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Unit3 LipidDigest1 > First Unit3 Lecture Goodridge > Flashcards

First Unit3 Lecture Goodridge Flashcards

1
Q

How many grams of water to store gram of fat?

A

1 gram of water to store 1 gram of fat

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2
Q

Describe amounts of total energy (Kcal) stored in body

A

Fat>Protein>Carbohydrates

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3
Q

Human Metabolism obeys First Law of Thermodynamics

A

deltaU = Q - W
deltaU=Kcal of chemical energy stored (mostly as fat) = change in energy stored in a physical system
Q=Kcal in food intake = energy input to the system
W=Kcal of metabolic and skeletal muscle = work done by the system

Also delta U=Triacylglycerol (adipose tissue), Glycogen (liver and muscle), Protein (all tissues)

W

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4
Q

Why Regulate Metabolism of Triacyglycerol and Fatty acids?

A
  1. Store energy in times of plenty
  2. Use stored energy during starvation
  3. Accommodate intake of varying ratios of triacylglycerols, carbohydrates, proteins
  4. Provide insulation to reduce heat loss
  5. Cushion body in case of falls or assault
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5
Q

Cholesterol Esters

A

Formed by esterification with Fatty Acids
More lipophilic than cholesterol
Storage form of cholesterol

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6
Q

How many excess calories in a year based on 2000 calorie diet to gain one pound of fat (including its water component)?

A

3500Kcal excess calories in a year will gain 1 pount (or 10Kcal per day excess)

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7
Q

In humans on an “average” American diet, what is the major source of cholesterol (where does it come from)?

A

Synthesis DE NOVO from in Liver and other tissues is the MAJOR SOURCE of cholesterol

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8
Q

Sources of Cholesterol (on average diet)

A

DE NOVO SYNTHESIS = 700mg/day

  • Liver = 70 (makes 10% of the cholesterol)
  • Intestine = 70 (makes 10% of the cholesterol)
  • Other tissues = 560 (almost all tissues make cholesterol)

DIET=400mg/day
-Transported to liver and extrahepatic tissues in blood

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9
Q

Sources of Cholesterol

A

Most Dietary Cholesterol is free cholesterol; balance is cholesterol ester

Cholesterol in diet is HIGHLY VARIABLE (vegetarians have zero from their diet, because plant sterols are not useable/metabolized in same way by animals, so they get ALL their cholesterol from DE NOVO SYNTHESIS)

DE NOVO cholesterol synthesis is INHIBITED BY DIETARY CHOLESTEROL

Amount of cholesterol in blood affects cardiovascular disease

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10
Q

Why Regulate Metabolism of Cholesterol

A
  1. Cholesterol is NOT a significant energy source
  2. Cholesterol is an important component of plasma and other organellar cell membranes
  3. It is a precursor to bile acids
    • Major Player in quantitative turnover of total body cholesterol
  4. It is a precursor to Hormones and Vitamins
    • Not significant in quantitative turnover of total body cholesterol
  5. It (cholesterol/Free Cholesterol) is Secreted into Bile. This is a Major Route of Removal of cholesterol from the body! So if you have too much cholesterol there are mechanisms to bring it back to liver, and then the liver excretes it into bile, and then a significant portion of it will go out in the stool.
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11
Q

Cholesterol and Fat (why hamburger is worse than egg even though egg has more cholesterol)?

A

Answer: Hamburger has a lot more fat (saturated fat)

Fat is important in energy balance, but fat ALSO influences the metabolism of cholesterol and exacerbates effects of cholesterol on cardiovascular function.

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12
Q

Gastric Lipase (first part of Digestion)

A

The first part of digestion of Fat occurs in the stomach. Gastric Lipase (an enzyme that HYDROLYZES triacylglycerol) is secreted by glands in the stomach
Acid pH in stomach is optimal for this enzyme (stomach acid pH is about 2)
Reaction:
triacyglycerol —-> fatty acid + 1,2-diacylglycerol
10-30% of intestinal triacylglycerol hydrolysis occurs in the stomach (by the enzyme catalyzed reaction by Gastric Lipase)

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13
Q

Overview of Lipid Digestion

A

Entering is Biliary Cholesterol (2000mg/day, because 2g per day of cholesterol is secreted into the Bile) and Dietary Cholesterol (400mg/day) as well as Dietary Triacylglycerol

98% of the Triacylglycerol that you eat will end up being absorbed!

Of the 2400mg/day of Cholesterol (total value), you will absorb only about 1200mg (so 50%) and the other half will be excreted in stool! This is the major way that cholesterol will be removed from the body if you have too much!

The Cholesterol is packaged into chylomicrons and sent to the lymphatic system (the 50% of cholesterol mentioned gets absorbed in the ILEUM, which is the lower end of the Small Intestine)

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14
Q

Biliary Lipids

A

Biliary Lipids=Bile, and it is made of the following components

Class Daily Secretion (g)
Bile Salts 24g
Phospholipids 11g
Cholesterol 2g

Biliary Lipids=Bile, and these are the components of bile. Most of the 24g of Bile Salts in the Bile will be reabsorbed. Bile Salts are also important in cholesterol metabolism in addition the fat/lipid absorption.

All of these components of Bile contribute to the emulsification and ultimately the creation of micelles with the lipids, which facilitates the digestion of fat.

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15
Q

Info About Bile Acids

A

They are synthesized in Liver

Stored in Gall Bladder

Fat in Duodenum causes release of cholecystokinin to blood (this is realized from the duodenal cells)

Cholecystokinin stimulates contraction of gall bladder, forcing bile into the duodenum

Bile acids are AMPHIPATHIC

Bile acids initially emulsify di- and triacylglycerols (emulsification particles are MACROscopic)

They ultimately form mixed micelles with products of fat hydrolysis (the micelles are MICROscopic particles in solution)

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16
Q

Bile Acid Synthesis First Step (Rate Limiting Step/Enzyme)

A

Bile Acids are Synthesized in the LIVER!

Rate limiting enzyme (slowest step and first step in Bile synthesis) = 7alphahydroxylase enzyme

You start with cholesterol and 7alpha hydroxylase uses NADPH,H+ (converting it to NADP+) and O2 (molecular oxygen) in order to convert it to 7alphahydroxycholesterol

7alphahydroxylase enzyme is the REGULATORY enzyme/step in pathway (All regulation of production of bile acids is regulated here!). It is STIMULATED BY HIGH LEVELS OF CHOLESTEROL IN THE LIVER (so feed-forward activator) and INHIBITED BY BILE ACID (the product, so bile acids are feed-back inhibitiors). Several hormones regulate the pathway as well! (don’t need to know names)

17
Q

Bile Acid Synthesis Continued (After 1st/Regulatory Step)

A

Once cholesterol is 7alphahydroxylated to 7alphahydroxy cholesterol by the rate-limiting enzyme “7alphahydroxlase,” it can the go through either of two different paths:

1) It can either be 12alphahydroxylated and activated with proponyl-CoA
OR
2) It can just be activated with proponyl-CoA
(these are several steps but we won’t talk about)

The proponyl-Coa serves to “Activate” compounds (similar to how fatty acids get activated with CoA before beta oxidation)

This gives you either Cholyl-CoA or Chenodeoxycholyl-Coa (only difference is one product is 12hydroxylated and one is not)

These molecules can be conjugated either by GLYCINE amino acid or TAURINE amino acid

This leads to a total of 4 PRIMARY BILE ACIDS/SALTS  (The four products are MADE IN LIVER and are SECRETED INTO THE BILE) when this amidation/conjugation occurs (amino acid linked to the molecule)
1) Tauracholic (amino) acid 
2) Glycocholic (amino) acid
OR
3)Taurachenodeoxycholic (amino) acid
4) Glycochenodeoxycholic (amino) acid

Once the bile get into the intestine, it undergoes a 7alphadehydroxylation and deconjugation of all four compounds, so you end up with TWO SECONDARY BILE ACIDS (These are the two FUNCTIONAL BILE ACIDS that will help with emulsification and creation of miscelles). They are DEOXYCHOLIC ACID and LITOCHOLIC ACID. *This reaction of dehydroxylation/removal of 7allpha hydroxyl and deconjugation/removal of aminoacid is carried out by BACTERIAL ENZYMES IN YOUR GUT (NOT Human enzymes!)

18
Q

Anatomy Description (Bile Acids: STORED in Gallbladder, DELIVERED to Duodenum

A

The ducts that connect from the liver cells are called Canaliculi (“Bile Canaliculi”). Canaliculi=Ducts.

From the liver, the bile goes to the “right and left hepatic ducts”, these merge into the “common hepatic duct”.

The Gall bladder has it’s own duct called the “cystic duct” and when the bile goes out of the gallbladder into the cystic duct it then merges with the common hepatic duct in what we call the “Common Bile Duct” (where cystic duct and common hepatic duct merge).

The pancreas also has it’s own “pancreatic duct,” which connects to and join the common bile duct. All of these secretions will go through the “SPHINCTER OF ODDI” and enter the “Duodenum” of small intestine.

This duodenum is the very top portion of small intestine that comes right after the stomach, so it will have the food/lipids that have been partially (10-30% from Triacyglycerol have become 1,2 diacylglycerol and free fatty acid by Gastric Lipase, as well as the rest remaining as triacyglycerols).

The Sphinctor of Oddi prevent all of the secretions that enter the duodenum of the small intestine from refluxing back into the common bile duct.

19
Q

Bile Acids are Amphipathic

A

Bile Acids are AMPHIPATHIC (contain BOTH polar and nonpolar regions)

Glycocholate (Glycocholic Acid) is the example of Bile Acid that he showed in picture. Bile acids have have an “apolar side with CH3 groups attached” (hydrophobic side) AND “polar side with OH groups attached near ring area and a carboxylic acid polar group on way end” (hydrophilic side).

20
Q

Bile Salts Emulsify Dietary Fats

A

Intestine contains “lipid droplet” from food that came from stomach and was only partially digested by Gastric Lipase (diacylglycerol, triacyglycerol, cholesterol ester).

The Bile Acids/Salts (Bile) will surround/emulsify this fat droplet (some Phospholipid will surround it too, which came from body secretion and possibly a little from diet).

“Pancreatic Lipase and Colipase” will bind to the surface of emulsified lipid to start digesting/breaking it down more.

Pancreatic Lipase will catalyze the next steps that will hydrolyze the majority of the Triacyglycerols that came from the diet.

21
Q

Hydrolysis of Dietary Triacyglycerol (Step 1)

A

Triacylglycerol + H20 (adding water to hydrolyze) —–enzyme PANCREATIC LIPASE ——-> 1,2-Diacylglycerol + Unesterified Fatty Acid

This removes the Fatty Acid from the THREE POSITION/C3 (THREE position of the glycerol,” making 1,2-Diacylglycerol and FFA.

Note: Unesterified Fatty Acids are sometimes called Free Fatty Acid, but actually it is on albumin or something and not just free, floating around. So Unesterified Fatty Acid is more correct, but it is the same as saying Free Fatty Acid.

22
Q

Hydrolysis of Dietary Triacylglycerol (Step2)

A

The second step uses Pancreatic Lipase to remove the second Fatty Acid by adding water (hydrolysis). This time it removed the FA from the One Position/C1 (ONE position of glycerol) in the 1,2-Diacylglycerol. This forms another FFA (unesterified FA) and a 2-Monoacylglycerol (2-MG).

1,2-Diacyglycerol + H2O —–Pancreatic Lipase—-> 2-Monacylglycerol + FFA

IMPORTANT: About 70% of Triacyglyceried are hydrolyzed to this step/product and then enter the ENTEROCYTES/MUCOSAL CELLS as “2-MG (2-Monoacylglycerol) + FFA”. So, the majority of the time (70% of the time) the hydrolysis process stops after this step. Most of the Time the fatty acids and monacylglycerols enter the cell by “Fatty Acid Transport Protein (FATP)”. This FATP is present on all cells; here we are talking about the mucosal/enterocytes/epithelial cells of small intestine.

23
Q

Hydrolysis of Dietary Triacylycerol (Step 3 and 4)

A

Step 3 (uses ISOMERASE enzyme):

2-Monoacylglycerol ——“ISOMERASE”—– 1-Monoacylglycerol

Step 4 (uses PANCREATIC LIPASE now that it can work on the ONE position, because it could NOT WORK ON TWO POSITION before), forming Glycerol and FFA as the final products:

1-Monoacylglycer + H20 —–Pancreatic Lipase —-> Glycerol + FA

IMPORTANT:

***The Glycerol is EXCEPTION and will enter mucosal cells/enterocytes and then go to the “Portal Vein” and travel to the LIVER. This is because there is not very much glycerol kinase to make use of it in the enterocytes, but the liver has plenty, so it will be more useful in the liver.

*****The rest of molecules (1,2-Diacyglycerol, 1-Monoacylglycerol, and FA formed) will enter mucosal cells/entoryctes, get REPACKAGED INTO TRIACYLGLYCEROL onto CHYLOMICRONS, and then ENTER THE LYMPHATIC VESSELS.

**Therefore AQUEOUS hyrophilic digestion products (like glycerol) are taken up by portal system (Portal Vein) versus hydrophobic (like cholesterol, cholesterol ester, triacylglycerol) are taken up by Lymphatic System (Lymphatic Vessels)

24
Q

Cholesterol Esterase

A

Cholesterol Esterase is an enzyme made in the PANCREASE and secreted into the gut/small intestine.

Cholesterol Esters are broken down by “Cholesterol Esterase” into Cholesterol + Fatty Acid

Cholesterol Ester —–Cholesterol Esterase–> Cholesterol + Fatty Acid

Note: Most of Cholesterol in DIET is UNESTERIFIED. If there is any small amount, it will be hydrolyzed by Cholesterol Esterase and broken into unesterified fatty acid (FFA) and unesterified cholesterol (sometimes called free cholesterol).

25
Q

Bile Acids Form Mixed Micelles with Products of Lipid Digestion

A

Bile Acids Form Mixed Micelles with Products of Lipid Digestion

The products of digestion of Triacylglycerol are AMPHIPATHIC

Amphipathic Agents:

  • 2-Monoacylglycerol (2-MG)
  • Bile Acids (BA)
  • Phospholipids (PL)
  • Fatty Acid (FA)

Micelles

  • Submicroscopic
  • Soluble
  • Essential for lipid absorption
26
Q

Quick Overview of Digestion of Dietary Fat

A

Triacylglycerol gets EMULSIFIED and then worked on/broken down a little by pancreatic lipase, MICELLES are formed from the increased amount of amphipathic particles, and these get broken down a lot more by pancreatic lipase. Then the FFA and Monoacylglycerols that are NOT IN MICELLE (unstirred layer) will fall out and be transported into the Gut Cells/mucosal cells/enterocytes.

***So the “unstirred layer” that is not miscelles which get absorbed by gut cells is what drives the digestion process forward so that more and more of these MG and FFA get formed.

***Know that it is a SINGLE LAYER OF CELLS that line the intestine, and these are what absorb the FFA and MG.

27
Q

IMPORTANT SLIDE:

Sites of Lipid Digestion and Absorption

A

STOMACH
-Fat Digestion BEGINS (GASTRIC LIPASE)

DUODENUM
-Site of MOST DIGESTION (PANCREATIC LIPASE)

JEJUNUM
-Site of MOST TG ABSORPTION (I think he means the TG gets absorbed here, but it’s actually absorbed in the form of DG, MG, and AG)

ILEUM
-Absorption of BILE ACIDS and CHOLESTEROL

28
Q

Optimizing/Making Digestion Efficient by INCREASING SURFACE AREA

A

There are a number of tricks used to INCREASE SURFACE AREA for digestion.

VILLI (macrovilli) and MICROVILLI are the two main ways to increase surface area.

The macrovilli are folds within the folds of the small intestine that amplify the surface area by many fold.

Each macrovilli has microvilli (extensions) that amplify the surface area even more fold.

Villi Line the intestine (and have microvilli extensions). The Micelles diffuse to Intestinal Walls and Deliver Lipids to the “Brush Border”(another term for MICROVILLI).

IMPORTANT PHYSIOLOGICALLY: The intestinal contents is full of hydrolases, so the cells keep dividing and the cells at the top get sloughed off. This can lead to loss of some cholesterol (one method of losing cholesterol), because those cells contain cholesterol and will get digested/become digestive product over time. It can also caused IRON LOSS, because the cells contain iron.

IMPORTANT PATHOLOGICALLY: Cancer drugs/chemotherapy target rapidly dividing cells (suppose to be the cancer cells), but the side-effect is that the “crypt cells”/dividing intestinal cells get targeted because they are also rapidly dividing. This leads to a reduced number of cells coming up from the crypt cells. This causes nausea, vomiting, and diarrhea (digestion problems caused by inhibition of division of the crypt cells).

29
Q

Disposition of Micellular contents

after micelles are formed, describe the absorption process

A

The UNESTERIFIED Fatty Acids and 2-MG fall off from miscelles and get absorbed at brush-border of enterocytes by the “FATP” (fatty acid transport protein) to go into the enterocytes/JEJUNUM cells).

The unesterified FA gets added to CoA (with ATP being used) to make FA-CoA. This FA-CoA can now either join the 2-MG to form a Triacylglycerol again or it can be added to glycerol 3-phosphate to form the Triacyglycerol again. So either way, the FA and 2-MG are again made into Triglycerides, and this will be packaged into chylomicrons and sent into chyl/lymphatic vessels (NOT portal vein).

Also, the Bile acids that were used in emusificiation will keep moving down the lumen of small intestine and be ABSORBED at ILEUM of small intestine.

Cholesterol from diet (that has been broken down to unesterified form if not already in that form) also gets abosrbed in ILEUM. It will also be transported by a membrane protein (NPC1L1) into the enterocyte cell. Cholesterol can get re-esterified if used by “acyl-coA: cholesterol acyltransferase” enzyme and “FA-CoA” joins it to re-form the “cholesterol ester” inside the Ileum enterocyte cell. This will get packaged into chylomicrons and sent in lymphatic system. OR cholesterol can be used by enteorycte cells/crypt cells for it’s own membrane OR cholesterol can exit the enterocyte by “ABC G5/ABC G8 membrane DIMER-FORMING/protein” (Atp Binding Cassette protein=ABC). This requires use of ATP to send cholesterol back out/AGAINST cholesterol gradient to the lumen for excretion in stool!

Summary

  • Digestion begins in stomach/gastric lipase (10-30% broken to make 1,2-diacylglycerol)
  • Most digestion occurs in Duodenum of Small Intestine (forming FFA and 2-MG which can now enter Jejunum enterocyte membrane/microvilli=brushborder).
  • Jejunum ABSORBS the FFA 2-MG (so it is site of most Triglyceride absorption, and 98% of dietary triglycerides will get absorbed!)
  • ILEUM absorbs Bile acids and Cholesterol (Note: 50% of cholesterol will be absorbed by the NPC1L1 transporter, and ALMOST ALL BILE ACIDS will get absorbed)

(maybe double check notes incase but i think it’s correct)

30
Q

IMPORTANT:
Inhibition of TG uptake from intestine
(Alli = Orlistate = Anti-obesity drug)

A

Alli (orlistat) - Anti-obesity drug

  • INIHIBITS PANCREATIC LIPASE
  • About a third of Triacylglycerol remains intact and unabsorbed
  • Causes intestinal problems + steatorrhea with high fat diet
  • Patients become averse to fat in diet
  • Modest weight loss (because patients aren’t compliant with their high fat diet due to discomfort)
31
Q

IMPORTANT:

AGENTS that INHIBIT Cholesterol Uptake from Intestinal Lumen

A

1) Benecol and Promise Take Control
- Margines that contain plant stanol esters or plant sterols. They:
* Inhibit uptake of cholesterol into micelles
* Inhibit lumenal cholesterol esterase of intestine

2) Zetia = Ezitimibe
- Inhibits enterocyte cholestrol transporter (NPC1L1)

3) Cholestyramine and colestipol
- Non-absorbable resins that bind bile acids
- Reduce recylcing of bile acids to the liver
- Hepatic cholesterol is re-directed to synthesis of Bile Acids

Important note: The problem with all three of fhese is that they inhibit cholesterol uptake. This will just lead to stimulating cholesterol synthesis. So, these drugs are usually taken IN ADDITION to the drugs that inhibit cholesterol synthesis (like Statins which inhibit HMG CoA reductase since they are cholesterol transition state analogs, leading to increase of LDL receptors and decrease LDL cholesterol/increase HDL/decrease blood triglycerides).

32
Q

SUMMARY Slide:

Digestion of Triacylglycerol and Cholesterol Ester

A
  • TG and cholesterol ester in emulsified fat hydrolyzed by lipases and cholesterol esterase, respectively.
  • MG, FA, (unesterified) cholesterol will be incorporated into micelles (but GLYCEROL will NOT!)
  • MG, FA, (unesterified) cholesterol. glycerol will all get transported or diffuse into intestinal epithelial cells/enterocytes
  • MG and FA get re-esterified in cells/Ileum to make TG again, unesterified cholesteral also gets re-esterified
  • TG (mainly reformed after absorbption in Jejunum) and Cholesterol Ester (mainly reformed after absorbed in Ileum) will be packaged into chylomicrons and secreted to lymphatic system
  • Glycerol will get abosrbed by enterocytes and sent to the portal vein/NOT LYMPHATIC but GO TO LIVER by venous system!
33
Q

Important: Generalized structure of plasma lipoproteins

A
  • SURFACE LAYER (outer layer) of AMPHIPATHIC lipids of chylomicron/lipoprotein: PHOSPHOLIPID and unesterified CHOLESTEROL (along with apo proteins)
  • CORE of nonpolar lipids: TG and CHOLESTEROL ESTER
  • APOLIPOPROTEINS (B, A, C, E proteins on surface of the lipoproteins) can be PERIPHERAL (A,C,E on HDL all peripheral and on the surface) OR can be INTEGRAL (B-48 of chylomicrons and B-100 of VLDL/IDL/LDL have lots of HYDROPHOBIC amino acid residues that anchor in the hydrophobic core)
  • Different types of lipoprotein particles (HDL, LDL, etc) contain specific lipoproteins
  • Lipid/protein ratio DETERMINES DENSITY!
34
Q

Important: Generalized Function of Apolipoproteins

A
  • Part of structure of lipoprotein
  • Co-factors/activators for enzymes (like C-II activates Lipo-protein-lipase/LPL)
  • Inhibitors for enzymes (like C-III inhibits LPL)

-Ligands for apolipoprotein receptors
(like the LDL receptor on all cells which binds apoB-100 and apoE and the LDL-receptor related protein on liver which binds apoE of the IDL(VLDL remnant) as well as the Apo100 of the LDL (since LDL doesn’t have any other apoliprotein other than B-100…explaining why mutations of B-100 lead to high LDL levels and can’t be treated by PCSK9 monoclonal antibodies)

-

35
Q

Primary Function of MAJOR LIPOPROTEINS

AND my own IMPORTANT SUMMARY bottom!!!!

A

CHYLOMICRONS (largest molecules, mostly TG, and highest lipid/protein ratio!)
-Deliver DIETARY TG from intestine to ADIPOSE TISSUE and, to lesser extent, to liver and other tissues
-Deliver DIETARY Cholesterol to the LIVER
(Starts as nascent chylomicron with B-48 and A that is made in Rough ER of enterocytes…gets C,E, and some more A from HDL to make it mature chylomicron)

Very Low Density Lipoprotein = VLDL (starts by being made in Liver as nascent VLDL from B-100,C,E made in rough ER I think…then more C,E get added by HDL to make it mature VLDL and then TG goes to adipose and E sent back to HDL to make it IDL=vldl remnant=just B,E some TG and lost of cholesterol….then more TG gets deliverd and E falls off/probably goes back to HDL and this form the LDL with cholesterol only and only apo-B100)

  • Deliver HEPATIC TG to ADIPOSE TISSUE and other tissues
  • Precursor to LDL

Low Density Lipoprotein = LDL
-Deliver CHOLESTEROL from LIVER to PERIPHERAL TISSUE (since it only contains B-100 and Cholesterol, but some will go back to the Liver as well even though most will go to peripheral tissue)

Note: ApoC and E only made in Liver
ApoA made in intestine and liver
ApoB48 made in intestine (integral apolipoprotein)
ApoB100 made in liver (integral apolipoprotein)
HDL = A,C,E source (only peripheral apolipoproteins)

   nascent chylomicron = B-48, A
   mature chylomicron = B-48,A,C,E,
   remnant chylomicron (gives A,C back to HDL) = B-48 and E, so it can be taken up by LDL and LDL-protein like receptors since they can attach to the apo E (but they can't attach to B-48 since they only attach to B-100 and E)
      nascent VLDL = B-100, E, and C
    mature VLDL = B-100 and more E and C (which it gets from HDL)
     IDL (VLDL remnant) = B-100 and E with cholesterol and less triglyceride (it gave C back to HDL)
     LDL = B-100 only and just cholesterol (lost E and rest of triglyceride)
   LRP=LDL-Receptor-Related-Protein which is on liver and binds to apE of chylomicrons, IDL, and LDL
   LDL Receptor = Binds B-100 but not B-48 and binds apoE of IDL,LDL, and chylomicron remnants since they have apoE 
    So the LIVER CLEARS chylomicron remnants by the LRP and LDL receptor binding the apoB of remnant chylomicrons
  *All apolipoproteins are made in ROUGH Endoplasmic Reticulum (Rough ER) since they are proteins (apoB-100,B-48,etc) and then go to smooth er to get lipid added (TG, chosterol, cholesterol ester, phospholipid) then go to golgi to get packaged into secretory vesicles, and then get sent out of cell....for chylomicrons ApoB48 andA are made in rough ER, etc happens, and then the nascent chylomicron in the vesical gets secreted out of the cell into the chyle of lymphatic system....chylomicrons in the lymphatic system eventually enter venous system at the "left sublavein vein" so they go to circulation system and then go to liver later......vs polar/aqeous compounds (like glycerol) that go to PORTAL VEIN/portal system from the enterocyte/small intestine so these aqeous/polar/glycerol/amino acids/glucose/MC-fa/aqeous drug metabolites go DIRECTLY TO LIVER! Also medium chain FA go directly to portal Vein (they are quite soluble in aqeous solution since smaller)!
36
Q

Medium chain TG/FA: go directly to liver!

A

MC triglycerides are less than 11 carbons

  • Hydrolyzed and absorbed in stomach and small intestine
  • Better digested by gastric lipase than long-chain TG
  • Resulting FA are quite soluble in aqeous solution
    * Absorbed in molecular form
    * Transported in LIVER via PORTAL VEIN (so they don’t go to lymphatic system and are not packaged into chylomicrons)
  • **MC supplements used to treat patients with pancreatic, billiary, or intestinal problems (maybe cancer blocking something, etc)…..also MC supplements are sometimes used by body-builders and athletes

Unit3 LipidDigest1 (9 decks)

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