Cobalamin (B12) Flashcards
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| 9090370150 | how is cobalamin produced? | anaerobic bacteria, not produced by plants or animals but can be found in animals | 0 | |
| 9090370151 | what increases B12 absorption? | IF | 1 | |
| 9090370152 | cobalamin | generic term for a group of compounds called corrinoids bc of its orrin nucleus | 2 | |
| 9090370153 | corrin nucleus | 1. macrocyclic ring of 4 pyrrole rings 2. for B12 center of the ring has cobalt attached, group attached to cobalt determines the form of cobalamin | 3 | |
| 9090370154 | active forms of cobalamin | only 2 1. adenosyl cobalamin 2. methyl cobalamin | 4 | |
| 9090370155 | sources of cobalamin | made by bacteria, found in animal products (no plant products) 1. meat, poultry, fish 2. clams & oysters 3. eggs 4. milk & milk products in lesser amounts | 5 | |
| 9090370156 | cobalamin in meat | adenosylcobalamin & hydroxocobalamin | 6 | |
| 9090370157 | cobalamin in milk | methylcobalamin & hydroxocobalamin | 7 | |
| 9090370158 | cobalamin bioavailability | 40-89% bioavailable from food. stability: resistant to light, heat, oxidation | 8 | |
| 9090370159 | digestion of cobalamin | eaten in all forms. absorption requires *digestion in stomach*: 1. pepsin/HCl release cobalamins from polypeptides 2. R proteins found in saliva & gastric juices in stomach binds to B12 & protects it from bacterial use 3. IF made & released in stomach (parietal cell) but functions in intestine | 9 | |
| 9090370160 | absorption of cobalamin | 1. cobalamin released from R protein by pancreatic proteases 2. IF binds to freecobalamin 3. B12-IF complex is absorbed by ileum via passive diffusion (pharmacological doses) & binds to IF receptor at physiological doses | 10 | |
| 9090370161 | polarized cells | 1. cubuilins: protein receptor, IF receptor (cubam) 2. B12-IF complex enter cell by receptor mediated endocytosis IF degraded so B12 can enter cell | 11 | |
| 9090370162 | non-polarized cells | 1. transcobalamin receptor (TC) 2. in blood, bound to TC | 12 | |
| 9090370163 | role of R, IF, & TC | assist cobalamin to get around bc its so big & complex | 13 | |
| 9090370164 | transpiration of cobalamin | transport in blood, bound to 1 of 3 transcobalmins: 1. TCI 2. TCII 3.TCIII | 14 | |
| 9090370165 | TCI | circulating storage form | 15 | |
| 9090370166 | TCII | carries newly absorbed cobalamin to tissues | 16 | |
| 9090370167 | TCIII | delivery from peripheral tissues to liver | 17 | |
| 9090370168 | storage of cobalamin | ONLY water-soluble vitamin that can be stored in body for long periods of time even years. 50% storage in liver, mainly as adenosylcobalamine (70%) but methylcobalamine is main form in blood. can be stored up to 11 years | 18 | |
| 9090370169 | how long would a deficiency of cobalamin take to develop? | may take 2-5 years bc of great storage | 19 | |
| 9090370170 | function of cobalamin | coenzyme-methyl carrier. homocysteine => methionine. step 1: formation of methylcobalamine-enzyme complex step 2: methylcobalamin donates methyl group to homocysteine to form cobalamin & methionine so methionine synthase becomes oxidized (inactive), eventually becomes reduced (active) again by methionine synthase reductase & NADH | 20 | |
| 9090370171 | where does the methionine synthase-CbI complex take the methyl group from? | 5-methyl THF (folate) | 21 | |
| 9090370172 | methyl-folate trap | irreversible 5-methyl THF formation. lack of vit B12 prevents formation of THF & traps folate in 5-methyl THF form | 22 | |
| 9090370173 | what is interaction of the methionine & folate cycle mediated by? | B12 | 23 | |
| 9090370174 | secondary function of cobalamin | adenosylcobalamin form. formation of succinyl CoA from methylmalonyl CoA. defieicny of CbI leads to accumulation of methylmalonyl CoA & used to assess vitamins status. succinyl CoA is KREBs is intermediate of KREBs while methylmalonyl is intermediate step | 24 | |
| 9090370175 | propionyl to methylmalonyl is dependent on what? | biotin | 25 | |
| 9090370176 | excretion of cobalamin | no degradation prior to excretion. very little in urine. turnover .1% per day. *most of vitamin is excreted in bile (enterohepatic circulation) but is reabsorbed* | 26 | |
| 9090370177 | deficiency of cobalamin | occurs in stages: 1. serum: low levels holotranscobalamin II 2. cell concentrations diminish 3. biochemical deficiency occurs => decreased DNA synthesis, elevated homocysteine in serum, elevated methylmalonic acid in serum | 27 | |
| 9090370178 | what does elevated homocysteine in serum cause? | increased risk for CVD, decreased methionine = decreased SAM & SAM is essential for nerve function | 28 | |
| 9090370179 | what does deficiency of cobalamin progress to? | megaloblastic macrocytic anemia. may be caused by pernicious anemia | 29 | |
| 9090370180 | pernicious anemia | auto immune condition where antibodies attack parietal cells causing decreased IF function | 30 | |
| 9090370181 | general deficiency symptoms | pale skin, short breath, insomnia, aboral gait, dementia, fatigue, palpitations, paresthesia, loss of concentration, neuro probs | 31 | |
| 9090370182 | severe B12 deficiency | -neuro symptoms -degeneration of spinal cord -presentation: absent reflexes, ataxia, no sense of touch -results: severe irreversible brain & NS damage & if untreated => death | 32 | |
| 9090370183 | at risk population for B12 deficiency | vegetarians & malabsorption: atrophic gastritis, gastrectomy, achlorhydria, decreased absorptive area in intestine, medications including proton pumps, H2 blockers | 33 | |
| 9090370184 | genetic disorder deficiency | common genetic mutation TCII associated w/ substitution of C for G results in TC protein unable to bind to CbI. 20% pop is homozygous for GG variant, leads to low levels of B12, high levels of homocysteine which is risk factor for CVD. GG instead of CG | 34 | |
| 9090370185 | toxicity of B12 | no toxicity & no benefit from excessive intake | 35 |