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CardioPulm Pre-Midterm > Lipids and Lipoproteins > Flashcards

Lipids and Lipoproteins Flashcards

1
Q

Major storage form of fatty acids are:

A

Triacylglycerols

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2
Q

Sources of Triacylglycerol

A

Dietary and de Novo (liver hepatocytes and adipocytes)

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3
Q

Progression of TG synthesis in Intestinal Cells

A

Dietary triacylglycerols → FA’s → Fatty acyl CoA → Diacylglycerol (DAG) → Triacylglycerol (TG) + apolipoproteins + other lipids → Chylomicron

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4
Q

What enzyme converts fatty acids to fatty acyl CoA?

A

fatty acyl CoA synthetase

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5
Q

Progression of TG synthesis from glucose in Hepatocytes

A

Glucose (via glycolysis) → DHAP + NADH → Glycerol-3-P

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6
Q

What enzyme is specific to TG synthesis in hepatocytes?

A

Glycerol kinase

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7
Q

Progression of TG synthesis from glycerol in Hepatocytes

A

Glycerol (free floating) + ATP + Glycerol kinase → Glycerol-3-P

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8
Q

Progression of TG synthesis de novo in Hepatocytes

A

Acetyl CoA (via de novo fatty acid synthesis) → fatty acid (enzyme fatty acyl CoA synthetase uses ATP to add CoA)→Triacylglyerol + apolipoproteins + other lipids→VLDL

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9
Q

VLDL stands for:

A

Very Low Density Lipolipids

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10
Q

What glucose membrane transporter imports glucose into adipocytes?

A

GLUT4

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11
Q

Chylomicron and VLDL + ?? lipase produces fatty acid

A

capillary lipoprotein lipase

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12
Q

Progression of TG synthesis from chylomicrons and VLDL in adipocytes

A

Via action of enzyme capillary lipoprotein lipase: Chylomicrons + VLDL (from intestinal and liver pathways) → fatty acid → Triacylglycerol (stored here in adipocytes)

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13
Q

Capillary lipoprotein lipase is stimulated by what hormone?

A

Insulin

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14
Q

DHAP (from glycolysis) becomes Glycerol 3-Phosphate via what adipocyte based dehydrogenase?

A

Glycerol 3-phosphate dehydrogenase

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15
Q

Breakdown of triacylglycerol occurs in

A

adipocytes

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16
Q

Promoters of triacylglycerol breakdown:

A

glucagon, epinephrine, norepinephrine

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17
Q

Inhibitor of triacylglycerol breakdown:

A

insulin

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18
Q

Which enzyme releases one fatty acid from triacylglycerol?

A

Hormone - sensitive lipase

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19
Q

Which enzyme releases one fatty acid from diacylglycerol?

A

Lipoprotein lipase

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20
Q

Which enzyme releases one fatty acid from monoacylglycerol?

A

Monoacyl-glycerol lipase

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21
Q

What is the product molecule following removal of all three fatty acids?

A

Glycerol

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22
Q

Short chain fatty acids are released into what? Where do they go?

A

Into blood stream and then the liver

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23
Q

Longer-chain fatty acids are bound to what and go where?

A

They are bound to albumin and go to the liver

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24
Q

Hormone-sensitive lipase (HSL) is activated via phosphorylation by what kinase?

A

PKA

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25
Q

PKA is activated by what?

A

Glucagon and epinephrine via cAMP and a GPCR signaling cascade

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26
Q

Hormone-sensitive lipase (HSL) is inactivated via dephosphorylation by what phosphatase?

A

Protein phosphatase 1 (PP1)

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27
Q

Protein phosphatase 1 is activated by what hormone?

A

Insulin

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28
Q

What is perilipin and why does anyone care?

A

Perilipin is a family of proteins that coat lipid droplets in adipocytes and muscle cells. They are a target of obesity treatment.

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29
Q

What do perilipins do?

A

They regulate lipolysis by controlling physical access of hormone-sensitive lipase to the fatty acids

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30
Q

The phosphorylation of perilipin allows what?

A

Phosphorylation allows Hormone-sensitive lipase access to fatty acids. Promotes lipolysis.

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31
Q

What phosphorylates perilipin?

A

PKA!

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32
Q

Olestra is what?

A

A synthetic fat

33
Q

Olestra is made of what?

A

a sucrose backbone with 6-8 fatty acids

34
Q

What was the point of olestra?

A

It is not absorbed in small intestine, therefore has no caloric value. Used as a fat substitute.

35
Q

What was the problem with olestra?

A

ANAL LEAKAGE. Also, too much of it caused deficiency of vitamins A,D,E and K.

36
Q

What are lipoproteins?

A

Proteins responsible for the transportation of cholesterol, triacylglycerols and fat soluble vitamins

37
Q

How many different types of lipoproteins are there?

A

5

38
Q

What are the five types of lipoproteins?

A

Chylomicrons, VLDL, IDL, LDL and HDL

39
Q

Give three distinguishing characteristics of Chylomicrons

A

Of the lipoproteins, they are the: Largest, Least dense and have the highest triacylglycerol content

40
Q

What apolipoproteins proteins are located in a Chylomicron?

A

ApoB-48, ApoC-II and ApoE

41
Q

What apolipoproteinsproteins are located in VLDL?

A

ApoB-100, ApoC-II and ApoE

42
Q

What apolipoproteinsproteins are located in IDL?

A

ApoB-100 and ApoE

43
Q

What apolipoproteinsproteins are located in LDL?

A

ApoB-100

44
Q

Is LDL a good or bad cholesterol particle?

A

Bad

45
Q

Is HDL a good or bad cholesterol particle?

A

Good

46
Q

What apolipoproteinsproteins are located in HDL?

A

ApoA-I, ApoC-II, Apo-E

47
Q

Three properties of HDL:

A

Smallest, most dense and has high protein and phospholipid content

48
Q

What are the three main roles of apolipoproteins?

A

Structural, transport and enzyme cofactors

49
Q

Type I Hyperlipoproteinemia is also know as:

A

Hyperchylomicronemia

50
Q

Type I Hyperlipoproteinemia is characterized by:

A

Inability to hydrolyze triacylglycerols in chylomicrons and VLDLs

51
Q

What causes Type I hyperlipoproteinemia?

A

Deficiency in either: Lipoprotein lipase (LPL) or ApoC-II

52
Q

How many forms of LPL deficiency are there?

A

Two, Primary LPL deficiency and ApoC-II deficiency

53
Q

When does primary LPL deficiency manifest?

A

In infancy

54
Q

When does ApoC-II deficiency manifest?

A

Post-adolescence

55
Q

Typer I hyperlipoproteinemia is characterized by triacylglycerol levels of what?

A

> 1000 mg/dL

56
Q

What are three clinical symptoms of Type I hyperlipoproteinemia?

A

Abdominal pain, acute pancreatitis and cutaneous eruptive xanthomas

57
Q

What is a treatment of Type I hyperlipoproteinemia?

A

Low fat diet

58
Q

Type II Hyperlipoproteinemia is also know as:

A

Familial Hypercholesterolemia

59
Q

What causes Type II hyperlipoproteinemia?

A

Defects in uptake of LDL via LDL receptor

60
Q

What does Type II hyperlipoproteinemia present with?

A

Increased cholesterol in blood and subsequent atherosclerosis

61
Q

Type II hyperlipoproteinemia causes impaired ability to recognize which apolipoprotein?

A

ApoB 100 on LDL

62
Q

Type II hyperlipoproteinemia is what type of inheritance?

A

Autosomal dominant

63
Q

Normal cholesterol levels are:

A

130-200 mg/dL

64
Q

Heterozygous LDL receptor mutation cholesterol levels:

A

300-500 mg/dL

65
Q

Homozygous LDL receptor mutation cholesterol levels:

A

> 800 mg/dL

66
Q

What do Type II hyperlipoproteinemia homozygous mutants die of if untreated? And when?

A

Coronary artery disease before teenage years

67
Q

What do Type II hyperlipoproteinemia heterozygous mutants die of if untreated? And when?

A

Coronary artery disease by age 40

68
Q

Physical symptoms Type II hyperlipoproteinemia:

A

Xanthomas, arcus senilis, corneal deposits in eye, angina pectoris

69
Q

What treatment do Type II hyperlipoproteinemia heterozygous mutants respond to?

A

Diet, statins and bile acid binding resins

70
Q

What treatment do Type II hyperlipoproteinemia homozygous mutants respond to?

A

LDL apheresis and liver transplantation

71
Q

What is the relationship between HDL cholesterol and Coronary artery disease?

A

More HDL cholesterol is correlated with less coronary artery disease

72
Q

HDL has anti______ and anti_____ properties

A

antioxidant and antiinflammatory

73
Q

HDL levels increase with:

A

weight loss, exercise, smoking cessation and moderate consumption of alcohol

74
Q

Antihypercholesteremic drugs, fibrates, niacin, antidiabetic thiazolidine drugs, estrogens, omega 3 fatty acids do what to HDL-C levels?

A

Increase them

75
Q

Smoking, progestins, androgens, beta blockers and high intake of omega-6/poly unsaturated fatty acids do what to HDL levels?

A

Decrease them

76
Q

What are statins?

A

Cholesterol lowering drugs

77
Q

Statins mimic what?

A

Structure of HMG CoA and Mevalonate

78
Q

What do statins do?

A

They competitively inhibit HMG CoA reductase, causing reduced cholesterol levels

CardioPulm Pre-Midterm (14 decks)

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