mainly tracylglycerols

phospholipids

cholesterol

• core lipids- endogenous CE
• apoproteins- A, C, D, E
• mechanism of lipid delivery (apoprotein moved from one particle to another)
  • transfer CE to IDL and LDL
  • recycle excess in liver

• major core lipids- endogenous triacylglycerides
• apoproteins- B100, C, E
• mech. of delivery
  • hydrolysis by lipoprotein lipase

• major core lipids- cholesterol esters
• apoproteins- B100
• mechanism of lipid delivery
  • receptor mediated endocytosis by liver and other tissues

• major core lipids- endogenous CE
• apoprotein- B100, E
• mech. of delivery
  • receptor mediated endocytosis by liver
  • conversion to LDL

• origin- intestines, liver
• lipoprotein- HDL
• function
  • activate LCAT
  • ABCA1 dock (activates its ATP binding cassette, which is a cholesterol pump)

• origin
  • B100- liver
  • B48- intestines
• apoprotein
  • B100- VLDL/LDL
  • B48- CM
• function
  • B100- bind LDL, scaffold
  • B48- scaffold, diet fat transport

• origin- liver, intestines
• lipoprotein- HDL
• function- inhibit LCAT

• origin- liver
• lipoprotein- CM, HDL
• function- activate LCAT, C transport

• origin- liver
• lipprotein- CM, VLDL, HDL
• function
  • C2- activate lipoprotein lipase
  • C3- inactivate lipoprotein lipase

• cleaves off Fatty acid chains that act as soaps
• end with mix of triacylglycerides, fatty esters, monoacylglycerides

• intestines has cytosine deaminase that convert C to U
• this causes CAA to go to UAA (STOP codon)
• causes functional change so it can deliver fat to cells
  • liver uses apopB100 to make membrane building material (lipid traffficking of building material)

• binds to Asp residues on VLDL/LDL receptors
• if you eliminate Lys, it cant bind with receptors

1. dietary fats diffuse into intestinal epithelium
2. form chylomicron
3. go into lymphatic system
4. begin talking with HDL allowing them to pick up specific apoproteins
5. bind to lipoprotein lipase in adipose and muscle cells
6. they will begin to unload TAG, free FA's
7. chylomicron remnants start talkin with HDL and pick up apoC
8. apoE left on remnant causes it to dock on liver
9. uses remnants to make AA's
   1. left over TAG's, cholesterol will synthesize bile salt from it

1. undergo FA synthesis
2. makes nascent VLDL (make pick up some apoproteins in its normal pathway)
3. HDL passes off apoprotein B100, A, C, E to VLDL
4. makes mature VLDL
5. bind to lipoprotein lipases on membranes of muscle cells and adipose and offloads fatty acids
6. left with VLDL remenant called IDL
7. IDL will crosstalk with HDL
   1. if HDL very effcient, apoB100 cant be pulled off, leads to stripping off all apoproteins, making LDL
   2. another option is to be reprocessed in the liver surface to form LDL

1. lipoprotein lipase bind with Lys residues to membrane bound anchor protein
2. chylomicron and VLDL (apoC- activate lipase) bind to LPL
3. leads to offloading of many free FA's as possible and going off of glycerol

This is all at the membrane of adipose and muscle cell.

1. FA's and CoA make fatty acyl CoA
2. via transferases with carnitine, reproduce fatty acyl CoA in the matrix
3. undergo beta oxidation

1. FA's are converted to fatty acyl CoA
2. underg TAG synthesis
3. lead to TAG storage
   1. on surface of storage vesicle is perillipin

1. acts on receptor via G protein-cAMP second messanger system
2. PKA phosphorylate hormone sensitive lipase and opens up membrane of storage vesicle by binding to perillipin
3. lipase goes into storage vesicle and breaks down TG to form glycerol and FA's

1. LDL binds to LDL receptors (IDL could bind as well due to its apoB100)
2. forms endosome
3. esterfy LDL and decrease pH (use pump), leading to its separation from its receptor
   1. one endosome w/receptor goes back to membrane
   2. another endosome with LDL fuses with lysosome will be broken down via degradative enzymes
      1. release phospholipids
      2. convert cholesterol esters back to cholesterol and FA;s
      3. degrade apoB100 to AA's that can be recycled in cell protein population

• seven 40 AA repeats that are Asp rich (can bind with Lys rich domain on LDL)
  • if I added positive charges, LDL will dissociate
• Cys S-S Cys links
• 4 AA adaptin binding domain (adaptin clatherin endocytosis)

• clatherin bind to LDL receptor
• anchoring and concentrating the LDL receptors in one particular region
• once LDL bound in, we remove clatherin and adaptin to reassemble complex that forms pit

1. via pancreatic lipase, we form a collection of DAG, MAG, TAG, glycerol, free FA, and cholesterol
2. these combine with bile salts to form micelles
3. micelles offload contents into the enterocyte
4. free FA and glycerol combine to reform TAG
5. as TAG concentration increases in cell, aggregate with apoprotein B48 to form the nascent chylomicron in smooth ER
6. ApoB48 brings TAG's into nascent chylomicron
7. nascent chylomicron goes into central lacteal aka lymphatic system
8. HDL delivers apoproteins C and E to nascent chylomicron to form mature chylomicron