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30 Cards in this Set

  • Front
  • Back
in mammals, can cholesterol be degraded to CO2 and water?
what are the fates of the degradation products of colesterol?
excreted in modified form or converted into other compounds (ie. bile acids, steroid hormones)
where 'can' cholesterol synthesis occur? what are the major sites of this action?
most other tissues.
liver and intestine main sites.
what is the precursor of all carbons in cholesterol?
what are the two fates of HMG-CoA and where do the processes take place in the cells?
conversion to mevalonate for cholesterol synthesis in the Endoplasmic Reticulum or degredation to ketone bodies in the mitochondria.
what cofactor (and how many) is required for the commited step of cholesterol synthesis?
in what state is the body when cholesterol synthesis is active?
Fed state
what effects do increases glucagon levels during fasting have on HMG-CoA reductase? does this result in the activation of inactivation of the enzyme?
glucagon binding leads to the phospholylation of HMG-Coa reductase, subsequently inactivating the enzyme (therefore, no cholesterol synthesis)
what effects do increases insulin levels during the fed state have on HMG-CoA reductase? does this result in the activation of inactivation of the enzyme?
insulin inding leads to the dephosphorylation of the enzyme, subsequently activating it and the synthesis of cholesterol.
what effect do increased levels of cholesterol have on HMG-CoA reductase (be specific)?
theoretically, cholesterol reduces the transcription and translation of HMG-Coa reductase, ultamately inhibiting cholesterol snythesis
what class of pharmacudicals acts to inhibite HMG-CoA reductase?
what colesterol intermediate is a branch point for synthesizing molecules for many other functions? (ie, glycoproteins, membrane proteins...) (terrible question I know...)
What are the catagories of products that can arise from farnesylpyrophosphate? (5)
ubiquinones(oxidative phosphorylation), glycoproteins, farnesylated proteins, geranylgeranylated proteins. (only about 1/1000 mevalonate's do end up as these) the rest go to cholesterol...
in the stucture of glycerophospholipids, what position has the highest incidence of unsatturated fatty acids?>
the C-2 position
what is the major function of cholesterol esters?
storage form of cholesterol in cells.
in cells, esterification of cholesterol is catalyzed by what enzyme?
in the plasma, esterification of cholesterol is catalized by what enzyme? also, what phospholipid is involved in this reaction?
LCAT catalyzes the transfer af a fatty acid from the 2-C position of phosphatidylcholine (PC).
LCAT deficiency presents with low levels of ____ __ and ____ in the serum accompanied by increased serum ____ and _______. (good luck)
low cholesterol esters and lysolecithin (lyso PC).
high PC and free cholesterol.
what is the only organ capable of converting cholesterol to bile acids?
the liver.
what is the major mechanism by which the body eliminates cholesterol?
by conversion to bile acids.
what is the name of the microsomal mixed oxidase enzyme found in the liver that is involved in the synthesis of bile acids?
cytochrome P 450.
what is the rate limiting enzyme in bile acid synthesis? what promotes and inhibits its activity?
colesterol-7-alpha hydroxylase. cholesterol promotes, bile acids inhibit..
name the 4 primary bile acids.
taurocholic acid
glycochoic acid
taurochenodeoxycholic acid
glycochenodeoxycholic acid
what simple reaction prevents cholesterol reabsorption in the small intestine? what performs this action?
the reduction of the delta-5-C double bond...
bacteria perform this reaction.
what are the two cholesterols that are excreted?
coprosterol, cholestanol.
what is the overall function of bile salts? what are a few of the specific actions?
bile salts promote the effective absorption of fat soluble substances.
-accelerate the action of pancreatic lipase
-keep cholesterol in solution, promoting its secreation.-
-bile acid reabsorption stimulates intestinal motility and the secretion of more bile by the liver.
through what structure are bile salts reabsorbed and delivered to the liver?
the portal vein
the reabsorption of bile acids promotes and inhibits two different things, what are they?
promoted liver secretion of more bile acids.
inhibits the synthesis of more bile acids from cholesterol.
what effects does the administration of bile-acid resins have?
binds to the bile salts in the small intestine and promotes their secretion. this lowers the reabsorption of bile acids to the liver and promotes the synthesis of more of them from cholesterol, therefore, lowering cholesterol levels...
what effect can prolonged antibiotic teatments have on cholesterol levels?
cholesterol levels would increase do to less bacterial degredation by bacteria...