Lipoproteins, Lipids Week 2 Flashcards Preview

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Flashcards in Lipoproteins, Lipids Week 2 Deck (31):

Lists the types of lipids (8) 

1. Fatty Acids (r-COOH)

2. Triglycerides- esters of 3 fatty 

3. Phospholglycerides 

4. Sphinolipids (sphingosin containing lipids)

5. Steroids- contains sterol group (cholesterol, bile)

6. Fat Soluble vitamins - DEKA

7. Eicosanoids- prostagladins

8. Ketone bodies- short lipids prodcued during fasting


Fatty acids


Most abundant in the body- often as troglycerides which can be stored. Fatty acids (and triglycerides) mostly taken up by food or stored away to be used for energy, while  most other lipids are not for that purpose. 

Part of many other types of lipids



Chemical nature of lipids

Most are hydrophobic and at best they are amphipatic (mainly hydrophobic with little hydrophillic nature- like phospholipid byayer of membrane)

Most lipids contain fatty acis and are stored as triacylglycerols


Function of lipids

1. storing energy,
2. providing a nonpolar surface (cell membrane)
3. supporting lung alveolar integrity (surfactant)
4. solubilizing nonpolar substances in body fluids
5. serving as hormones with highly potent and specific physiologic roles in control of metabolic processes 


Sources of lipids

Dietary: triacylglycerol, short- and medium chain fatty acids, cholesterol ester, phospholipids, lipid-soluble vitamins (DEKA can be hard to excrete excessive stroage in liver can cause probs)

Synthesized by liver: triacylglycerols, cholesterol, bile acids and salts, phospholipids, ketone bodies

Synthesized by some other cells: phospholipids, eicosanoids, cholesterol derivatives (examples: immune cells, specialized glads, etc) 


What composes the majority of dietary fat?

How are they present in the body? 

TAGs, Choleterol, cholesterol ester, phospholipids. 

Because they are water insoluble, they are present as fat droplet-water emulsion


First step in digestion of fats is where and with what?

Who's this particularrly important for?

In the stomach where acid-stable lipase (both linguall and gastric origin) makes TAGS into short and medium FA side chains. 


IMportant in newborns and people with pancreatic insufficiency because fatty acids are much easier to handle by GI system and cells


What happens with lipids digestion in the SI

What enters the SI is mainly unchanged except some FA have been liberated. Here lipids are emulsified by bile salds and peristalis. 


What is bile? Structure function?

Bile is a choleterol derivative made in liver, stored in gallbladder and is surfactant that solubulize fatty acids and monoglycerides, cholesterol, dietary lysophospholipids and fat-soluble vitamins and form mixed micelles


Enzymes of digestion from the pancreas and their functions

1. Pancreatic lipase- TAGs digestion- anchored to fat by colipase and cleaves TAG into two fatty acids (2-monoglycerides) 

2. Cholesterold esters are digested by cholesterol esterase

3. Phospholipids digested by phospholipase A2 which cleaves off one fatty acid making lysophospholipids which is further degraded by 4. lysopholipase



What happens to bile at the ileum

They are reabsorbed, return to the liver and participate in cycles of micelle formation.


Dicuss lipid absorption- transporters? Formation of the lipids?

The micelles transport these lipids (2-monoacylglycerol, cholesterol and glycerylphosphoryl base) to the surface of the enterocytes where the micelles disaggregate and lipids enter the cells mainly by passive diffusion.

Absorption of
long-chain fatty acids is enhanced by a transporter (FATP4) and that of cholesterol by a channel (NPC1L1). SHort and medium FAs don't need any transporter and on the other they can directly do to portol blood by binding to albumin-- this is good because it's ready made source of energy (hence why they are good for babies). Other classes are apolar so make a bubble (like chylomicron) which have to go through lymphatics and then venous before they reach the body. 


However, sterols can be pumped out of the cells by an ABC transporter, thus only 30-40% of cholesterol is absorbed.


What are chylomicrons and where are they formed?

TAGs are resynthezisex from FAs in the ER OF MUCOSAL CELLS and cholesterol is reesterified with fatty acids-- then they are collectively packaged into lipoproteins called chylomicrons which go into the lymphatic system (through thoracic duct) and then the systemic venous system. 

Remnants of chylomicron are taken up by the liver after the needed part has been delivered to peripheral organs. 


Regulation of digestion

Secretion of enzymes stimulated by food, CCK and secretin

Secretin- producd by endocrine cells of the duodenal wall and stimulate bicarb release

CCK-  release dby endocrine cells of duodenum and act on acinar cells and cause gallbladder to release bile


Secretin function

 produced by endocrine cells of the duodenal wall, stimulates bicarbonate
secretion by ductule epithelial cells of the pancreas. 


CCK function

also released by endocrine cells of the duodenum, acts on acinar
cells of the pancreas to stimulate digestive enzyme secretion and causes the gallbladder to contract and deliver bile into the duct. 


Define steatorrhea and possible causes. 

Fat absorption and digestion disorder resuling in lipids in feces. 


Possible causes 

1. problem with bile salt synthesis/secretion,
pancreatic problems
2. defective absorption by enterocytes.


Interorgan transport of lipids

1. Adipose tissue= TAGs stored--this is realeased as FA when energy is needed and hormonal trigger. THe glycerol produced from the hydrolyssi of TAG goes to the liver for energy or gluconeogenosis  (FA bound to albumin)

2. Blood/intestine- intestine have chylomicron that can appear in blood after eating a fatty meal

3. LIver- place to synthesize a lot of lipids and can enter the blood stream by VLDL and that goes to the peripheral cells 


Where are lipoproteins made? Structure?

Synthesized in the liver and intestine

They are a heterogenous group of lipid-protein complexes that solubulize fats for transportation in blood. And carry fats to and from tissues 

single layer phospholipds- polar to outside and nonpolar to inside and we distinguish between the class of lipoporteins by the apoprotein on the surface 


What happens to the unesteridifed cholesterol in the lipoproteins

The polar portein embeds in the cell membrane. 


Sizes of the lipoproteins and their sources and functions

1. Chylomicron-made in the intestine (store TAGs and that's what most of our fatty diet it)

2. VLDL made in the liver( (take up liver synthesized TAGs and cholesterol and the liver makes all of the lipids---again more TAGs then choelsterol)

3. LDL- breakdown of VLDL (this is the remants of VLDL which must be taken up by the liver)

4.HDL-made in the liver and intestines ( very small ebcause it's almost empty and picks up unwanted lipids especially cholesterol) 


Steps of chylomicron metabolism

1. Intestinal cells secrete TAG rich chylomicrons with Apo B 48

2.  When released frm the SI, the circulating HDL transfer two additional apoproteins (Apo C-II and Apo E) to the surface of chylomicrons. These are needed for regnition and for the release and recylcing by the liver. 

3. Apo C-II has to be on the surface and activates lipoproteins lipase which degardes the TAGs allowing the free fatty acids to go to the cells and glcyerol to go back to the liver. 

4. Once it's released TAGS,  it's a chylomicron remnant and it has more choelsterol than TAGs which can cause a problem because it can be oxidized. 

5. The Apo E receptor (from the HDL) are needed for recycling back to the liver. 


VLDL  (and LDL) metabolism

LDL is a derivative of VLDL so metabolim is the same 


1. LIver secretes VLDL with Apo Protein B-100 rich in TAG

2. When in circulating HDL gives it two apoproteisn Apo C-11 for regocnition and Apo E to release TAGs to any cell. 

3. When in circulation Apo C-II activates lipoprotein lipase which degrades the TAG in the VLDL releasing the lipid content to cell (sending glycerol to liver) 

4. the VLDL is now called IDL which released the APo E and Apo CII back to the HDL, making LDL with only Apo B-100 apoprotein

5. Apo protein B- 100 only has one receptor - LDL receptor which can be problemmatic if there is a problem with this receptor or if it's overhwlemed then LDL circulates for a long time and can get into the intima of blood cells. 


HDL metabolism

1 Synthesized by the ilver and small intestines with Apoportein A-1 and C-II- and E( which it gives to VLDL and chylomicron)

2. Apo-1 is imporant for picking up cholesterol from the cells. Apo-1 activate LCAT which esterifies cholesterol making it hydrophobic and packing it into the core of HDL. (if it was esterified the cholesterol would be in the membrane making the HDL very rigid) 

3. The full HDL is taken up by the liver. through Apo 1 it binds to its own receptor (so that receptor is unlikely to be backed up) 

But  since the choelsterol is so expensive to synthesize it can be exchnaged between the VLDL and the HDL through CETP.  


What is the LDL receptor specific for?

Apo B 100- which is unique to VLDL and literautre shows maybe Apo E 


What does the recycled cholesterol do? 

Make steroid hromones

Mkae bile acids

Temporary storage of cholesterol esters (very small)


Overproduction of intracellular cholesterol the liver stops the de nuvo synthesis


What is type I hyperlipoproteininemia

Chylomicron higher in circulation than it should be. Lipoprotein lipase deficiency (the enzyme that release the TAGs/FAs). When it's missing you get high chlomicrons and can't release the TAGs.


Doesn't affect VLDL as much becaus when chylomicron is high tells the liver to stop fatty acid synthesis so the liver stops making VLDL. VLDL is also not as huge and as many as chylomicron. 


What is familiarl type iii hyperlipoproteinemia?

Defecieincy in APoprotein E. So there is an increase in the chlymicron and VLDL remnants because they can not be taken up by the liver


What is Type II hyperlipidemia?

Most well known and a problem with the LDL receptor because it's missing from the liver, so LDL can't be cleared from the blood. 


Familiar LCAT deficiency is what?

Defeciency in LCAT which is the enzyme that takes cholesterol from periohery into HDL by esterfying it. If it's not there cholesterol can still enter the membrane so part of it will be recycled.


What is hepatic steatosis?

Fatty liver. imbalance between TAG synthesis and VLDL secretion. Sometimes missing the apoprotein