Term
| What are the three major lipid membrane components and which are rigid vs. flexible? |
|
Definition
1. Phospholipid - flexible
2. Sphingolipid - flexible
3. Cholesterol - rigid |
|
|
Term
| What is the general composition of a phospholipid? |
|
Definition
| A diacylglycerol with a phosphodiester bridge that links the 3rd glycerol carbon to a head group, usually a nitrogenous one with a charge on it |
|
|
Term
| What are the four phosphlipases and what does each cleave? |
|
Definition
Phopholipase A1 - cleaves the 1st fatty acid
Phopholipase A2 - cleaves the 2nd fatty acid
Phopholipase C - completely cleaves the head group
Phopholipase D - partially cleaves the head group, leaving the phosphate in |
|
|
Term
| What are sphingolipids? Where are they located and what is their function? |
|
Definition
| Sphingolipids are parts of plasma membranes (most commonly found in white matter) are fatty acids bound to sphingosine. They play a role in cell interactions, growth, and are antigenic |
|
|
Term
| What are ceramides? What are they made from and how are they made? |
|
Definition
1. Fatty acid amide derivatives of sphingosine
2. They are made by adding a fatty acid (most commonly behenic acid, a 22 carbon FA) to the amide group of sphingosine |
|
|
Term
| Describe the precursor and structure of cholesterol |
|
Definition
1. Sterane is the precursor
2. A 27 carbon structure with a hydroxyl ant the 3, a double bond at the 5, and methyls at 18 and 19 carbons |
|
|
Term
| What are the functions of cholesterol? |
|
Definition
1. Major sterol (essential in membranes), abundant in CNS myelination
2. Precursor of bile salts, steroid and sex hormones, and vitamins D2 and D3
Note: Only found in mammals, not plants (important for diet) |
|
|
Term
| Where is cholesterol synthesized and what are its precursors? What are the energy sources for synthesis? |
|
Definition
It is synthesized in the ER of liver, intestine, adrenal cortex, and reproductive tissues
2. Its precursor is acetyl CoA, and acetate is the carbon source
3. Thioester bonds from Acetyl-CoA and ATP are the energy source |
|
|
Term
| What are the 4 major steps in cholesterol synthesis and which one is regulated? |
|
Definition
1. Accetate is converted to mevalonate <-- regulated step
2. Mevalonate becomes and activated isoprene
3. Isoprene becomes squalene
4. squalene becomes cholesterol |
|
|
Term
| Describe the steps in the regulated part of cholesterol biosynthesis |
|
Definition
1. Two acetyl CoA combine to make acetoacetyl CoA
2. Acetoacetyl CoA combines with another acetyl CoA to make HMG CoA
3. HMG CoA is turned into Mevalonate by reducing it with NADPH and the enzyme HMG CoA Reductase (this is the rate limiting, regulated step, NOT committed) |
|
|
Term
| How is cholesterol is stored? |
|
Definition
| As a cholesteryl ester, where a fatty acid is attached to the hydroxyl group on the 3 carbon (making it a completely non polar lipid) |
|
|
Term
| How does cholesterol become soluble? |
|
Definition
| Binds to lipoproteins to make them soluble in water |
|
|
Term
| How does the liver regulate cholesterol levels and synthesis |
|
Definition
1. It is the major site of conversion for cholesterol to bile acids
2. It has the most LDL receptors for internalization of LDL (suppresses biosynthesis by raising cholesterol levels in cells)
3. It has the most HMG CoA reductase |
|
|
Term
| Explain the regulation of HMG-CoA and LDL receptors |
|
Definition
| The SREBP transcription factor is necessary for their production. It exists in the ER bound to SCAP, which makes it inactive. When sterol levels are low, it migrates to the Golgi where it is cleaved from SCAP and becomes active. High sterol levels prevent migration to the golgi |
|
|
Term
| Explain the hormonal regulation of cholesterol synthesis |
|
Definition
Insulin (GLOBAL STORE ENERGY) promotes HMG CoA Reductase activity
Glucagon (GLOBAL RELEASE ENERGY) inhibits HMG CoA reductase activity |
|
|
Term
| What are statins and how do they work? |
|
Definition
| Pharmaceutical drugs that mimic the structure of HMG CoA reductase and mevalonate to lower cholesterol levels |
|
|
Term
| How is cholesterol excreted? What regulates this process? What does a deficiency in this pathway lead to? |
|
Definition
1. Conversion to bile acids
2. Cholic acid (product inhibition) inhibits the conversion. Increased cholesterol promotes the conversion.
3. Gallstones |
|
|
