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WVSOM - Biochem
Cholesterol and Bile Acid Synthesis
| Question | Answer |
|---|---|
| Cholesterol Synthesis Starting materials | Acetyl CoA NADPH ATP |
| HMG-CoA reductase | rate limiting step (target of drug therapy) |
| Products of cholesterol synthesis | Cholesterol NADP+ ADP |
| Location of Cholesterol synthesis | hepatocytes |
| regulated enzyme of cholesterol synthesis | HMG CoA reductase |
| Increasing levels of cholesterol __________ cholesterol synthesis | decreases |
| HMG CoA is active when | dephosphorylated |
| HMG CoA is dephosphorylated with ___________ insulin to glucagon levels. | high |
| HMG CoA is inactivated by ____________ and is then _____________ | Glucagon; phosphorylated |
| Most significant factor in regulation of cholesterol biosynthesis | decreasing HMG CoA reductase synthesis |
| Proteolysis of HMG CoA reductase increases as ____________ | sterol levels rise |
| Which drug class inhibits this enzyme | statins |
| Extrahepatic cholesterol synthesis | occurs under certain pathological conditions |
| Why is cholesterol esterified | regulation |
| where is cholesterol esterified | on lipoprotiens and in cells |
| How does esterification change regulation | cholesterol ester CANNOT regulate HMG CoA reductatse |
| Two enzymes that esterize cholesterol | LCAT (Lecithin) ACAT (acyl CoA) |
| LCAT | Esterifies cholesterol on lipoprotein that can be transferred from HDL to LDL |
| ACAT | esterifies cholesterol within the cell |
| Extrahepatic cholesterol synthesis | under certain pathological conditions |
| Where are cholesterol esterified/de-esterified in cells? | lipoproteins |
| Esterifcation of cholesterol | changes the properties of cholesterol especially with regard to its control functions |
| LCAT | Lecithin: chelesterol acyl transferase Esteerifies cholesterol on lipoproteins |
| What is transfered to LDL and HDL | Esterfied cholesterol |
| ACAT | esterfies cholesterol within the cell |
| Cholesterol esterase | reveses LCAT and ACAT esterification |
| Bile Salt Synthesis Location | hepatocytes |
| Starting compounds of Bile Salts | Cholesterol, ATP, NADPH |
| 4 conjugated bile salts | taurocholic glycocholic taurochenocholic glycohenocholic acids |
| Conjugation of bile salts increases ____________ | solubility |
| Solubility enables bile salts to act as | detergents |
| Conjugated bile salts composed of | primary bile salts, cholic acids and chenocholic ascid conjugated to taurine or glycine which are hydrophobic |
| How much bile salts are recycled | > 95% |
| Liver synthesis of bile acid _____ g/day | .2 - .6 |
| Amount of bile salts reabsorbed | 12-32 g/day |
| bile removed by feces | .2-.6 g/day |
| Why would we want to decrease bile salt reabsorption | drugs which bind to bile acids prevent their reabsorption to increase cholesterol excretion |
| Cholesterol esterase | reverses LCAT and ACAT by de-esterifying cholesterol |
| Bile Salt Exrection | in feces |
| Primary Bile Salts | chenocholic acid and chlic acid |
| Location of bile acid synthesis | hepatocytes |
| starting compounds of bile acid synthesis | cholesterol ATP NADPH |
| Controlled step of bile acid salts | products and substrate!!!! |
| Products of bile acid synthesis | cholic acid and chenocholic acids |
| Conjugated bile salts | primary bile salts bound to hydrophobic taurine or glycine |
| 4 conjugated bile salts | taurocholic glycocholic taurochenocholic glyochenocholic acids |
| Bile Salts recycled | > 95% 12-32 g/day |
| Why would we want to pharmachologically bind drugs to bile acids | to prevent reabsorption to increase cholesterol excretion |
Created by:
tjamrose
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