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Cardio/Pulm Final > Lecture 17: Lipids and Lipoproteins > Flashcards

Lecture 17: Lipids and Lipoproteins Flashcards

1
Q

Major storage form of FA’s?

A

TAG’s

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2
Q

TAG’s are made de novo where?

A

Hepatocytes and Adipocytes

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3
Q

Dietary TAG’s are processed where?

A

Intestinal cells

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4
Q

Dietary TAG’s are broken down into what in the intestinal lumen?

A

MAG and FFA

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5
Q

Resynthesizing TAG’s by intestinal cells uses what as the backbone and which enzyme?

A

MAG as the backbone; Fatty acyl CoA synthetase

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6
Q

TAG’s made by intestinal cells are packaged with apolipoproteins and other lipids to form?

A

Chylomicrons

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7
Q

Where are chylomicrons released and enter blood via?

A

Lymphatic system and enter blood via thoracic duct

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8
Q

What are the starting molecules for TAG synthesis in the liver?

A

Glucose + Glycerol

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9
Q

Glucose and glycerol combine to form the backbone for TAG synthesis in liver, which is?

A

Glycerol 3-phosphate

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10
Q

What enzyme is ONLY present in the liver?

A

Glycerol kinase

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11
Q

Fatty acids in hepatocytes are synthesized how?

A

De novo

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12
Q

TAGs packaged with apolipoproteins and other lipids from hepatocytes form?

A

Very Low Density Lipoproteins (VLDL)

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13
Q

Where are VLDL’s released?

A

Bloodstream

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14
Q

Source of the glycerol (G-3-P) backbone in adipocytes?

A

Glucose

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15
Q

What are the source of FA’s for TAG synthesis in adipocytes?

A

Come from the breakdown of Chylomicrons and VLDL’s

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16
Q

What cuts the TAG’s from VLDL’s and Chylomicrons, releasing the FA’s for adipocytes to use in resynthesizing TAG’s?

A

Capillary lipoprotein lipase

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17
Q

What happens to the TAG’s made by adipocytes?

A

Stored in adipocytes

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18
Q

3 major lipases for breakdown of TAGs?

A

1) Hormone sensitive lipase (HSL)
2) Lipoprotein lipase (LPL)
3) Monoacylglycerol lipase (MAG lipase)

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19
Q

Long chain fatty acids require what for transport?

A

Complexed with Albumin

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20
Q

HSL activity is modulated by?

A

Phosphorylation

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21
Q

The 2 major signals that promote mobilization of TAGs; hormones involved?

A

1) Hunger - glucagon

2) Exercise - epinephrine

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22
Q

What inhibits the mobilization of TAGs?

A

Insulin inhibits lipolysis (FED STATUS)

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23
Q

What acts before HSL and activates it during lipolysis?

A

ATGL - adipose triglyceride lipase

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24
Q

What is Perilipin?

A

Family of proteins that coat lipid droplets in adipocytes and muscle cells.

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25
Q

How does Perilipin regulate lipolysis?

A

By controlling physical access to HSL (surrounds the lipid droplet)

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26
Q

In mice with overexpression of Perilipin what is observed?

A

Inhibition of lipolysis

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27
Q

In mice with Perilipin knocked out what is observed; significance?

A

Increases lipolysis; target of obesity tx

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28
Q

Perilipin is regulated by, how?

A

PKA, phosphorylation causes release of lipid droplet so it can associate with HSL, promoting lipolysis.

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29
Q

Function of lipoproteins?

A
  • Serve as transport vehicle for cholesterol, TAGs, and fat soluble vitamins
  • Contribute to the metabolism of lipids
30
Q

What is contained in the outer shell of lipoproteins?

A

Monolayer of phospholipids, free cholesterol, and apolipoproteins

31
Q

What is contained in the inner core of lipoproteins?

A

Packed with hydrophobic TAG’s, cholesterol esters

32
Q

What are the 5 types of lipoproteins?

A

1) Chylomicrons
2) VLDL
3) IDL
4) LDL
5) HDL

33
Q

Properties of Chylomicrons?

A
  • Largest
  • Least dense
  • High TAG content
34
Q

Function of ApoB-48 on chylomicron?

A

Facilitates transport

35
Q

Function of ApoC-II on chylomicron?

A

Activates capillary lipoprotein lipase which degrades the TAG

36
Q

Function of ApoE on chylomicron?

A

Facilitates uptake into liver (binds receptor)

37
Q

What makes LDL worse than VLDL?

A

LDL contains less TAG’s and more cholesterol

38
Q

Properties of HDL?

A
  • Smallest
  • Most dense
  • High protein and phospholipid content
39
Q

What can HDL do with ApoC-II and ApoE?

A

Can exchange with other lipoproteins allowing them to be more active

40
Q

When a chylomicron is first assembled with dietary lipids in the intestine what is it referred to, why?

A
  • Nascent Chylomicron

- Doesn’t have ApoE or ApoC-II

41
Q

When a chylomicron becomes mature what happens to it?

A

Acted on by capillary LPL, which hydrolyzes TAG’s into glycerol and FFA’s, creates a Chylomicron remnant

42
Q

What happens to a chylomicron remnant?

A

Endocytosed by the liver via binding of ApoE to its receptor

43
Q

VLDL’s are assembled in liver and already contain?

A

ApoC-II and ApoE

44
Q

Describe what happens during the processing of VLDL in the blood?

A

VLDL is acted on by capillary LPL, hydrolyzing the TAG’s into FFA and glycerol. ApoC-II is released back to HDL, and IDL remains

45
Q

What happens to cholesterol in IDL?

A

Cholesterol in IDL is delivered to the liver via bind of ApoE to IDL receptors on hepatic cells.

46
Q

How does IDL lose more TAG’s; becomes?

A

Via action of hepatic lipoprotein lipase; becomes LDL

47
Q

What happens to LDL?

A

Delivers cholesterol load to the liver and peripheral tissue via binding of ApoB-100 to LDL receptors on target cells

48
Q

Function of ApoB-100?

A

Binds the LDL receptor on cells, allowing for the cell to internalize the LDL

49
Q

What happens upon internalization of LDL by cells?

A

LDL is sent to lysosomes where it is chopped up, and the raw materials are released

50
Q

What happens when there are defects in the LDL receptor?

A

LDL is NOT taken up and will sit in blood forming plaques (familial hyperlipidemia)

51
Q

Where is HDL synthesized?

A

Liver and Small intestines

52
Q

What does nascent HDL do?

A

Picks up cholesterol from peripheral tissues

53
Q

What enzyme allows for the esterification of cholesterol inside of HDL?

A

Lecithin cholesterol acyl transferase

54
Q

Function of cholesterol ester transfer protein?

A

Allows for HDL to transfer cholesterol esters to VLDL, IDL, and LDL in exchange for TAG’s and phospholipids

55
Q

HDL has the ability to reverse what?

A

Cholesterol transport from peripheral tissues to liver

56
Q

What are some recently discovered properties of HDL?

A

Antioxidant and Anti-inflammatory

57
Q

Type I Hyperlipoproteinemia (aka hyperchylomicronemia) is caused by?

A

A deficiency in Lipoprotein Lipase (LPL) or ApoC-II

58
Q

Type I Hyperlipoproteinemia effects?

A

Inability to hydrolyze TAG’s in chylomicrons and VLDL

59
Q

A primary LPL deficiency manifests when?

A

Infancy (more serious)

60
Q

ApoC-II deficiency manifests when?

A

Post-adolescence

61
Q

Type I Hyperlipoproteinemia follows what genetic inheritance pattern?

A

Autosomal recessive (both alleles need to be bad)

62
Q

Clinical symptoms and tx for Type I Hyperlipoproteinemia?

A

Sx: Abdominal pain, acute pancreatitis, cutaneous eruptive xanthomas

Tx: Low fat diet

63
Q

Plasma TAG levels will be at what level in Type I Hyperlipoproteinemia?

A

> 1000 mg/dL (very high)

64
Q

Type II Hyperlipoproteinemia (aka hypercholesterolemia) is caused by?

A

Defects in uptake of LDL via LDL receptor; impaired ability to recognize ApoB-100 on LDL

65
Q

75% of the clearance of LDL in plasma is accomplished via?

A

Receptor mediated endocytosis via LDL receptor

66
Q

Type II Hyperlipoproteinemia follows what type of inheritance pattern?

A

Autosomal dominant (only need one bad allele)

67
Q

Heterozygous Type II Hyperlipoproteinemia manifests when and correlates with what cholesterol level?

A
  • In middle age

- 300-500 mg/dL

68
Q

Homozygous Type II Hyperlipoproteinemia manifests when and correlates with what cholesterol level?

A
  • In teens

- >800 mg/dL

69
Q

If untreated homozygous Type II Hyperlipoproteinemia patients will die of?

A

Coronary artery disease (CAD) before teenage years

70
Q

Tx for heterozygous Type II Hyperlipoproteinemia?

A

Statins, diet, and bile acid binding resins

71
Q

Tx for homozygous Type II Hyperlipoproteinemia?

A

LDL apheresis and liver transplantation

Cardio/Pulm Final (18 decks)

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