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CP Exam 2 > Lipids and Lipoproteins > Flashcards

Lipids and Lipoproteins Flashcards

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1
Q

TAGS are the major storage form of fatty acids with a glycerol backbone and 3 FA.

TAGS have ____ more energy than stored glycogen (carbs).

A

7x

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2
Q

What are our three sources of TAGS?

A
  1. Dietary TAGS, processed in our intestinal cells.
  2. De novo TAG from our hepatocytes and adipocytes
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3
Q

Describe the process of TAG synthesis in the intestines

A

1. Dietary TAGS are consumed

2. Pancreatic lipases in the intestinal lumen [TAG–> MAG and 2 FA].

3. MAG and 2 FA go absorbed into the intestinal cell

4. [MAG + 2 FA] –> [fatty acyl CoA synthetase]–> Fatty acyl CoA

5. Fatty acyl CoA–> DAG

6. DAG–> TAG

7. TAG + apolipoproteins + other lipids–> [CHYLOMICRONS]

8. Chylomicrons then enter the lymphatic system

9. Exit the thoracic duct

10. Go into the blood.

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4
Q

If we are starving, are we forming chylomicrons?

A

No, because we are not ingesting dietary TAGS.

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5
Q

What promotes TAG synthesis in the intestines?

A

Dietary TAGS

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6
Q

What are the two ways we can make TAGs in the liver?

A

1. Glycolysis

2. De novo synthesis

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7
Q

Describe the process of TAG synthesis in the liver

A

A. Glycolysis

  • Glucose (main driver) undergoes glycolysis–> DHAP
  • DHAP–> [GAP3DH]–> G3P

*Glycerol–>[Glycerol kinase]–> G3P

B. De novo synthesis

-Acetyl coA–> FA

FA–> [Fatty acyl CoA synthetase]–> Fatty acyl coA

C. Common pathway

  • G3P + FFA
  • DAG–> TAG
  • TAG + apolipoproteins+ lipids+ cholesterol–> VLDL
  • VLDL–> bloodstrem
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8
Q

If you want to inhibit the formation of of G3P from glycerol, and not impact any other cell in the body, what enzyme would you target?

A

Glycerol kinase- it is SPECIFIC to the liver.

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9
Q

What makes the backbone of our TAG?

A

Glycerol is made from G3P

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10
Q

What promotes the TAG synthesis in hepatocytes?

A

Excess carbohydrates

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11
Q

What are our sources of TAG in adipocytes (3)?

A

1. Chylomicrons

2. VLDL

3. Glucose

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12
Q

Describe the process of TAG synthesis in the adipocytes

A

A. Glycolysis

  • Glucose enters the adipocyte via GLUT-4 transporters
  • Glucose–> GAP3DH–> G3P

B. Chylomicrons and VLDL

  • Chylomicrons and VLDL in the bloodstrem are broken down via capillary lipoproitein lipase into FA
  • FA–> Fatty Acyl Co-A

C. Common Pathway

  • Fatty acyl Co-A+ G3P
  • DAG–TAG

–> stay in adipocytes; stored.

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13
Q

In adipocytes, what causes glucose to enter the cell and VLDL and chylomicrons to be broken down into FA, which will then enter the adipocyte?

A

+ insulin

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14
Q

TAG synthesis in the adipocytes is promoted by excess _______.

A

Carbs

and

fats

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15
Q

What is the only cell that stores TAGs?

A

Adipocytes

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16
Q

Where does mobilization of TAGS occur?

A

Adipocytes, because they are the only cell that stores the adipocytes.

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17
Q

Describe the process of mobilization of TAGs.

A

Occurs in the adipocytes

1. TAGS–>[ATGL* and hormone sensitive lipase]–>DAG, with release of a FA

2. DAG–>[hormone sensitive lipase* and lipoprotein lipase]–> MAG, with release of a FA

3. MAG–> [MAG lipase]–> free glycerol, with release of a FA

4. Short chain FA leave the adipocyte and undergo B oxidation in mT (long chain FA do the same, however they have to be bound to albumin).

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18
Q

Describe how we activate hormone sensitive lipase.

A

+ Glucagon

+NE

+ EPI

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19
Q

What enzymes are involved in the breakdown of TAG? (4)

A
  1. ATGL
  2. Hormone-sensitive lipase (activated by glucagon, EPI and NE)
  3. Lipoprotein lipase
  4. MAG lipase
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20
Q

What modulates the activity of HSL?

Study These Flashcards
A

Hormones (glucagon, EPI) bind to a GCPR.

  • Glucagon is relased when we are hungry
  • EPI is released when we are excercising

GCPR will then increase AC, cAMP, PKA

PKA phosphorylates HSL to activate it.

Thus, phosphorylation.

21
Q

What inhibits HSL phosphorylation?

Study These Flashcards
A

Fed status (insulin)

because we do not want to break down the TAG

22
Q

When we are in fed state, how do we inacitvate HSL?

Study These Flashcards
A

Protein phosphatase 1 (PP1) dephosphorylates and inactivates HSL

23
Q

What happens if we knockout hormone sensitive lipase?

Study These Flashcards
A

Increase in DAG

24
Q

What are perilipins?

Study These Flashcards
A

Perilipins control lipolysis by coating lipids in adipocytes and muscle cells, proteing them from being targeted by HSL.

25
Too much perilipin causes what? What about knocking it out?
Overexpression- Inhibits lipolysis Knocking out- increase in lipolysis
26
Cholesterol is made by what cells and what is its fate? What is the substrate for cholesterol?
The substrate for cholesterol is **acetyl-coA**. Cholesterol is made by the **liver**, and then packaged into **VLDL**.
27
Lipoproteins transport cholesterol, cholesterol esters, TAGS and fat soluble vitamins. Cholesterol is hydrophobic and not soluble in the blood. Thus, why is its concentration in the blood high?
**Cholesterol concentration is high in the blood because it is packaged into VLDL.**
28
What is the structure of lipoproteins?
Outside of the lipoprotein is made of one layer of **phospholipids**, **free cholesterol** and **apoplipoproteins**. The inside, has **TAGS** and **cholesterol esters.**
29
**Lipoproteins contribute to lipid metabolism.** **How?**
**-Act as ligands** that bind to receptors and internalize lipoproteins -Also activate many enzymes
30
What are the **5** different types of lipoproteins?
**1. Chylomicrons** **2. VLDL** **3. Intermediate density lipoproteins** **4. LDL (bad cholesterol)** **5. HDL (good cholesterol)**
31
Which lipoprotein has the most TAGs and least proteins? Which lipoproteins have the least TAGS and most proteins?
**Chylomicrons**--\> most TAGs and least proteins **HDL**--\> most proteins and least TAGS
32
What apoproteins are on chylomicrons?
1. **ApoB-48**--\> helps transport in blood 2. **ApoC-II--\>** -activates the capillary lipoprotein lipase 3. **ApoE**--\> allows reuptake by the liver
33
What apoproteins are on VLDL?
**1. ApoB-100--\> allow uptake into cells** **2. ApoC-II--\> activate capillary lipoprotein lipase** **3. ApoE--\> Allows uptake by the liver**
34
What apoproteins are on IDL?
Same as VLDL except ApoC-II- thus does not activate CLL
35
What apoproteins are on LDL?
**Only ApoB-100-** allow uptake into cells. If LDL is taken up by a cell, its good. If it lingers in our blood, it can cause a build up of plaque.
36
What apoproteins are on HDL?
**1, ApoC-11 (activates CLL)** **2. ApoE (allows utake by the liver)** **3. ApoA-I**
37
How do we process chylomicrons (make and degrade)?
**----Maturation---** 1. Nascent chylomicrons (those with only Apo-B48) are made in the SI--\> lymphatic system--\> thoracic duct--\> blood stream 2. HDL adds **ApoC-II** and **Apo-E** to the nascent chymicron--\> mature chylomicron **----Breakdown----** 3. Capillary lipoprotein lipase breaks down TAG--\> *glycerol* and *FFA* and releases *ApoC*-II 4. Chylomicron remant is made. 5. ApoE binds to its receptor on the liver and it is endocytozed
38
**Describe the process of VLDL, IDL and LDL processing.**
1. **VLDL (ApoC-II, ApoE, ApoB-100**) are made in the liver--\> blood stream 2. [VLDL]--\>+capillary lipoprotein lipase is activated, causing the release of ApoC-II, glycerol and FFA--\> [IDL] 3. ApoE on IDL binds to the ApoE-R on the hepatic cells, delivering cholesterol 4. Hepatic lipoprotein lipase acts on IDL and causes it to lose TAGS and ApoE --\>[LDL] 5. ApoB-100 on LDL binds to ApoB-100-R and deliver cholesterol to liver and peripheral tissue.
39
How do we uptake LDL?
**LDL receptor gets recycled and goes to the surdface of the cell to attract more LDL.**
40
What are the beneficial effects of HDL?
1. High HDL--\> decrease risk for coronary artery disease (CAD) 2. important for maturation of chylomicrons 3. Reverse cholesterol transport: removes LDL from periphery and takes it to the liver where it is recycled and processed. 4. Anti-oxidant and anti-inflammatory effects 5. Weight loss
41
What helps in the maturation of the chylomicron?
HDL- donates Apo-E and Apo-C-11
42
**Type I hyperchylomicronemia** ## Footnote Cause: Effects:
Cause: **Deficiency in Apo-CII or lipoprotein lipase** Effects: **Increase chylomicrons and TAGS**
43
**Type II hypercholesterolemia** ## Footnote Cause: Effects:
Cause: LDL receptor is completely (IIa) or partially defective (IIb) Effects: Increases cholesterol and LDL, TAGs are normal in IIa but inncreased in IIb, VLDL is increase in IIb
44
Type 1 hyperchylomicronemia is the same thing as type I hyperlipoproteinemia. In this, we cannot do what? What cause it?
We cannot hydrolyze TAGS in **chylomicrons and VLDL** due to a deficiency in lipoprotein lipase or Apo C-II.
45
Type 1 hyperchylomicronemia (type I hyperlipoproteinemia) ## Footnote **Primary LPO deficiency occurs when?** **Apo C-defiency occurs when?** **Plasma TAG levels are?** **Clinical symptoms?** **Tx?**
**Primary LPL deficiency occurs when?** Infancy **Apo C-defiency occurs when?** Adolescence **Plasma TAG levels are?** \>1000mg/dl **Clinical symptoms?** Xanthomas **Tx?** low fat diet
46
Type II hyperlipoproteinemia (hypercholesterolemia FH) is caused by? What contrinutes to the 75% clearance of LDL in plasma?
- Defects in the LDL receptor uptaking LDL. - Receptor-mediated endocytosis contributes to the 75% clearance of LDL in the plasma.
47
Type II hyperlipoproteinemia (hypercholesterolemia FH) causes
Artherolscerosis. -Cant recognize ApoB-100 on the LDL xanthomq
48
Type II hyperlipoproteinemia (hypercholesterolemia FH) - Normal cholesterol - Differences between heterozygous and homozygous
- Cholesterol is normally is 130-200 mg/dl - Heterozygous is 300-500 mg/dl, while those that are homozygous have \>800. - Those **heterozygous can use diets, statins, bile acid binding resins** - **Homozygous needs LDL apheresis and liver transplantation.**
49
Type II hyperlipoproteinemia (hypercholesterolemia FH) sx?
Xanthomas CAD (arthersclerosis)

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