biochem mini 3

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sweetlu
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114917
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biochem mini 3
Updated:
2011-12-04 15:45:51
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BIOCHEM MINI
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biochem mini 3
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  1. LCAT
    • - only in plasma
    • -esterifies free dietary cholesterol
  2. ACAT 1
    • - steroid producing tissues and phagocytes
    • - esterifies dietary colesterol
  3. ACAT 2
    • - liver
    • - esterifies dietary cholesterol
  4. rate limiters in cholesterol synthesis
    • - HMG CoA reductase (inhibited by statins)
    • - Mevalonate- rate limiting substrate
  5. SREBP
    • "sterol regulatory element binding protein"
    • -initiates HMG CoA reductase synthesis
    • - controlled on gene expression level
    • - activated what cholesterol levels are low inside cell
  6. apo A-1
    • -major protein of HDL
    • - activates LCAT
    • -HDL and chylomicrons
  7. apo B-48
    • - chylomicrons only
    • - lack LDLr binding domain
  8. apo B-100
    • - only protein of LDL
    • - ligand for LDLr
    • - VLDL, IDL and LDL
  9. apo C-2
    • -activates lipoprotein lipase
    • - not on LDL
  10. apo C-3
    • - lipoprotein lipase inhibitor
    • - not on LDL
  11. CETP
    • - HDL only
    • - cholesterol ester transfer (say to VLDL in LDL syn)
  12. apo E
    • - binds to B/E receptors on hepatocytes
    • - 3 alleles, E3 most common
    • - E2/E2 is seen in HLP 3
    • - (E4/E4) associated with alzheimers (amyloid deposits)
  13. apo (a)
    • - extremely atherogenic
    • - forms complex with LDL
    • - resembles plasminogen and slows blood clot b/d
  14. chylomicron synthesis
    • - intestinal mucosa
    • - acquires apo C-2 and apo E from HDL
  15. VLDL synthesis
    • - liver
    • - trigs are transferred from VLDL to HDL in exchange for cholesterol esters (via CETP) resulting in the formation of LDL
  16. Type 1 HLP
    • - LPL or apo C-2 defeciency
    • - strawberry milkshake blood
    • - increased chylomicrons, huge increased trigs
    • - turbid retinal vessels,red eruptive xanthomas
    • -Tx- low fat, high CHO diet
  17. familial hypercholesteremia
    • - Type 2a HLP, autosomal dominant
    • - LDLr defect
    • - reduced LDL clearance=> increased LDL
    • -CAD and plaques, xanthalasmas(eye), increased chol synthesis
    • - achilles tendon xanthalomas, arcus senilis (grey ring eye)
    • - homozygous Tx- liver transplant
    • hetero Tx- statin therapy
  18. Type 2b HLP
    • - increased LDL, delayed VLDL clearance
    • - strongly associated with CAD
  19. Type 3 HLP
    • - apo E2 homozygous
    • - xanthomas (increased trigs via increased chylomicrons)
    • - CAD/ plaques
  20. Type 4 HLP
    • - elevated VLDL production
    • - associated with metabolic syndrome(insulin resistance), EtOH consumption
  21. Wolmans disease
    • - defect in lysosomal cholesterol esther hydrolase
    • - reduced LDL clearance
  22. fibrates
    increase lipoprotein lipase activity
  23. resins
    bind bile acids in the intestine
  24. niacin
    inhibits FA release from adipose tissue
  25. statins
    HMG CoA reductase inhibitor
  26. lipoprotein lipase
    hydrolyzes FA from the chylomicrons into adipocytes
  27. isocitrate DH
    • - commited step of TCA (most important ez)
    • - isocitrate--> alpha KG
    • -first CO2 released, NADH produced
    • - downregulated by NADH and ATP
  28. PDH
    • - pyruvate--> AcCoA
    • - E1- inactivated by phosphorylation (T)
    • - E2- inactivated by Ar (L,C)
    • - E3- makes NADH (F,N)
  29. aconitase
    • - cis-aconitase--> isocitrate
    • - inhibited by fluorocitrate
  30. alpha KG DH
    • -alpha KG--> succinyl CoA
    • -TLCFN
    • -succinyl CoA feedback inhibits
    • - # ez complex, NOT controlled by phosphorylation
    • - NADH inhibits
  31. succinyl CoA sythetase
    • succinyl CoA---> succinate
    • - substrate level phosphorylation
  32. citrate synthase
    • - AcCoA+ozaloacetate-->citrate
    • -irreversible
    • - citrate can then down regulate PFK-1 except in the liver
    • - ATP and NADH inhibit
  33. glycerol phosphate shuttle
    • - high activity in brain
    • - NADH shuttles into Mt matrix via FADH2
  34. malate aspartate shuttle
    - high activity in liver and heart
  35. complex 1 inhibitors
    • -block e- flow from NADH to CoQ
    • - rotenone
    • - barbituates (amytal)
    • - demerol
  36. complex 3 inhibitors
    Antimycin A
  37. complex 4 inhibitors
    • Cn, CO, H2S and azide
    • - keeps Fe in 3+ state (prevents reduction, thus stopping e- flow)
  38. uncoupling agents
    • - 2,4 DNP, pentacholrophenol, high dose ASA, thermogenin
    • -stimulate ETC, but bypass ATP synthetase
    • - cause hyperthermia because all E is given off as heat instead of 50% used for ATP prod. and 50% to heat
  39. oligomycin
    ATP sythase inhibitor

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