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159 Cards in this Set
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- 3rd side (hint)
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vit b1 aka
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thiamin. it stands for:
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thi (S)
amin (amino) |
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do all vits contain an amino group?
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no
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what is the biologically active form of thiamin?
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TDP (thiamin diphosphate). it is also the most abundant form in animal tissues
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what form is thiamin absorbed in?
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NOT TDP form. just regular. The phosphates are cleaved by a phosphatase before being absorbed.
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at low thiamin conc how is it absorbed?
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through active transport into the enterocyte by sodiom depentdent transporters
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If thiamin conc is high, how is it absorbed?
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through passive transport
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after thiamin is absorbed into the enterocyte, where does it go?
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portal vien to liver
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how does the normal thiamin which is absorbed get the two phosphates added to it to make it active?
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ATP gives it two phosphates (or just one or three, but two phosphates is what it needs to be biologically active)
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where is most B1 found in the body?
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muscles (50%)
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After B1 gets phosphates donated to it in the liver, where does it go?
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blood --> muscle, heart, brain, kidney and liver
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what forms of thiamin circulate in the blood?
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free thiamin, TMP, TDP, TTP
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what form is thiamin in when it leaves the enterocyte?
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free thiamin. what form is it in when it leaves the liver?
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TMP, TDP or TTP (also maybe free thiamin)
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TDP is used for what type of reactions?
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decarboxylation reactions. where specifically?
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pyruvate to AcCoA
aKG to succinyl CoA |
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tanic acids interfere with the absorption of
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B1
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What interferes with B1 absorption?
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tanic acids (coffee and tea), caffeine, thiaminase (raw fish), Ca, Mg
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what is required for the decarboxylation of the BCKA
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B1 (TDP)
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thiamin deficiency in US?
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rare
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thiamin deficiency would result in
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inhibition of pyruvate --> AcCoA,
therefore increased anaerobic ATP production = lactic acidosis |
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maple syrup urine disease is a result of
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genetic disorder. b/c of....
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BCKA dehydrogenase is insufficient. Resulting in increased BCAA and BCKA in the blood. w/o thiamin, the BCKA can't be oxidized resulting in MSUD.
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dry beriberi is
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muscle weakness and muscle wasting
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wet beri beri
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congestive heart failure and edema
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excessive thiamin =
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100 x
headaches, convulsions |
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vit b2 is
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riboflavin
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what forms is riboflavin found in?
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free, bound to protein, FMN, FAD
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FAD and FMN are
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coenzymes. they stand for
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flavin adenine dinucleotide
flavin mononucleotide |
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structure of FAD has
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two extra P's and an adenine
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FMN structure has
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extra P
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B2 absorption:
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absorbed into entercyte in free form. Some converted and used in enterocyte. The rest goes to liver and is converted to other forms. Then circulated to other tissues
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high B2 in:
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liver, kidney and heart
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free riboflavin in extrahepatic cells:
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converted to FMN and FAD to keep it from diffusing out
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FMN and FAD participate in what kind of reactions?
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redox. they accept H.
They are ___ agents: |
oxidizing
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rxns that use FAD
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pyruvate to AcCoA (intermediate e- carrier, NADH is the final acceptor)
succinate to malate AcCoA to Trans acyl CoA (beta oxidatoin) |
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FMN's job
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part of ETC
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Riboflavin deficiency:
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cheilosis (fissures/cracks on the outside of lips)
glossitis (swelled tongue) hyperemia (redness of oral cavity) |
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riboflavin toxicity symptoms:
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no known toxicity
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vit b3 isi
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niacin
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Nicotinamide structure?
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has an amine group that replaces an OH group
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NAD structure?
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Nicotinamide + adenine + 2P's
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how is niacin absorbed?
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high conc: passively
low conc: actively (Na dependent) |
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After niacin is absorbed into enterocyte?
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some used in enterocyte
rest goes to liver where it is converted to NAD The nicain not needed by the liver leaves and goes to cells where it is converted to NAD or NADP (or NAD leaves and in other cells is converted to nicotinamide) |
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niacin can be synthesized from
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tyrptophan. How much trp to make niacin?
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60 mg trp = 1 mg niacin
(remember that trp isn't only used to make niacin, also makes seratonin) |
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necessary cofactor for niacin synthesis from trp?
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b6
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what percent of typical protein intake is trp?
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10%
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recommended protein intake per day per kg?
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0.8 g/kg for males?
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what type of reactions does niacin help facilitate?
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dehydrogenase.
can accept or donate electrons |
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pathways that use niacin
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hexose monophosphate shunt
BCKA dehydrogenase-->energy glycolysis pyruvate-->lactate pyruvate--> AcCoA tca x 3 Acyl CoA --> AcCoA malate aspartate shunt? citrate pyruvate shuttle? |
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NADPH does NOT transfer electrons and H to ETC. instead used as
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reducing agent in pathways:
cholesterol and fa synthesis |
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where is NADPH produced?
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hexose monophosphate shunt
citrate pyruvate shuttle |
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pellagra symptoms:
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dementia
dermititus diarrhea death |
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niacin toxicity symptoms:
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flushing
itchy liver damage hyperglycemia gastrointestinal distress |
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what is niacin sometimes used to treat?
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hypercholesteremia
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6 forms of vit b6
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pyridoxine (PN)
pyridoxine phosphate (PNP) pyridoxal (PL) Pyridoxal phosphate (PLP) pyridoxamine (PM) pyridoxamine phosphate (PMP) |
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active forms of vit b6?
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PMP
PLP |
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pyridoxine structure?
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OH group
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pyridoxal sturcture?
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aldehyde group
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pyridoxamine structure?
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amine group
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the Phosphate added to b6 structures does what?
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replaces and OH group
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when can B6 be rephosphorylated?
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in the enterocyte or liver
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too little riboflavin =
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potential b6 deficiency b/cit can be absorbed
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needed for the synthesis of heme
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b6
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needed for the synthesis of trp from niacin
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b6
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b6 deficiency:
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irregular EEG (brain waves), insomnia, cheilosis (cracking of tissue around the mouth), irritability, and convulsions in infants
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hypochromic microcytic anemia is from
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b6 deficiency. B/C
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bone marrow can't make heme w/o b6. Results in Fe accumulation in bone marrow
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b6 toxicity =
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nerve degeneration
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b12 aka
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cobalmins
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cobalmins are part of
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corrinoids. They are what contribute the large ring structure (corrin nucleus)
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what is in the center of corrin nucleus?
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cobalt atom
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what is bound to the cobalt in the corrin nucleus?
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lots of things. ex: cyanid
cyanocobalmin |
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active form of cobalmin:
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methylcobalmin
adenosylcobalmin |
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how is b12 typically found in food?
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bound to polypeptides
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what releases b12 from food?
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pepsin
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which tissues in the body have a receptor for TCII?
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all tissues
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what is the primary protein that delivers B12 to the boyd?
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TCII
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how is b12 and TC uptaken by cells?
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endocytosis
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people with b12 deficiencies?
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stomach partial removal
ileal removal |
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PRIMARY function of adenosylcobalmin:
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transfer adenosine to other compounds.
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adenosylcobalmin is key in the reaction of
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L-methylmalonyl CoA --> succinyl CoA
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propionyl CoA eventually is metabolized to
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succinyl CoA and enters the TCA cycle
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Met, Val, Ile, Thr, and odd chained FA all produce
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propionyl CoA
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primary function of methylcobalmin
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transfer its methyl group to things
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cobalmin accepts a methyl group from
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folic acid (N5 THF).
Cobalmin then donates this methyl group to |
homocysteine. which becomes...
methionine |
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b12 deficiency in US is b/c of
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malabsorption (not deficiency)
when do deficiency symptoms occur? |
not for up to several years b/c thebody stores it in the liver
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b12 deficieny symptom
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megaloblastic anemia
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two deficiencies that can cause megaloblastic anemia
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b12 and folic. Why folic?
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folic acid donates the methyl to cobalmin
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b12 deficiency results in what other deficiency?
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folic acid. B/c the methyl has nothing to donate to and folic acid remains in the THF state and is "trapped."
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folic acid is used for the synthesis of
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DNA
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deficiency of __ inhibits cell's that undergo rapid division
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folic acid or b12.
What kind of cells are affected? |
rbc
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megaloblastic anemia is characterized by
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large, immature rbc. incapable of carrying oxygen.
How to treat it: |
folic acid and/or b12
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cobalmin is used for:
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synthesis of sphingomyelin,
generation of methionine |
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what results in decreased SAM
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decreased b12 (b/c then decreased met, which is used for SAM)
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how is b12 used for the production of myelin sheath?
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b12 donates methyl to homocystein to make met.
Met is used in SAM SAM donates methyl to choline part of sphingomyelin. |
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nerve degeneration is a result o __ deficiency?
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b12.
What can solve this problem? |
b12 or met therapy
(NOT folic acid) |
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pernicious anemia is:
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megaloblastic anemia + nerve degeneration
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not enough b12 may result in:
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elevated homocysteine.
This results in: |
increased CAD
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b12 toxicity?
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no known
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folic acid aka
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pteroylglutamate
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three components of folic acid:
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glutamate
PABA (para aminobenzoic acid) pteridine |
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pteroic acid is:
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pteridine + PABA
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can the body make folate?
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yes it can make all the three separate parts.
BUT it lacks the enzyme to bind pteridine to PABA |
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Where do we get folate?
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diet only
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active form of folate?
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4-7 glutamates
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pteroylpolyglutamate is?
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folic acid with multiple glutamates
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what form is folic acid absorbed in?
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monoglutamate form
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what enzyme hydrolyzes the excess gluatmates from folic acid so it can be absorbed?
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conjugases
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where are conjugases found?
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brush border
intestinal lumen |
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what do conjugaes (hydolyze Glu from folic acid) need to function?
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zn
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__ deficiency inhibits folic acid?
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zn
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how is folate absorbed? passive v active?
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30% passive
70% active |
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key to folic acid being absorbed?
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must be bound to FBP to get into enterocyte.
Once in...? |
reduced to THF
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what is required to reduce folic acid to THF?
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NADPH
where does this happen? |
enterocyte
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THF methylated produces:
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N5 methyl THF
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THF is formylated to produce:
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N5 or N10 formyl THF
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what forms of THF are circulated from enterocyte to liver?
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N5 or 10 formyl THF
N5 methyl THF THF |
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forms of THF in the liver are:
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THF,
N5 methyl THF N10 formyl THF. |
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what forms of THF can be reabsorbe in the bile?
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N5 methyl THF and N10 formyl THF
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WHAT form is THF in in the blood?
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all forms, but bound to FBP.
Primarily monoglutamate form |
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what form of THF i the cells?
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converted to polyglutamate form. (active form. also keeps it from diffusing out of the cell)
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folic acid is required for the synthesis of
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purines and pyrimidines
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metabolism of ___ requires folic acid:
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aa (some)
serine methionine glycine histidine |
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folic acid deficiency results in:
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megaloblastic anemia
decreased cell division enterocytes affected dementia depression nerve dgeneration elevated homocysteine cancer risk CAD risk |
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folic acid toxicity
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GI distress
irritability insomnia |
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lysine is a part of what nutrient?
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biotin
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lysine is bound to biotin how?
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amide (not peptide)
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active form of biotin?
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biocytin (biotin + lysine)
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what forms of biotin are removed from food?
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biocytin
biotin biotinyl peptides |
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biotinase does what?
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converts some of the biocytin and biotinyl peptides into free biotin
(in SI) |
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what forms of biotin can be absorbed in the enterocyte?
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biotin and biocytin
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is biotin absorbed actively or passively?
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unknown
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if biocytin isn't converted to biotin...
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excreted in urine
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where is biotinidase?
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SI and other tissues of the body
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biotin deficiency:
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depression
dermatitis hallucinations anorexia nausea muscle pain hair loss |
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CoA has ___ as a compoent of it?
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pantothenic acid
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CoA is made up of?
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pantothenic acid + cysteine + ATP
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do we synthesize pantothenic acid?
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no
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what form is pantothenic acid in in the diet?
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CoA
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pantothenic acid is active or passive absorption?
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passive mainly
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CoA forms what kind of linkage with other compounds?
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thioester with a carboxyl group
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pantothenic deficiency:
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vomiting
burning in legs weakness fatigue |
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vit C aka
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ascorbic acid
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can we make vit c?
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nope
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what is reduced in the reaction of ascorbic acid --> dehydroascorbic acid
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glutathione
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ascorbic acid is primarily absorbed via
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active transport.
How is dehydroascorbic acid absorbed? |
passive or glc transporters
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when is absorbed dehydroascorbic acid changed to ascorbic acid??
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in the enterocyte
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what is required for dehydroascorbate reductase?
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glutathione
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what is glutathione made of?
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glutamate, cysteine, glycine
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what kind of reactions does vit c help with
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hydroxylation reactions
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vit c is used for the hydroxylation of
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proline and lysine on procollagen by acting as a reducing agent for iron 3+
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vit c is a reducing agent for
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iron +3 to iron +2
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how does vit c affect collagen?
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it hydroxylates proline. That is necessary for the formation of the helical structure of collagen.
The hydroxylation of lysine is also important. |
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vit c is used for the synthesis of
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neurotransmitters
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vit c hydoxylates these aa (or at least plays a part in it)
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trp
pro lys. What's the point of doing it to trp? |
to make serotonin eventually
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vit c relation to bile?
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hydroxylation of rate limiting step of bile acid synthesis
(7-alpha-hydroxylase) |
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vit c is a good antioxidant b/c
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it has good reducing power. Donates H atoms to free radicals
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excess vit c
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interferes with Cu absorption
diarrhea kidney stone destory b12 if greater than |
500 mg vit c/day
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retinoids can be derived from
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carotenoids.
examples:? |
lycopene
beta carotene gamma carotene |
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provitamin A =
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carotenoid from which vit a is derived
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what form is vit a in in food?
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carotenoid or
retinyl ester bound to a FA. ex: |
retinyl palmitate
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beta ionone ring found in what compounds?
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vit a compounds
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what is vit a bound to in food?
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protein
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