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77 Cards in this Set
- Front
- Back
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Cholesterol ring structure
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can not be broken down by humans
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Cholesterol can not be catabolized to
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CO2
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Cholesterol is a component of
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membranes
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Rate limiting step of drug therapy
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HMG-CoA reductase
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Cholesterol is starting material for
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Bile, Vitamin D synthesis, Steroids
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Cholesterol ester levels do not
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Alter the rate of cholesterol synthesis
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Proteolysis of HMG CoA reductase increases as
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sterol levels rise
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high insulin:glucagon then HMG coA reductase is
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dephosphorylated and active, signals ATP and acetyl coA available for chol synthesis
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Statin
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inhibits HMG coA reductase
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Cholesterol is esterified/de-esterified on lipoproteins by
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LCAT or ACAT- esterifies cholesterol
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Cholesterol stored in cell for use later as
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cholesterol ester
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Esterified cholesterol can be trasnferred
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from HDL to IDL
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Bil acid synthesis takes place in
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hepatocytes
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Bile acid synthesis starts with
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cholesterol, ATP and NADPH
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Bile acid synthesis regulation step
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7 alpha-hydroxycholesterol production from cholesterol is feedback inhibited by high bile salt level
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Products of bile acid synthesis
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primary bile salts: cholic acid and chenocholic acid
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Four different conjugated primary bile salts
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taurocholic, glycocholic, taurochenocholic and glycochenocholic acid
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Conjugation
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increases bile acid solubility allowing bile salts to be detergents
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Four secondary bile salts
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deoxycholic acid, lithocholic acid, deocychenocholic acid, and lithochenocholic acids made by bacterial action on 4 conjugate primary bile salts once in intestine
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Serum tryglyceride levels are proprotional to VLDL levels when
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fasting
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Chylomicrons
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transport dietary lipids
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What state do chylomicrons occur in?
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fed
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Are chylomicrons synthesized by liver?
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No only lipoprotein that isnt, making them the lightest (float)
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What do chylomicrons form
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Nascient chylomicrons by picking up dietary triglycerides and cholesterol
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HDL transfer what to nascent chylomicrons
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Apo E for hepatic receptors and Apo C11 activates liporprotein lipase
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Mature chylomicrons transport to adipose and skeletal muscle cells
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LPL ocnvert chylomicron trigylcerides to FFA and glycerol
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Apo C on chylomicrons activates
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LPL
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Insulin also activates LPL by
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inducing its synthesis
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Skeletal muscle prefers
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chylomicron triglycerides, lower Km for it than adipose lipoprotein lipase
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Chylomicron remnants
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enter liver and broken into component molecules
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Dietary cholesterol
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carried from intestine to liver on chylomicron remnants
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Dietary cholesterol results in down regulation of
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HMGCoA synthesis and increases proteolysis of it
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Dietary cholesterol unused goes to
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VLDLs + cholesterol made in liver
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VLDLs high
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tyrglyceride concentration makin them least dence of liver lipoproteins
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VLDL are made in
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liver
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VLDL deliver triglycerides to
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skeletal muscle and adipose tissue
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Donation of Apo C to VLDL for
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Lipoprotein lipase allows VLDL to break into fatty acids and glycerol
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VLDL become IDL when ____ are removed
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triglycerides
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2 fates of IDL
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to become LDL or return to the liver
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Cholesterol made in liver or delivered to liver by chylomicron remnants leave with
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VLDL exported out the liver
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Liporprotein lipase action on VLDL causes them to become
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more dense density more like an IDL
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IDL may return to
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liver
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IDL are recognized by
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LDL receptors, endocytosed and degraded in liver
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Triglyclerides removed from IDL
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increase their density and help them become LDLs
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Triglyceride removal occurs in and uses
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hepatic sinusoids and uses hepatic triglyceride lipase
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Cholesterol esters are transferred from HDL to IDL
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As the IDL becomes LDL
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Amount of IDL entering liver vs becoming LDL
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depends on hepatic LDL receptors which depends on amount of cholesterol in liver
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LDL deliver cholesterol to
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extra-hepatic cells
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acetyl coa comes from
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glucose, fatty acids, amino acids
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Almost all bile salts are
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reabsorbed
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Drugs decreasing bile salt reabsoprtion increase
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cholesterol excretion
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Specific uptake of LDL by extra-hepatic cells occurs by
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LDL receptors on surface of cell
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cholesterol ester (free cholesterol) leads to
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down regulation of genes for LDL receptor synthesis and HMG coA synthesis
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LRP proteins dont depends on
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amount of cholesterol cellular levels
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LRP help decrease
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serum levels of lipoproteins
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High hepatic cholesterol levels prevents IDL
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return to liver
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Excess LDL in serum can be oxidized by
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reactive oxygen species
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Antioxidants can decrease
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oxidative species
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genetically defective LDL receptors occurs=
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high serum LDL levels early in life
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HMGcoA is still expressed in LDL defected receptors
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Can't get into the cell so cholesterol levels still appear low
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with defected LDL receptors extra-hepatic cholesterol synthesis is
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turned on
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Specific uptake of LDL by extra-hepatic cells occurs by
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LDL receptors on surface of cell
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cholesterol ester (free cholesterol) leads to
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down regulation of genes for LDL receptor synthesis and HMG coA synthesis
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LRP proteins dont depends on
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amount of cholesterol cellular levels
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LRP help decrease
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serum levels of lipoproteins
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High hepatic cholesterol levels prevents IDL
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return to liver
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Excess LDL in serum can be oxidized by
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reactive oxygen species
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Antioxidants can decrease
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oxidative species
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genetically defective LDL receptors occurs=
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high serum LDL levels early in life
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HMGcoA is still expressed in LDL defected receptors
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Can't get into the cell so cholesterol levels still appear low
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with defected LDL receptors extra-hepatic cholesterol synthesis is
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turned on
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Increase in VLDL
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increase in IDL and LDL
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HDL pick up
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cholesterol from degrading membranes and esterify it w LCAT
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most hepatic uptake of HDL occurs via
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non-specific scavenger receptor SR-B1
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SR-B1 do not down regulate with
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high heaptic cholesterol levels
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limiting dietary cholesterol, trans fatty acids may lower
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LDLs
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Lp(a) found elevated
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post-MI
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