Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

69 Cards in this Set

  • Front
  • Back
How are cholesterol and cholesterol esters made soluble?
By lipoproteins
What are the 2 functions served by proteins in lipoproteins?
1. Solubilize lipids
2. Cell-targeting signals
Density/diameter of Chylomicron:
Richest in:
Density <1.006
Diameter 75-1200 nm
Rich in Triglyceride (85%)
*acquires C/E*
Density/diameter of VLDL:
Richest in:
Density 0.95 - 1.006
Diameter 30-80nm
Rich in Triglyceride (50%)
Density/diameter of IDL:
Density 1.006-1.0019
Diameter 25-35nm
Density/diameter of LDL:
Richest in:
Density 1.0019-1.063
Diameter 18-25 nm
Rich in Cholesteryl Ester
Apo B100
Density/diameter of HDL:
Richest in:
Density 1.063-1.210
Diameter 5-12 nm
Rich in Protein
Where are chylomicrons assembled? Released?
Assembly = intestine

Release = Enterocytes
What is the first step in chylomicron metabolism?
Hydrolysis by LPL (lipoprotein lipase) at extrahepatic tissue.
What tissues mainly have LPL?
Adipose and Skeletal muscle
What are the products of LPL hydrolysis of chylomicrons?
FFA + monoacylglycerol
What happens to the hydrolyzed products of chylomicron?
-FFA Storage (fat cells)
-FFA B-oxidation (muscle)
-Monoacylglycerol is sent to liver for gluconeogenesis.
Where exactly is LPL located?
How is it held in place?
On the endothelial surface of blood vessels in fat/muscle.
-Held in place by Heparan Sulfate proteoglycans.
What is necessary to activate LPL?
So how is it that chylomicrons can activate LPL?
They acquire Apo-CII and Apo-E from HDL remodeling.
How is LPL activated in adipose tissue? Under what conditions?
By INSULIN - in ANABOLIC condtns
What happens in step 2 of chylomicron metabolism (to the remnants of LPL hydrolysis)?
Residual triglycerides & dietary cholesterol delivered to liver.
How does the liver take up chylomicron remnants? (2 receptors)
-LDL receptor
-Hepatic lipase
What is required for LDL receptor uptake?
Apo-E (acquired from HDL remodeling)
(Apo-B100 works too, but not as high affinity as Apo-E)
What is required for Hepatic Lipase activity?
What happens after hepatic uptake of chylomicron remnnats?
Endocytosis in lysosomes; released cholesterol has 3 fates.
What are the 3 fates of cholesterol released in hepatocytes?
1. Form bile acids
2. Secreted into bile as such
3. Incorporate into nascent lipoproteins (HDL)
How are both LPL and Hepatic lipase bound to cell membranes?
By Heparan Sulfate Proteoglycans.
Why are VLDLs made?
When triglycerides are in excess VLDLs provide a way to export them from the liver.
So VLDLs are made and secreted from?
What causes excess triglyceride? (3 things)
1. Lipogenesis
2. Plasma FFA
3. Chylomicron remnants taken up by LDL/Hepatic Lipase
What does VLDL metabolism consist of?
Basically same as Chylomicrons
Step 1: Apo-CII activates LPL; releases FFA to tissues
Step 2: VLDL remnant taken up by liver LDL receptor.
What is the VLDL remnant called?
What happens to IDL after hepatic endocytosis into lysosomes?
It goes to the 3 fates of released cholesterol.
What happens to IDL if it bumps into hepatic lipase?
Hepatic Lipase binds and removes Apo-E, which results in LDL
What 2 things does Heparan Sulfate bind?
-IDL (vldl remnant)
Does this principally
-Chylomicron remnant
What 2 things can LDL do?
1. Bind LDL receptor (but low affinity b/c only has Apo-B100
2. Go to peripheral tissues
What does LDL do at peripheral tissues?
Binds the LDL receptor and gets endocytosed into lysosomes.
What is the purpose of LDL at peripheral tissues?
Regulation of de novo cholesterol synthesis
What is the consequence of LDL receptor having a much higher affinity for ApoE than ApoB100?
IDL (as ApoE) has a much shorter T1/2 than LDL (only ApoB100) and more gets taken up at liver.
What regulates whether LDL will be taken up by the liver of peripheral cells?
The amount available.
Where does HDL originate?
-Small intestine
What is the initial form of HDL described as? Why?
Nascent/discoidal - b/c it is mainly protein w/ little cholesterol or cholesteryl esters.
How does cholesterol get incorporated into HDL?
What is ABCA1?
ATP-Binding cassette transporter
How exactly does ABCA1 work?
It delivers cholesterol to Apo-A1
How is Mature HDL formed?
By the addition of cholesteryl esters to ApoA1 - done via LCAT.
What are the 2 functions of HDL?
1. Lipoprotein remodeling
2. Cholesterol transport to liver/cells for steroid hormone synthesis.
What 2 molecules on HDL are responsible for lipoprotein remodeling?
PLTP: phospholipid transfer protein
CETP: Cholesteryl ester transfer protein
What does PLTP do?
Transfers phospholipids and cholesterol INTO HDL.
What does CETP do?
Removes Cholesteryl esters FROM HDL.
What molecule allows uptake of HDL by liver/adrenal gland for steroid hormone synthesis?
SR-B1 - scavenger receptor b1
What is the main purpose of LCAT?
Synthesis of cholesteryl esters from free cholesterol in plasma lipoproteins.
Where is LCAT made?
Liver cells
Where does LCAT act?
In circulation (blood) on HDL.
What is the mechanism of LCAT?
Transfers a fatty acyl residue from lecithin (phosphatidyl choline) to free cholesterol.
What are the 2 products of the LCAT reaction?
Cholesteryl Ester
Why does LCAT have a high preference for HDL?
B/c it is activated by ApoA1 which is only on HDL.
What are the steps in HDL circulation?
1. Apo A1 (depleted HDL) picks up C from periph. cells
2. Nascent HDL picks up CE from circulation via LCAT
3. Mature HDL binds SRB1 on liver/adrenals to make steroid hormones. Depleted HDL recycles
Is there a normal ref range for lipids in people?
No; widely varies.
What is the most important disorder of plasma lipoproteins?
LDL receptor disorder
What is LDLreceptor deficiency called, and what results?
Familial hypercholesterolemia - can't take up cholesterol from IDL/LDL via the LDL receptor.
List 3 Clinical characteristics of Famlial hypercholesterolemia:
1. High plasma LDL levels
2. LDL-derived cholesterol deposts in tendons/skin/arteries
3. Autosomal dominant
What genetic effect results from FH being autosomal dominant?
Dosage - homozygotes get it worse than heterozygotes.
Occurence of FH-heterozygotes?
1/500 - most common inborn error of metabolism!!
Occurence of FH-homozygotes?
1/1 million
Who is at higher risk of having coronary heart symptoms - m/w?
Men - women have protective effects via estrogen
What is an Atheroma?
Atherosclerosis in coronary arteries
What is Atheromas characterized by?
1. Accumulated Cholesteryl esters in foam cells
2. Smooth muscle proliferation
3. Fibrosis
Why is LDL receptor deficiency so bad?
B/c it is the main way that nonhepatic cells obtain cholesterol for membranes.
How do cells get cholesterol via LDL?
By receptor-mediated endocytosis
What component of LDL does the LDL receptor bind?
Apo B100
What 3 things does oversupply of cholesterol in nonhepatic cells result in?
1. Inhibited HMG-CoA reductase
2. ACAT activation
3. Inhibited synthesis of LDL receptor.
What happens to cholesterol if it accumulates in a nonhepatic cell?
-ACAT esterifies it w/ long chain FA
-Stored as cholesteryl ester droplets