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  1. Respiration
    Energy from carbohydrates, lipids, or proteins to turn ADP+Pi into ATP
  2. ATP per gram of tissue
    The kidneys win with skeletal muscle (running) as a close second, then the heart
  3. Function of glycolysis
    • Glucose to pyruvate
    • All cells do this
    • Generates 2 ATP and 2 NADH per glucose
    • Aeorbic or anaerobic
    • Makes precursors for other pathways
    • Occurs in cytosol
  4. Glucose into the cell
    • Diet and glycogen, a branched chain of glucose with two types of links
    • Sodium glucose symport in and a sodium potasium ATPase
  5. Glucose to ?
    • Glucose 6-phosphate
    • Hexokinase I -Glucose 6 Phosphate +Pi (located on surface of mitochondria in cytosol)
    • Glucokinase (hexokinase IV) no inhibition (located in cytosol in liver and beta cells of the pancreas)
    • Hexokinase II and III are used in glycogen synthesis and pentose phosphate -glucose 6 phosphate -Pi
  6. Fructose 6 phosphate to ?
    • Fructose 1,6 bisphosphate
    • Phosphofructokinase 1 +AMP +Fructose 2,6 bisphosphate -ATP -citrate (citrate is related to insulin glucagon ratio)(also ATP is substrate though so does both)(PFK2 makes fructose 6 phosphate into fructose 2,6 bisphosphate in excess f6p)
  7. PEP to ?
    • Pyruvate and ATP
    • Pyruvate kinase +Fructose 1,6 bisphosphate -ATP (this means work faster because I've got a lot of f1,6bp)
  8. Fructose metabolism
    Breakdown via fructose 1 phosphate to glyceraldehyde 3 phosphate, so it skips the citrate (insulin regulated steps)
  9. Galactose metabolism
    Goes through a UDP galactose to be converted to UDP glucose (higher energy) to glucose 1 phosphate to glucose 6 phosphate
  10. Polyol pathway
    Reduces sugars like glucose and galactose to sorbitol and galactitol to oxidize NADPH to NADP
  11. Anaerobic glycolysis
    Pyruvate to lactate to make 2 NAD
  12. Fatty acid transport
    Fatty acyl CoA synthesized in cytosol ATP to AMP+PPi, then transfered by carnitine palmitoyl transferase I (CPTI) -malonyl CoA to the intermembrane space where it becomes fatty acylcarnitine which is shuttled into the matrix and the CoA is added back on by carnitine palmitoyl transferase II
  13. Beta oxidation steps
    oxidation, hydration, oxidation, cleavage to shorten it by 2 carbons and make an acetyl CoA for the TCA cycle -NADH -FADH2 (sensitive to electron transport chain which is -ATP -ADP)
  14. Odd chain fatty acid oxidation
    At last 3 carbons it adds a CO2 using biotin and makes succinyl CoA
  15. Unsaturated fatty acid oxidation
    Only trans (cis must be transed which moves the bond)
  16. Very long chain fatty acid oxidation
    In peroxysomes and generates H2O2 from FADH2 generated until it is about 8C. Acetyl CoA still goes to matrix
  17. Branched fatty acid oxidation
    In peroxysomes by alpha oxidation (one carbon shortening)
  18. Omega oxidation
    When beta oxidation is insufficient this takes over in the cytosol. It makes dicarboxylic nose
  19. Ketone body oxidation
    • Makes 2 acetyl CoA and 1 NADH. Uses succinyl CoA at one step
    • In the liver and other tissue
  20. Pyruvate to ?
    • Acetyl CoA by pruvate dehydrogenase +NAD +CoASH -Acetyl CoA -NADH. Pyruvate dehydrogenase is dephosphorylated to be activated +Ca2+ and phosphorylated to inactivate +Acetyl CoA +NADH -ADP -Pyruvate
    • Reaction is called oxidative decarboxylation
  21. Concentrations in TCA
    Citrate is high then isocitrate and alpha ketoglutarate are rapid and low. Oxaloacetate is also low
  22. TCA regulation
    • Acetyl CoA to citrate by citrate synthase -citrate
    • Isocitrate to alpha ketoglutarate -NADH +ADP +Ca
    • Alpha ketoglutarate to succinyl CoA -NADH +Ca
    • Malate to oxaloacetate -NADH
    • These are all the steps that produce NADH
  23. Alcohol metabolism
    • Ethanol goes to Acetyl CoA via oxidation steps making 2 NADH and ATP to AMP+PPi
    • Disulfiram blocks this to cause acetylaldehyde buildup to cause getting sick and flushing
    • A different enzyme on ER surface in cytosol can do this too which reduces O2 to water and NADPH to NADP
  24. Outer membrane of mitochondria
    VDAC (voltage gated) beta barrel lets in a lot so its more permeable
  25. Inner membrane permeability
    Less permeable, uses ANT
  26. Electron transport complexes
    • Ubiquinone aka CoQ transfers electrons from NADH dehydrogenase (complex I) to cytochrome c reductase (complex III) and cytochrome c transfers electrons from cytochrome c reductase (complex III) to cytochrome c oxidase (complex IV)
    • Succinate dehydrogenase (complex II) takes succinate to fumarate (technically makes FADH2) and transfers via ubiquinone (CoQ) to cytochrome c reductase (complex III)
    • Redox potential increases across chain
    • Each pumps a proton across membrane except for succinate dehydrogenase which is not transmembrane
  27. Getting NADH into mitochondria
    • Glycerol 3 phosphate shuttle produces FADH2 by conversion to dihydroxyacetone P
    • Malate-Aspartate shuttle produces NADH
    • Malate shuttled (antiport with alpha ketoglutarate) and converted to oxaloacetate (NADH production)
    • OAA transaminated with glutamate to make alpha ketoglutarate and aspartate (aspartate and glutamate antiport)
    • This happens in matrix and cytosol
  28. Proton motive force
    • electrochemical and pH driven
    • drives ATPsynthase (which is bidirectional)
    • Can be used to get things like ATP ADP phosphate pyruvate out or in
    • Causes calcium sink due to negative voltage in matrix
  29. Uncoupling
    • Allows protons other way to cross back into matrix
    • Drugs UCP and 2,4-dinitrophenol and brown fat can do this (weight loss!)
  30. Mitochondria and apoptosis
    Mitochondrial permeability transition pore where VDAC and ANT align and ATP and ADP and Ca and Ros all get out
  31. Erythrocyte shunt
    • NADH is used to reduce cytochrom b5 to reduce hemoglobin
    • 1,3 bisphosphoglycerate to 2,3bpg to regulate O2 curve and back to 3 phosphoglycerate
  32. Pentose phosphate pathway
    • This leads to nucleotide synthesis and uses NADP and loses CO2 to make ribose 5 phosphate, which can also go to fructose 6 phosphate if you don't need to make nucleotides
    • Or you can make more NADPH by taking ribulose 5 phosphate to glyceraldehyde 3 P (non oxidative!)
  33. NADPH uses
    • reduce hydrogen peroxide (and oxygen radicals)
    • fatty acid synthesis
    • amination (not transam!) of alphaketoglutarate to glutamate via glutamate dehydrogenase (this is backwards of entering urea cycle)
    • Rereduction of BH2 to BH4 for phenylalanine to tyrosine
    • Rereduction of thioredoxin for ribose to deoxyribose
    • Rereduction of dihydrofolate to tetrahydrofolate
  34. Additional ways of getting TCA intermediates
    • branched amino acids and odd chain fatty acids to propinyl CoA to succinyl CoA
    • Many amino acids and fatty acids and carbohydrates produce
    • Other amino acids can go to glutamate to alpha ketoglutarate or fumarate or aspartate to oxaloacetate
  35. Fatty acid synthesis initiation (prework)
    • Acetyl CoA to citrate in the mitochondria because it cannot cross
    • Citrate in cytosol needs ATP to go to OAA and Acetyl CoA for fatty acid, which goes to malate (NADH to NAD) then malate makes NADPH and loses CO2 to make pyruvate
    • Pyruvate can go straight to OAA by pyruvate carboxylase using biotin (adds CO2) +Acetyl CoA (this is how you regulate to keep OAA levels high)
  36. Fatty acid synthesis
    • Acetyl CoA bind to fatty acid synthase to make omega carbon
    • Acetyl CoA to Malonyl CoA using CO2 and biotin and ATP for addition of all carbons. To malonyl is via acetyl CoA carboxylase, which can be inactivatingly phophorylated +low energy levels or phosphatased to activate +insulin
    • Fatty acid synthase is a dimer that helps the other one and do two at once
    • CO2 loss, reduction, dehydration, reduction (uses NADPH)
    • Elongation beyond 16C uses different enzymes but its the same steps
    • Cytochrome b5 is oxidized to reduce to double bonds, but the reducing power ultimately comes from NADH
  37. Ketone body synthesis
    2 Acetyl CoA for start and makes acetoacetate, which can oxidize NADH to make hydroxybutarate or lose CO2 to become acetone
  38. Triacylglyceride synthesis
    • In liver ATP is used to get glycerol to glycerol 3 phosphate
    • In liver and adipose NADH is used to get glucose to glycerol 3 phosphate
    • 2 fatty acids link with dehydrated one typically at C2, removal of phosphate allows for third fatty acid
  39. Glycerophospholipid synthesis
    Use CTP to bind as CDP to either the head or the diacylglycerol for high energy transfer of head group
  40. Cholesterol biosynthesis
    • Starts with 3 acetyl CoA through steps to mevalonate -Statins
    • Goes through isopentyl PP (used in many other pathways)
    • Aminobisphosphonates can block
    • FTIs and GGTIs can block farnesyl transferase out of pathway (makes lamins and Ras) and geranylgeranyl transferase out of pathway (makes Rab and Rho)
  41. Gluconeogenesis overview
    • In liver
    • Same points are regulated
  42. Gluconeogenesis (getting PEP)
    • Pyruvate to PEP does not happen directly, rather malate or aspartate leave mitochondria and are converted to OAA through oxidation or transamination and OAA loses CO2 and takes GTP to get PEP
    • There isn't glycolysis happening so the carbons (pyruvate) come from amino acid break down
    • NADH inhibits pyruvate decarboxylase
  43. Gluconeogenesis (non reversible steps)
    • Steps involving phosphorylation/dephosphorylation
    • Use fructose 1,6 bisphosphatase -F2,6bp
    • Use glucose 6 phosphatase (somehow regulated)
  44. Glutamate to urea cycle
    • alpha ketoglutarate takes amine groups from amino acids to become glutamate, requires B6 (PLP, pyridoxal phosphate) and only lyseine, threonine, proline and hydroxyproline can't do this
    • Glutamate can give up NH4 via glutamate dehydrogenase to enter urea cycle
    • Glutamate can transaminate with OAA to form aspartate which can enter urea cycle via AST
    • ALT can turn alanaine and alpha ketoglutarate to pyruvate and glutamate
  45. Amines from peripheral to liver for urea cycle
    • In muscle ALT uses glutamate and pyruvate to make alpha ketoglutarate and alanine which can go to liver and use ALT to regenerate glutamate to urea cycle
    • In other peripheral tissue GDH generates glutamate from alpha ketoglutarate. Glutamate to glutamine requires ATP, and glutamine goes to liver where NH4 are directly removed
  46. Carbonium and NH4 to ?
    • Carbamoyl phosphate requires 2 ATP to 2 ADP (in matrix)
    • Carbamoyl phosphate synthetase I +N acetyl glutamate (from glutamate+acetyl CoA via ? +arginine)
  47. Proton motive force in urea cycle
    • Citruline ornithine transfer requires it
    • ornithine binds to carbamoyl phosphate to produce citruline
  48. Arginine to ?
    • Urea and ornithine
    • Arginine is an amino acid so this is sensitive to free amino acid levels
    • Arginine can also enter matrix to encourage formation of N acetyl glutamate
  49. Uses of glutamine
    • Transfers 2 amines to liver
    • Can transfer NH4 to kidneys to buffer
    • Used in brain to donate NH4 to purine and the resulting glutamate is a neurotransmitter and can be modified to make other nuerotransmitters
  50. Non-essential amino acids
    Asparagine, aspartate, alanine, arginine, glycine, glutamate, glutamine, serine, cysteine, proline, tyrosine
  51. Glycolysis to amino acids
    • pyruvate to alanine
    • 3 phosphoglycerate to serine (serine to glycine or cysteine)
  52. Cysteine synthesis
    (methionine to homocysteine) homocysteine and serine join via cystathione synthase -PLP (B6) to make cystathione which becomes alpha ketobutarate to propinyl CoA to TCA and cysteine
  53. Glutamate related amino acids
    • Glutamine, histidine, proline, arginine
    • Thus all can "enter" at alpha ketoglutarate
  54. Ketogenic amino acids
    All are ketogenic through acetyl CoA and tyrosine (so phenylalanine too) goes directly to acetoacetate, which leucine can also do but leucine has the option of going to acetyl CoA too
  55. Phenylalanine to tyrosine
    • Various breakdown points for different diseases
    • Uses tetrabiopterin BH4 which is recycled (reduced) by NADPH
  56. Purine production
    • Start with ribose 5 phosphate
    • Build base onto sugar with C and N coming from glycine, CO2, aspartate, glutamine and methyl and formyl FH4, resulting in IMP
    • IMP to AMP via aspartate donating NH4 using GTP
    • IMP to GMP via glutamine donating NH4 using ATP
    • AMP ADP ATP GMP GDP and GTP (all purine nucleotides)regulate at various points
  57. Purine degradation
    To uric acid, which can build up and cause gout so you stop this from happening with allopurinol
  58. Purine salvage
    • IMP and GMP can go to inosine and guanosine through dephosphorylation and then be lose the ribose to form hypoxanthine and guanine which can be reattached to PRPP to make IMP and GMP
    • AMP skips the step of going all the way back to a naked base. Once the phosphate is removed you can add it back on using ATP to ADP
    • Making AMP using ATP seems dumb but in skeletal muscle under intense excercise, AMP to IMP can join up with aspartate to form fumarate eventually to the TCA cycle for more energy and AMP is popped back out when it makes fumarate!
  59. Pyrimidine production
    • Uses glutamine and CO2 and aspartate (2ATP!) to build orotate, a free base that can attach to PRPP, which goes to UMP to UDP
    • UDP can go to UTP which can become CTP (to dCTP via CDP)or can go to dUMP (can get from dCDP via dCMP too) to make dTMP to dTTP of course
    • Regulation occurs at same steps by TDP CTP UTP and purine nucleotides downregulating but PRPP upregulating orotate formation
  60. Pyrimidine degradation
    To succinyl CoA to TCA to free amines and CO2 eventually
  61. Pyrimidine salvage
    • Free uracil and cytosine bases ban bind to ribose 1 phosphate
    • Free thymine bases can bind to deoxyribose 1 phosphate
  62. Ribose to deoxyribose
    • Requires NDP (that is any base on a ribose with two phosphates)
    • uses thioredoxin which is rereduced by NADPH
  63. One carbon pool donors
    Serine, glycine, histidine formaldehyde and formate doante a one carbon to FH4 (tetrahydrofolate) to make formyl methylene or methyl tetrahydroformate, which can be used for a variety of products
  64. Uses of tetrahydrofolate with 1C
    • dUMP to dTMP (can be blocked by 5-fluorouacil or methotrexate
    • addition of CH3 to B12
  65. B12 reactions
    • Homocysteine to methionine
    • Methylmalonyl CoA to succinyl CoA
  66. SAM
    • Methionine (made from homocysteine by B12) and ATP make S-adenosyl methionine (active methionine)
    • SAM is pretty much does every methylation that we haven't already said another enzyme does
    • After doing work it goes back eventually to homocysteine and must be made into methionine by B12 again
    • The methyl trap!
Card Set:
2014-09-25 07:02:52
foundations fnd1 biochem biochemistry tubberly

You can forget it all once the test if over
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