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CP Exam 2 > Lipids and Lipoproteins > Flashcards

Lipids and Lipoproteins Flashcards

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?

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?

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?

A

Protein phosphatase 1 (PP1) dephosphorylates and inactivates HSL

23
Q

What happens if we knockout hormone sensitive lipase?

A

Increase in DAG

24
Q

What are perilipins?

A

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

25
Q

Too much perilipin causes what?

What about knocking it out?

A

Overexpression- Inhibits lipolysis

Knocking out- increase in lipolysis

26
Q

Cholesterol is made by what cells and what is its fate?

What is the substrate for cholesterol?

A

The substrate for cholesterol is acetyl-coA.

Cholesterol is made by the liver, and then packaged into VLDL.

27
Q

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?

A

Cholesterol concentration is high in the blood because it is packaged into VLDL.

28
Q

What is the structure of lipoproteins?

A

Outside of the lipoprotein is made of one layer of phospholipids, free cholesterol and apoplipoproteins.

The inside, has TAGS and cholesterol esters.

29
Q

Lipoproteins contribute to lipid metabolism.

How?

A

-Act as ligands that bind to receptors and internalize lipoproteins

-Also activate many enzymes

30
Q

What are the 5 different types of lipoproteins?

A

1. Chylomicrons

2. VLDL

3. Intermediate density lipoproteins

4. LDL (bad cholesterol)

5. HDL (good cholesterol)

31
Q

Which lipoprotein has the most TAGs and least proteins?

Which lipoproteins have the least TAGS and most proteins?

A

Chylomicrons–> most TAGs and least proteins

HDL–> most proteins and least TAGS

32
Q

What apoproteins are on chylomicrons?

A
  1. ApoB-48–> helps transport in blood
  2. ApoC-II–> -activates the capillary lipoprotein lipase
  3. ApoE–> allows reuptake by the liver
33
Q

What apoproteins are on VLDL?

A

1. ApoB-100–> allow uptake into cells

2. ApoC-II–> activate capillary lipoprotein lipase

3. ApoE–> Allows uptake by the liver

34
Q

What apoproteins are on IDL?

A

Same as VLDL except ApoC-II- thus does not activate CLL

35
Q

What apoproteins are on LDL?

A

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
Q

What apoproteins are on HDL?

A

1, ApoC-11 (activates CLL)

2. ApoE (allows utake by the liver)

3. ApoA-I

37
Q

How do we process chylomicrons (make and degrade)?

A

—-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—-

  1. Capillary lipoprotein lipase breaks down TAG–> glycerol and FFA and releases ApoC-II
  2. Chylomicron remant is made.
  3. ApoE binds to its receptor on the liver and it is endocytozed
38
Q

Describe the process of VLDL, IDL and LDL processing.

A
  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
Q

How do we uptake LDL?

A

LDL receptor gets recycled and goes to the surdface of the cell to attract more LDL.

40
Q

What are the beneficial effects of HDL?

A
  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
Q

What helps in the maturation of the chylomicron?

A

HDL- donates Apo-E and Apo-C-11

42
Q

Type I hyperchylomicronemia

Cause:

Effects:

A

Cause: Deficiency in Apo-CII or lipoprotein lipase

Effects: Increase chylomicrons and TAGS

43
Q

Type II hypercholesterolemia

Cause:

Effects:

A

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
Q

Type 1 hyperchylomicronemia is the same thing as type I hyperlipoproteinemia.

In this, we cannot do what?

What cause it?

A

We cannot hydrolyze TAGS in chylomicrons and VLDL due to a deficiency in lipoprotein lipase or Apo C-II.

45
Q

Type 1 hyperchylomicronemia (type I hyperlipoproteinemia)

Primary LPO deficiency occurs when?

Apo C-defiency occurs when?

Plasma TAG levels are?

Clinical symptoms?

Tx?

A

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
Q

Type II hyperlipoproteinemia (hypercholesterolemia FH) is caused by?

What contrinutes to the 75% clearance of LDL in plasma?

A
  • Defects in the LDL receptor uptaking LDL.
  • Receptor-mediated endocytosis contributes to the 75% clearance of LDL in the plasma.
47
Q

Type II hyperlipoproteinemia (hypercholesterolemia FH) causes

A

Artherolscerosis.

-Cant recognize ApoB-100 on the LDL

xanthomq

48
Q

Type II hyperlipoproteinemia (hypercholesterolemia FH)

  • Normal cholesterol
  • Differences between heterozygous and homozygous
A
  • 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
Q

Type II hyperlipoproteinemia (hypercholesterolemia FH) sx?

A

Xanthomas

CAD (arthersclerosis)

CP Exam 2 (27 decks)

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