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intermediates of tca cycle
citrate, isocitrate, alpha-ketoglutarate, succinyl coA, succinate, fumarate, malate, oxaloacetate (cindy is kind so she forgives more often)
key enzymes of regulation in tca cycle (and what reactants they convert to what products)
1) citrate synthase (acetylcoA to citrate), 2) isocitrate dehydrogenase (isocitrate to alpha-ketoglutarate), alphaKGdehydrogenase (alphaKG to succinylcoA)
regulation citrate synthase
(TCA cycle, acetylcoA to citrate) inhibited by ATP (NADH, succinyl coA, fa co A, + ADP)
regulation of isocitrate dehydrogenase
(isocitrate to aKG) inhibited by NADH and ATP, activated by ADP and Ca [no succinylcoA]
regulation of aKGdehydro
(aKG to succinyl coA) inhibited by succinyl coA, NADH, ATP; activated by Ca
cofactors of aKG dehydro
same as PDH (B1,2,3,5,lipoic acid)
energy produced from TCA
3 NADH, 1 FADG2, 1GTP, (2CO2) for total of 12 ATP
steps at which energy produced TCA
succinyl coA to succinate (1GTP), succinate to fumarate (FADH2), (3NADH) at malate to oxaloacetate , isocitrate to aKG, and aKG to succinylcoA
what comes in in the succinyl coA step
odd chain FA (via propionylcoA and methylmalonylcoA)
aKG can be diverted from TCA to
AA (via glutamate transamination/deamination)
citrate can be diverted from TCA to
fa (this is how acetyl coA is transported out of mitochondria for fa synthesis--malonyl coA + acetyl coA)
amino acids can come into TCA at
fumarate step (fumarate also byproduct of urea cycle)
oxaloacetate may come from
aspartate (via transamination/deamination)
rxn of transamination/deamination
aa come in as glutamate and on conversion to aKG give off NH4 to urea cycle. then aKG converted back to glutamate while aspartate converted to oxaloacetate, enz PLP requiring B6.
steps of pentose P path (HMP shunt)
Glu6P to ribuloseP via G6PD (producing NADPH), to Fru 6P
ribuloseP can be used for
nucleotide syn (converted to ribose5P)
steps glycogen synthesis
Glu1P to UDP-Glu to Glycogen (where Glu1P converted from Glu6P of glycolysis)
regulatory enzymes of glycolysis
PFK (Fru6P to Fru1,6P rate limiting step), PK (PEP to Pyr), PDH (to enter TCA changes pyruvate to acetylcoA)⬦.also minor regulation HK (- by Glu6P)
steps glycolysis energy produced
Gly3P to 1,3GlyP (NADH), 1,3GlyP to 3PGly (ATP), PEP to Pyr (ATP)
steps glycolysis requiring energy
1) Glu to Glu6P, 2) Fru6P to F1,6P (at PFK rate limiting step)
regulation of HK
inhibited by Glu6P (its product)
HK throughout the body, GK only in liver, lower affinity, higher capacity (key to clearing hi concentration glu after meal)
rate limiting step glycolysis
Fru6P to Fru1,6P (PFK)
regulation PFK
(Fru6P to Fru1,6P); inhibited by ATP and citrate; activated by AMP and Fru2,6P
regulation of PK
(PEP to Pyr) inhibited by ATP and alanine, activated by Fru1,6P
regulation of PDH: phosphorylation state
(pyr to acetylcoA) active when deP
cofactors of PDH, specifics and the vitamin they're derived from
pyroP (thiamine B1), lipoic acid, coA (pantothenate B5), FAD (riboflavin B2), NAD (niacin B3)
steps urea cycle
ornithine + carbamoylP to citrulline (+asp) to Arginosuccinate, (-fumarate) to Arginine, (-urea) to ornithine (+carbamoylP) to citrulline
carbamoyl produced from
C)2 and NH4 from transamination/deamination
where difft steps of urea cycle occur
liver, carbamoyl is in mitochondria, rest in cytoplasm
purpose Cori cycle
transfer lactate from RBC and muscle to liver, allowing them to fxn anaerobically
steps cori cycle
glu (in mscl or RBC) hydrolyzed to pyr (gain 2ATP), converted to lactate via LDH, lactate taken up by liver converted to pyr by LDH, requires 6ATP to return to glu (in liver)
endpoints of pyruvate metabolism
oxaloacetate, alanine, acetyl coA, lactate
how pyr converted to oxaloacetate
via pyr carboxylase (w biotin) + ATP
how pyr converted to lactate? needs?
via LDH (+NADH)
how pyr converted to alanine
via Ala aa trxr
subunits of electron transport chain
NADH dehydro, (Q), cyto bcl, cytoC, cytochrome oxidase aa3
NADH comes in at which step
NADH dehydro
FADH2 comes in at which step
rotenone blocks
NADH dehydro to Q (also amylol)
antimycin A blocks
cyto bcl to cyto c
uncoupling of electron transport
2,4 DNP
inhibit transfer to 02
CN-, N3-, CO
inihibit ATPase
energy NADH produces in electron transport
energy FADH2 produces in electron transport
how is energy obtained from ketone bodies (what step do they enter metabol?)
enter as ketoacids as acetylcoA to TCA
fa syn precursor ____, is converted from ____ of TCA
fa syn precursor malonylcoA converted from acetylcoA
regulation of acetylcoA carboxylase
active when deP (insulin), insulin, citrate. inhibited by glucagon. NOTE: requires biotin
how is fatty acid use shut off during fa synthesis
malonylcoA inhibits CAT (carnitine transfer) for txr of fa into mito for beta-oxidation
what is needed for rxn for desaturation
need O2, NADPH, cytob5 can insert >9 to COOH end
why linolenate and lineleate impt
esstl fa bc only plants can insert dble bonds bw 9 and omega carbon (opp COOH)
steps of cholesterol syn
2 acetylcoA to HMGcoA through HMGCoA reductase (requiring 2NADH) making mevalonate
HMGCoA reductase: role? requires? regulation?
cholesterol synthesis, requires 2 NADH and inhibited by cholesterol
how ketones synthesized
HMGCoA to acetoacetate (to beta-OHButyrate and back)
pathway of how ketones be used
acetoacetate plus succinylcoA go thru thiotrxse and thiolase to TCA
HMGCoA reductase is found
NOT in the liver, so liver can't use the ketones it makes
regulation of glycogen synthase
when deP (insulin) this is stim in liver and muscle, activated by Glu6P and insulin, inhib by glucagon and epi
overall regulation of glyc syn and degradation,
liver v muscle regulation?
glucagon->increase in PKA inhibits gly synthase by P, and activ gly degradation. in liver gly degradation: activated by glucagon and epi, in muscle activated by epi, AMP, and Ca.
what types links gly synthase form
alpha 1,4
how form branches in gly syn
alpha 1,6 made by glucosyl 4:6 trxase
how body able to break down TAG in adipose, and its regulation
hormone sens lipase (+epi, - insulin) breaks into FFA which is carried by albumin, and glycerol which is transferred to liver for gluconeo
uses of biotin
1) gluconeo (carboxy of pyr in mito)
2) fa syn (carbosy of acetylcoA to form malonyl coA)
3) odd chain fa degradation (propionylcoA to methylmalonylcoA)
signs symptoms biotin defic
anorexia, (enteritis) N/V, glossitis, alopecia, derm
causes biotin defic
egg whites (avidin in egg whites binds biotin avidly), Abx
vit A
water soluble vitamins
all B, C, biotin, folate
common features B defic
dermatitis, glossitis, diarrhea
role of pyridoxal P
amino acid: transamination, decarboxy, deamination
role of THF
transfers one carbon units
signs/symptoms pyridoxal P defic
convulsion, derm, anemia
signs/sympt THF defic
megablastic anemia, neuro
role B12
methyl txr THF to homocys to form meth, also methylmal coA to succinylcoA in fa metab (myelination trbl?)
role of thiamine
thiamine pyroP: PDH, aKGdehydro, pentoseP (also oxidation of branched aa)
coenzA: role? requires what vit?
provides thioesters for acetylcoA, succinyl. Requires pantothenate.
role pantothenate
for transferring thioesters (part of CoA), cofactor for acyl txr, and fa synthase complex
signs/sympt pantothenate defic
dermatitis, enteritis, alopecia, adrenal insuff (listless, fatigue, burning feet)
role vitC
hydroxylation prolyne and lysine for collagen crosslinking, absorb Fe, anti-oxid, cofactor for dopamine to NE
main causes b12 defic
1) no animal products (STRICTEST VEGAN)
2) malabsorb (Sprue, protozoa)
3) no intrinsic factor (pernicious anemia)
4) no terminal ileum (crohns)
b12 nec in what 2 rxns
form TH4 (to make thymidine to make DNA), homocysteine to methionine
role vit E, defic causes...
antioxidant, defic leads to increased fragility of RBC.
E for Erythrocyte
defic vit A
night blindness, dry skin, impaired immune response
excess vit A
arthralgias, fatigue, HA, skin changes, sore throat, alopecia
defic in B1, name? clinical presentation?
(thiamine defic)=Beriberi and Wernicke-Korsakoff. Beriberi: polyneuritis, cardiac, edema. wet beriberi can lead to hi output cardiac failure
vit B2 defic
(B2=riboflavin) causes angular stomatitis, Cheilosis, Corneal vascul
causes of B3 defic
(B3 defic=pellagra), Hartnup dz, malignant carcinoid syndrome, INH
B3 defic
(Pellagra) Diarrhea, dermatitis, dementia, and beefy glossitis
role B3
(niacin) for NADH, NADPH.
thiamine in what specific enz, which is used in which rxns?
thiamine pyrophosphate, for PDH, aKG, and cofactor for transketolase rxn in HMP shunt
origin of melanin
(melatonin from tryptophan, both T's)
origin of melatonin
what need to make heme
what does tryptophan make
Niacin (NADH), Serotonin, Melatonin
what does phenylalanine make
tyrosine, which makes thyroxine and dopa. dopa makes NE, epi, and melanin
what does tyrosine make
thyroxine and dopa. dopa makes NE, epi, and mela
how NE made
phenylalanine to tyrosine to dopa to dopamine to NE
what made by arginine
creatinine, urea, NO
histamine comes from
role of B100
1) mediates VLDL secretion from liver
2)on VLDL, IDL, LDL so can bind liver
activates LCAT (esterifies 2/3 of plasma cholesterol)
chylomicron role
takes dietary tg to tissue, takes dietary chol to liver to make VLDL
apo B48
sxn of chylomicron (from intestine)
cofactor for LPL to work (both chylomicron and VLDL)
role of apoE, on which molecules for what function
mediates extra uptake by liver, for chylomicron to make VLDL and for IDL to make LDL send hep chol to tissue
role LDL
after VLDL used in tissue LPL, IDL comes back to liver. Hep tg lipase then adds hep chol to IDL to form LDL. So LDL transports hep cholesterol to tissues.
role IDL
after tg used out of VLDL comes back to liver to get reloaded with chol to take to tissues.
role HDL and where come from
reverse transport of cholesterol to liver. has apoC and apoE. secreted from both liver and intestine.
energy requiring steps of gluconeo
ATP for pyr carboxy, GTP for PEPCK
enzymatic steps different in gluconeo
1) pyr carboxylase (pyr to OAA) 2) PEPCK (OAA to PEP) 3) Fru1,6BP (Fru1,6P to Fru6P) 4) glu6P (glu6P to glu). 1,2 replace PK, 3 replaces PFK, 4 replaces GK
FA synthesis steps mito acetylcoA converted to citrate so enter cytosol.
acetylcoA + malonylcoA + 2NADPH each cycle, until desired length
how can glyceral (from TAG) enter gluconeo
via DHAP/G3P step
how is gluconeo turned on and glycolysis turned off
acetyl coA activates pyr carboxy and inactivates PDH (leading pyr to TCA). glucagon P turning off PK. glucagon also decreases Fru2,6BP which inhibits PFK and induce Fru1,6Phosphatase. low glucose inhibits GK. (levels ATP/NADH also influence)
phosphorylation states insulin v glucagon
glucagon put on P (via PK), insulin takes off P (via phosphorylase), so with glucagon enz-P, with insulin enz-noP
phosphorylation states of PFK2
when PFK2-deP kinase, when PFK2-P phosphatase
regulation and cofactors pyr carboxylase
requires biotin and ATP, activated by acetyl coA
relation of Fru2,6P to PFK activity?
PFK2 is a kinase when deP (insulin/meal) converting more Fru1P to Fru2,6P, activating PFK1 (increase glycolysis)
simple way to think of Fru2,6P as regulator?
fru2,6P hi when lot of reactant (fru1P)
way to remember irreversible enzymes in gluconeo
"Pathway produces fresh glu" Pyr carboxy, PEPCK, Fru1,6P, and Glu6P
what shuttle needed in gluconeo
Asp/Mal shuttle to get OAA out of mitochondria for PEPCK rxn
what substrates enter gluconeo
glucogenic aa, alanine, lactate (Cori cycle). GLUCOGENIC=Met, Thr, Val, Arg, His (+/-Ile, Phe, Trp either gluco or keto). KETO=Leu, Lys and acetoacetate.
where glu6phosphatase enzyme located
only liver and kidney, not muscle so muscle can only create glu6 which can't be exported (used glycolysis)
where malonyl coA from
product of acetylcoA carboxylase
3rd world-baby rapid onset tachycardia, vomit, convulsion
beri beri, defic B1 due to "polished rice"
in what clinical condition do you increase niacin, what does it do?
IIb combined hyperlipoproteinemia (where both VLDL and LDL are high)
inhibits lipolysis in tissue, decr TAG, decr VLDL which in turn decreases LDL (chol). NET: both TAG and chol decrease.
which of these vitamin defic unusual
biotin, pantothenate
when need supplement B6
secondary folate defic

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