
- b12 transp into mucosal cell and subsequently general circulation.
- carried by binding protein transcobalamin
- taken up and stored by liver, released in bile, reabsorbed in ileum
cause of malabsorption of cobalamin in elderly
reduced secretion of gastric acid (achlorydia)
what is pernicious anaemia
severe malabsorption of cobalamin
common cause of pernicious anaemia
- autoimmune destruction of gastric parietal cells that absorb IF
- partial/total gastrectomy become IF deficient and therefore b12 deficient.
effects of cobalamin deficiency
- anaemic (folate recylcing impaired)
- neuropsychiatric symptoms as disease develops. CNS effects irreversible
treatment of pernicious anaemia
lifelong treatment of
- high dose oral b12 or
- IM cyanocobalamin
why does b12 supplementation work
- approx 1% cobalamin uptake is by IF-independent diffusion
active form of vitamin C
ascorbic acid
Function of vit C
- act as reducing agent.
- coenzyme in hydroxylation reactions. e.g. hydroxylation of proline and lysyl residues in collagen.
- thus, required for maintenance of normal connective tissue + wound healing.
- facilitates absorption of dietary non-haeme iron from intestine by reducton of fe3+ to fe2+
- antioxidant
- forms collagen, bile acids, epinephrine and steroid hormones
Vit C deficiency
- scurvy; bleeding gums, haemorrhage, fatigue, bone, joint, teeth
- can be explained by defective connective tissue
- also causes microcytic anaemia
what is vit b6 a collective term for
- pyridoxine, pyridoxal and pyridoxamine; all derivatives of pyridine
which b6 is found in plants
- pyridoxine
which b6 is found in animal derived food
pyridoxamine and pyridoxal
biochemical function of b6 supp
- precursors to PLP (coenzyme)
- e.g. transulfuration of Hcy to cysteine
- transamination
- deamination
- decarboxylation
- condensation
clinicals b6 deficiency
- isoniazid used to treat TB induces b6 defic. bc forms inactive derivative with PLP.
- administered in conjunction w b6 supplementation
- dietary deficiencies in newborns, women taking oral contraceptive, alcoholism
b6 toxicity
- excess of 400x RDA causes sensory neuropathy
what is thiamine
vit b1
active form of b1 and how is it formed
thiamine pyrophosphate TPP formed by transfer of pyrophosphate grp from ADP
biochemical functions of b1
- formation/degradation of alpha ketols
- oxidative decarboxylation of a-keto acids
beri-beri + classification
- thiamine-deficiency syndrome found inn areas where polished rice is major comp of diet
- dry: peripheral neuropathy esp in legs
- wet: oedema bc of dilated cardiomyopathy
Wernicke-korsakoff syndrome
- dietary insufficiency/impaired intestinal absorption of thiamine
- mental confusion
- gait ataxia
- nystagmus
- opthalmoplegia: paralysis of eye muscles
- wernicke encephalopathy
- memory problems+ hallucinations with korsakoff dementia
why does b1 deficiency affect CNS
- oxidative decarboxylation of pyruvate and AKG is decreased
- less ATP produced
- impaired cellular function