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MCM test 2 > 2- Lipid Synthesis and Storage > Flashcards

2- Lipid Synthesis and Storage Flashcards

1
Q

When does fatty acid biosynthesis occur?

A

In the Insulin world. In the fed state

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2
Q

What are the ingredients for FA?

A

AcetylCoA- from citrate

CO2- from blood stream

NADPH - from HMP shunt (G6PD) and malate

ATP- mitochondria

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3
Q

Draw pathway from citrate to FA synthesis

A

citrate moved to cytoplasm

citrate > Acetyl CoA + CO2 (use ATP) > Malynyl CoA + NADPH > Fatty acid Palmitate + CO2

enzymes:
AcetylCoA carboxylase (ABC): acetyl CoA > Malynyl CoA
Fatty Acid Synthase: malynyl CoA + NADPH > fatty acid
palmitate

Fatty acid palmitate is the only FA made by scratch

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4
Q

Acetyl CoA carboxylase

A

ABC, acetyl CoA, biotin, CO2

Activated (+) by insulin and citrate

Inhibited by glucagon, and palmitoyl CoA

Co2 + Acetyl CoA (2C) > malynyl CoA

AcCoA carboxylase regulates fatty acid synthesis

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5
Q

What happens to FA after synthesis?

A

FA moves from cytoplasm to smooth ER.

FA elongated and desaturated (is that all?) in the ER.

FA then made into triglyceride, in the liver.

TGL combines with app-B100 (VLDL)

Then shifted into adipocytes.

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6
Q

How is fat absorbed from the gut?

A

lacteals (lymphatic vessels) so that blood is not clogged with fats.

Goes straight to the right atrium where it meets up with apoproteins and then gets shipped to the liver.

Whereas protein and glucose goes to the hepatic portal vein to the liver.

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7
Q

Why are alcoholics liver fatty?

A

alcohol stops VLDL from leaving the liver.

Alcohol disrupts VLDL assembly, TG stay in liver

Alcohol is found in the liver because it is absorbed very fast and will get to the hepatic portal vein to the liver. Also where alcohol dehydrogenase is found.

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8
Q

What does Malonyl CoA inhibit?

A

carnitine acyltransferase I

in order to prevent import and degradation of newly synthesized fatty acylCOA (?)

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9
Q

What are the 3 control points of FA synthesis?

A

Acetyl CoA

Malonyl CoA

Palmitoyl CoA

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10
Q

LPL

A

lipoprotein lipase- enzyme to facilitate movement of fat into the cell

Insulin activates it. So in diabetics, fats are made but can’t be stored

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11
Q

What are the sources of glycerol in the liver?

A

2 sources:

DHAP from glycolysis

Glycerol from the liver itself

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12
Q

Why is insulin important for FA synthesis? what all does it do?

A
  • Activates AcCoA carboxylase to turn on FA synthesis
  • Turns on gene for for LPL in adipocytes
  • Forces the liver to make TGL in abundance

-Also turns on glucokinase and PFK-2 in the liver during glycolysis

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13
Q

Why can’t TGL be stored in the liver in abundance?

A

Because TGLs are non polar, liver does not fit them well.

Adipocytes, however, are 90% anhydrous (do not contain water)

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14
Q

Where does cholesterol come from?

A
  1. Cholesterol itself- polar OH, can dissolve in some water.
  2. Cholesterol ester - nonpolar, does not mix in blood.
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15
Q

Recommended daily dose of cholesterol

A

300 mg

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16
Q

Cholesterol digestion

A

Chol and cholesterol ester are emulsified by bile and pancreatic esterase. Enzyme removes FA off of CE so that it can be absorbed into intestines

After absorbed, ACAT puts FA into Chol remaking CE (in intestinal mucosa)

CE packaged with TG+PL+ApoB-48 > Chylomicrons

Goes to lymph then blood stream via thoracic duct

17
Q

Chylomicron

A

ApoB-48

delivers dietary fats to tissues

lowest density chylomicrons

18
Q

What are the three types of lipase that break ester bonds of TGs?

A
  1. Pancreatic lipase- breaks down TGL
  2. LPL (lipoprotein lipase)- in lipoprotein metabolism. important for uptake into adipocytes
  3. HSL- hormone sensitive lipase- in adipocytes where it hydrolyzes stored triglycerides to free fatty acids.
19
Q

Normal blood cholesterol levels?

A

200 mg/dl

after meal takes 5-7 hours to return to normal levels. (compared to glucose takes 1-2 hours)

20
Q

Apo proteins and types

A

The protein part of lipoprotein

ApoA- activator of LCAT (enzyme found in blood)
ApoB- involved in receptor lipoprotein interactions
ApoE- involved in receptor lipoprotein interactions
ApoC- activator of LPL

21
Q

Draw the pathway of lipoproteins from intestine to destination.

A

Mucosal cells absorbs FA + Cholesterol, intestine, TGL and CE reunited in

Intestine > lymph chylomicron, (TGL some CE and apoB48 on surface)

Lymph > blood stream via thoracic duct > left subclavian vein > RA of heart (where fat and apo protein mix)

HDL donates ApoC and ApoE in blood > join chylomicron

ApoC activates LPL in adipocytes > LPL breaks down lipoproteins and TGL to FA > stored as TGL

ApoC is give back to HDL > Chylomicron starts to shrink > now chylomicron remnant (residual TGL, CE, apoE and apoB-48)

Remnant receptors on liver dock with apoE and apoB > endocytosis into liver > esterasere (cleaves CE) > FA and cholesterol

22
Q

How long after high carb meal can TGL be used?

A

90 - 120 minutes.

23
Q

Chylomicron remnant

A

After LPL does it’s job chylomicron now just ApoE ApoB-48 and residual TGL and some CE.

Attaches to remnant receptor in liver

24
Q

What is the liver going to do with dietary cholesterol?

A

send out to blood as VLDL (mostly TGL and Chol.) and surface is apoB100.

VLDL will encounter HDL. HDL gives ApoC and Apo E

VLDL will now activate LPL when near. Take in TGL and cleave 3FA + glycerol

Becomes IDL which goes to liver.

25
Q

What turns on LPL?

A

Apo C and insulin

26
Q

Similarities of chylomicron and VLDL

A

Made by organ
Apo B, C, and E
Mostly TGL
Huge

27
Q

Differences in chylomicron and VLDL

A

Intestine (Chylomicron) vs liver (VLDL)
ApoB48 (chylomicron) vs ApoB100 (VLDL)
CE (Chylo) vs Cholesterol (VLDL)
Lymph vs blood

28
Q

What happens to LDL

A

LDL rich in cholesterol and CE

LDL binds to receptor through ApoB100, brought in via endocytosis (Cathrin coat).

Brought into lysosome.

Lysosomal esterase breaks ester bond (CE to Chol and FA)

29
Q

What happens to LDL receptors?

A

They are recycled back to the membrane. But some are lost during recycling.

Genes are turned on to add more receptors to wall.

If receptors are not there LDL will be higher in concentration in blood.

30
Q

Where does cholesterol come from?

A

Diet

De nova synthesis- from acetyl CoA. But this uses a lot of ATP.

31
Q

HMG CoA Reductase

A

Important for Cholesterol synthesis

32
Q

What is activated/inhibited when there is an increase in Chol in the cell.

A

Inhibits: HMG CoA Reductase, LDL receptor

Activates: ACAT for storage

33
Q

Low cholesterol leves inhibit/stimulate what?

A

Stimulate: HMG CoA Reductase, LDL receptor

Inhibit: ACAT for storage

34
Q

How do statin drugs work.

A

Inhibits HMG CoA Reductase, inhibits De Nova synthesis in the liver.

Lower cholesterol intake and through synthesis.

MCM test 2 (15 decks)

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