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Exam3Lec2Lipoproteins Flashcards

1
Q

Definition of lipoproteins

A

transportation form of hydrophobic substances such as lipids

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2
Q

Where are lipids derived from?

A

fatty acids

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3
Q

What are some examples of lipids?

A

fats, oils, waxes, steroids, sterols

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4
Q

What are the functions of lipids?

A
  • Energy source
  • Component of cell membranes,
  • Hormones (cell to cell communication),
  • Insulation for nerves
  • Protection and insulation for organs
  • Vitamin A,D,E, K are lipid soluble
  • Buoyancy
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5
Q

Why do lipids present a special challenge?

A

lipids are hydrophobic

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6
Q

How does the body transport lipids: cholesterol and triglycerides

A

they are transposrted inside a lipoprotiens

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7
Q

What is the composition of a lipoprotein particle?

A

core: contains non polar lipids( tri glycerols and cholesterol esters)
outside: amphiphatic lipids (phosholipids heads and cholesterol)
**surface: apolipoprotiens

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8
Q

The higher the diameter of the lipoprotein, the___ density

A

lower

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9
Q

What is the order of lipoproteins from lowest to highest density?

A

Chylomicrons, VLDL, IDL, LDL, HDL, Fatty acids and Albumin

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10
Q

Chylomicron is made of

A

cholesterol:3%
phospholipid: 5%
triacylglycerol: 90%

largest diameter
Most amount triacyglycerol

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11
Q

VLDL is made of

A

cholesterol:10%
phospholipid: 10%
triacylglycerol: 70%

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12
Q

LDL is made of

A

cholesterol:26%
phospholipid:15%
triacylglycerol: 10%

most amt of cholesterol

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13
Q

HDL is made of

A

cholesterol:20%
phospholipid: 25%
triacylglycerol: 5%

smallest diameter

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14
Q

What are apoproteins?

A

on surface of lipoproteins to provide structure and function by indentifying receptors on cells its looking to bind to

They recognize receptors on organs so type of apo is essential for lipoprotein fxn and where it transports.

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15
Q

What is the fxn of apoprotein?

A
  1. solubility and structural integrity
  2. receptor-binding and targeting
  3. Enzyme activation
  4. Exchange
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16
Q

What is ApoA-1?

A

unique to HDL-Structural and enzyme activator (activates LCAT)

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17
Q

What is ApoB?

A

unique to non HDL particles-Structural and ligand for receptor binding

18
Q

What are the major lipoproteins for Apo B-100

A

VLDL, IDL, LDL

19
Q

What are the major lipoproteins for Apo B-48

A

chylomicrons, remnant

20
Q

Explain ApoB mRNA editing.

A

ApoB-48: Cytidine Deaminase Editing complex converts CAA to UAA and makes it a stop codon. Then gets translated into ApoB48 In the INTESTINES.

ApoB-100: no modifications in the liver

no modification in the liver, because it does not have the cytidine deaminase enzyme

21
Q

As a result of RNA editing, where is ApoB-48 and ApoB-100 expressed?

editing ONLY, not splicing, mutation, division, etc.

A

ApoB-48 is expressed only in the intestinal cells and is requored for the receptor to uptake chylomicron remnant in liver

ApoB-100 is expressed only in the liver and is required for LDL uptake by Liver

22
Q

After the small intestine, chylomicron has what ratio of TG to Chol and what two steps can occur.

A

10:1
(a) They can be given up as FFA to tissues
(b) Can be converterted to the Chylomicron remnant (1:1:) by LPL

23
Q

What is LPL?

A

Lipprotein lipase: enzyme required to hydrolyze chlyomicrons and VLDL to free fatty acids (FFA) and 1,2-diacylglycerols (DAG)

24
Q

What is the LPL reaction?

A

Tracylglycerol to 1,2 diacylglycerol + fatty acid

LPL hydrolyzes TG

LPL is located in adipocytes, striated muscles, pancreatic islets, macrophages

25
Overview of chylomicrons Synthesis location Secretion location Contains apoprotein Function
1. Synthesis location: small intestines in fed state 2. Secretion location: Lymph vessels to blood vessels 3. Contains apoprotein: ApoB 48 4. Function: deliver TAG to body cells to be used as fuel
26
VLDL LCAT reaction ## Footnote Lecithin-cholesterol acyltransferase
Esterifies cholesterol so that it can be easily transported cholesterol + lecithin turns into cholesterol ester and lysolecithin by LCAT ## Footnote Adds more cholesterol
27
VLDL ACAT reaction
uses acyl-coA to add acyl group to cholesterol in liver cholesterol + acyl-coA turns to cholesterol ester by ACAT | ACAT is only in liver ## Footnote `
28
Overview of VLDL Synthesis location Secretion location Primary component Contains: apoproteins Fxn
Synthesis location: liver Secretion location: bloodstream Primary component: rich in TG Contains: apoproteins ApoB-100 Fxn: deliver TAG to body cells
29
Overview of LDL synthesis location Function | low density lipoproteins
Synthesis location: liver as VLDL and uses LPL to release all FFA and convert cholesterol to cholesterol esters using LCAT Secretion location: bloodstream Primary component: cholesterol Apoprotein: none Function: deliver cholesterol to all body cells
30
Explain HDL reverse cholesterol transport
removes cholesterol from extra-hepatic tissues (aka body) 1. HDL removes free cholesterol from tissue and transports it to liver for excretion 2. Liver disposes cholesterol as bile acids and free cholesterol 3. HDL is called "good cholesterol" ## Footnote HDL to VLDL by CETP. VLDL to Remants of VLDL by LPL. Remnants of VLDL to liver
31
What is CETP (cholesterol ester transfer protein)
Transfers HDL to VLDL for uptake by the liver nore that there are differences of ratio betweem triaglycerols and cholesterol ester. And trasnfers can occur.
32
Overview of HDL Synthesis location: Secretion location: Primary component: Contains: Fxn:
Synthesis location: liver and intestines Secretion location: bloodstream Primary component: cholesterol Contains: apo-A1 Fxn: remove cholesterol from body and deliver to liver "good" form of cholesterol (reverse cholesterol transport). ## Footnote There is potential to help reverse heart disease
33
What is the general pathway of cholesterol uptake?
1. LDL binding 2. Internalization 3. Lysosomal hydrolysis (chol released) 4. Regulatory actions
34
Cholesterol is taken up via LDL receptors. What regulatory actions can occur?
1. DOWN regulation of HMG CoA reductase: do not need to make more chol. because we just received cholesterol from diet. (this makes chol) 2. UPregualation of ACAT: meed to store all the cholesterol we just absorbed (acat makes chol. esters) 3. DOWNregulation of LDL receptors: do not need to take in more cholesterol
35
Organs and pathways involved in plasma lipoprotein metabolism
Sources: HEPATOCYTES making VLDL, HDL, and LDL are in the liver. INTESTINE from dietary uptake : Chylomicron is in the Intestine Sources goes to Lipoprotein transport particle where we see different conversion which then goes to target organs Target organs: Peripheral (nonhepatic) cell, macrophage, muscle cell, adipocyte
36
Triglyceride and Cholesterol has a protein component: Apolipoproteins. What are the 4 functions
1. Solubility, structual integrity 2. receptor binding-targeting 3. enzyme activation 4. exchange
37
Hyperlipidemia/Hyperlipoproteinemia can lead to what
Increaed risk of atherosclerosis and cardiovascular diseases
38
What is familial Hypercholesterolemia
genetics: mutation in LDL receptor gene (you lack LDL receptors so there is decr degradation of LDL) Metabolic characterisitcs: high LDL and plasma cholesterol lvls Physical characteristics: orange-yellow xanthomas (large amt of LDL accumaulation w/chol bc of no receptor) note: Liver does not recognize body has too much cholesterol which leads to no down-regulation of HMG CoA reductase, so you keep making chol.
39
Cholesterol is found in what type of food?
ANIMAL FOOD ONLY (eggs, red meat, milk, cheese, etc) ## Footnote does NOT come from fruits, vegetables, grains, etc
40
What atherosclerosis?
Plaque formation within endothelial lining of arteries causing blockages in blood flow
41
What is the LDL hypothesis for Atherosclerosis?
1. Elevated lvls of LDL cholesterol and apoB100 directly contribute to atherosclerosis 2. Oxygen radicals in endothelial lining of the arteries oxidize LDL and retain them 3. Activated endothelial cells have increased inflammation (macrophages are attached to it) 4. Macrophages take up LDL and are saturated with cholesterol thus forming foam cells 5. Hemmorage/tissue damage from plaque micro vessels

Biochem (17 decks)

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