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Cardiopulmonary Exam 1 > Zaidi: Lipids and Lipoproteins > Flashcards

Zaidi: Lipids and Lipoproteins Flashcards

1
Q

TG

A

Triacylglycerols

Major storage form of fatty acids

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2
Q

TG composition

A

one glycerol group and three fatty acid chains

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3
Q

Dietary TG is processed where

A

in the intestinal cells

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4
Q

De Novo TG synthesis occurs

A

in liver hepatocytes and adipocytes

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5
Q

TG Synthesis in Intestinal Cells: sequence

A

TGs are broken down in the lumen of the intestine into

1) FAs
2) 2-monoacylglycerol
Both are transported across the epithelia. Inside, FAs are converted to
1) Fatty acyl CoA
and 2-monoacylglycerol is converted into
1) Diacylglycerol.
Fatty acyl CoA and diacylglycerol are combined to produce Triacylglycerols (TGs), which are packaged with
apolipoproteins and other lipids to form CHYLOMICRONS

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6
Q

After TGs are reassembled in the intestinal cell, what happens

A

they are combined with apoproteins and lipids = chylomicrons

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7
Q

In the liver, there are a number of events leading to TG synthesis: what are the “big” initial steps

A

Glucose is converted into DHAP, which is reduced and combined with an oxidized form of glycerol to form Glycerol-3-P.

G3P is combined with fatty acyl CoA to form a number of intermediates, eventually TG

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8
Q

fatty acyl coA is responsible for

A

activating fatty acids that have been transported from the lumen into fatty acyl CoA inside the cell

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9
Q

Glucose is converted into G3P by

A

G3P Dehydrogenase

Hepatocyes

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10
Q

Glycerol is converted into ___ by _____

A

Glycerol 3P by Glycerol Kinase

Hepatocytes

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11
Q

In the liver, de novo FAs are initially

A

converted into FA-CoA by FA-CoA Synthase, eventually combined with G3P, and subsequently comverted into TG and repackaged into chylomicrons

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12
Q

TG synthesis in adipocytes: what two processes occur before production of a TG happens?

A

Glucose is broken down via glucose and transformed into G3P.

FA is broken down into FA-CoA

G3P and FA-Coa are combined to eventually form TG and stored

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13
Q

What enzyme activates FA into FA-CoA?

A

FA-CoA Synthase

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14
Q

VLDL is produced in the

A

hepatocyte and released into the blood

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15
Q

Capillary Lipoprotein Lipase

A

Chylomicrons and LDLP are delivered to the adipocyte.

CLPL break these down into FA’s

found in the adipocyte:

breaks down lipoproteins and VLDL to form glycerol and FAs. these are internalized and used for TG formation

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16
Q

In which cell is glucose converted to glycerol by Glycerol kinase?

A

Hepatocyte. Does not happen in the adipose cell, which uses glycolysis followed by G3P Dehydrogenase to produce Glycerol-3-P

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17
Q

which enzyme is used by hepatocytes to form glycerol but not in adipocytes?

A

glycerol kinase

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18
Q

What is the source of glycerol in the hepatocyte

A

it’s moving around freely because of the breakdown of TG but also because of glycolysis

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19
Q

where is glycerol kinase found?

A

the liver only

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20
Q

CLPL

A

made by adipocyte but RELEASED out of the adipocyte

breaks down VLDL and chylomicrons into the FAs, which are then used to form TGs inside the cell

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21
Q

where is the source of glycerol in adipocyte?

A

glycolysis, but lacks the glycerol kinase

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22
Q

Insulin acts on which enzyme in the adipocyte?

A

capillary lipoprotein lipase

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23
Q

What does Insulin mobilize in adipocytes?

A

the breakdown of VLDL and chylomicrons by capillary lipoprotein lipase

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24
Q

TG are broken down where

A

adipocytes

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25
Q

why don’t hepatocytes or intestinal cells break down TG?

A

they deliver TGs to different locations, but its hepatocytes that are primarily responsible for breaking down the TGs

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26
Q

What three enzymes do we find in the adipocyte involved in TG breakdown (just name them)

A

hormone sensitive lipase
lipoprotein lipase
monoacyl-glycerol lipase

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27
Q

hormone sensitive lipase is activated ( -/+) by

A

norepinephrine and epinephrine and glucagon (+)

insulin (-)

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28
Q

hormone sensitive lipase does what?

A

mobilizes TGs into FA and DAG

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29
Q

Lipoprotein Lipase is found where and does what

A

adipocyte

converts DAG into an FA and a monoacylglycerol

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30
Q

monoacyl-glycerol lipase does what

A

converts monoacyl glycerol into FA and glycerol

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31
Q

FAs in the adipocyte leave according to size

A

shorts FAs are soluble and diffuse out, long FAs are combined with albumin to exit

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32
Q

HSL is activated directly by

A

Hormone Sensitive Lipase is activated by phosphorylation by PKA

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33
Q

PKA does what

A

“ultimately” activates HSL

is activated by hormones via cAMP (GCPR) signaling cascade

it phosphorylates Hormone Sensitive Lipase (HSL) to initiate TG breakdown

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34
Q

Hormone Sensitive Lipase is inactivated by

A

Protein Phosphatase 1 (DP1)

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35
Q

How does DP1 act in the cell?

A

it is INACTIVATED by insulin

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36
Q

Epinephrine and Glucagon promote

A

lipolysis

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37
Q

Insulin inhibits

A

lipolysis

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38
Q

Glucaon is released in response to

A

hunger

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39
Q

Epinephrine is released in response to

A

exercise

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40
Q

Insulin is released in response to

A

high carb meal

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41
Q

Perilipin

A

family of proteins that coats lipids in adipocytes and muscle cells

REGULATED BY PKA

regulates LIPOLYSIS by blocking physical access to HSL

overexpression leads to inhibition of lipolysis and knock out the revers effect

target of anti-obesity drugs

42
Q

what does perilipin do exactly? who controls it?

A

it blocks physical access HSL

PKA

43
Q

Perilipin coats

A

lipid droplets and prevents HSL from activating their degradation

44
Q

Synthetic FATs

A

Olestra

45
Q

what are synthetic fats made from?

A

synthetic fats made of sucrose backbone with 6-8 fatty acids

no absorbed in small intestine

no calories

excreted out in stool

absorb vitamins A, D, E, K

high amounts of olestra

cause deficiency in these vitamins

abdominal cramps, bloating and diarrhea

46
Q

Olestra

A

synthetic fatty acid that humans lack an enzyme to breakdown

absorbs K.A.D.E, so depletes you of vitamins

causes bloating, diarrhea etc

sucrose with a backbone of 6-8 fatty acids

47
Q

Lipoproteins serve what purposes,

A

transport form for TG, cholesterol, and fat soluble vitamins

48
Q

Structure of the lipid: outershell and inner shell

A

outer: monolayer of phospholipids, free cholesterol, apoproteins

inner hydrophobic TGs, cholesterol esters

49
Q

ACAT

A

Acyl CoA Acyl Transferase (ACAT)

50
Q

ACAT

A

Transfers acyl groups to cholesterol to make them hydrophobic (cholesterol —> cholesterol-estor)

cholesterol ester

51
Q

5 different types of lipoproteins

A
  1. chylomicron
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
52
Q

Chylomicrons

A

largest and least dense of the lipoproteins
High TG content

ApoB-48 and ApoC-II and ApoE

53
Q

What the three surface apoproteins associated with chylomicrons?

A

ApoB-48
Apo-E
Apo-C-II

exogenous, formed from dietary fats

54
Q

VLDL

A

ApoB-100
ApoE
ApoC-II

55
Q

IDL

A

ApoB-100

ApoE

56
Q

LDL

A

ApoB-100

57
Q

HDL properties

A

smallest, most dense, high protein and phospholipid content

58
Q

swelling in LNs found in infections and cancer

A

non-Hodgkin lymphoma

59
Q

Apolipoprotein functions

A

Structural, Transport, Cofactors for Enzymes

60
Q

Apolipoproteins function: structural

A

stabilizes lipoproteins

61
Q

Apolipoproteins function: transport

A

redistribution of lipids between tissues

62
Q

Apolipoproteins finction: coenzymes

A

Apo-CII activates LPL

63
Q

Type I Hyperchylomicronemia

A

AKA hyperchylomicronemia

Deficiency in Apo-C-II OR

defective lipoprotein lipase

the effect is to elevate chylomicrons and TGs

inability to hydrolyze TAGs, chylomicrons, VLDL

64
Q

When is Type I Hyperchylomicronemia diagnosable?

A

Primary LPL deficiency in infancy

ApoC-II deficiency, post adolescence

65
Q

What is a treatment for Type I Hyperlipoprotenemia?

A

low fat diet

66
Q

Clinical symptoms of type I hyperlipoprotenemia

A

abdominal pain, acute pancreatitis

67
Q

Type II hyperlipoproteinemia

A

AKA familial hyperchylomicronemia (FH)

68
Q

Type II hyperlipoproteinemia: Cause

A

defects in LDL uptake via LDL receptor

69
Q

Type II hyperlipoproteinemia: what is impaired?

A

LDL receptor fails to recognize ApoB 100 on LDL

70
Q

Type II hyperlipoproteinemia: long term problems

A

LDL adding to athersclerosis

71
Q

Type II hyperlipoproteinemia: genetics

A

autosomal dominant inheritance

72
Q

Normal cholesterol is

A

130-200 mg/dl

73
Q

cholesterol for heterozygous Type II hyperlipoproteinemia is

A

300-500 mg/dl

74
Q

homozygous for Type II hyperlipoproteinemia is

A

> 800 mg/dl

75
Q

untreated homozygous die from

A

coronary heart disease CAD befroe teenager years

76
Q

untreated homozygous develop CAD by

A

age 40

77
Q

Two sources of G3P in the liver

A

when glycerol kinase phosphorylates glycerol or when DHAP is reduced

78
Q

insulin stimulates adipocytes to secrete

A

capillary lipoprotein lipase, which recognizes ApoC-II in chylomicrons and VLDL

79
Q

PKA is activated by ___ which allows the PKA to do what?

A

glucagon, phosphorylate HSL

80
Q

Protein Phosphatase 1 does what?

A

it dephosphorylates HSL

81
Q

PP1 is activated by

A

insulin

82
Q

Good Cholesterol: content and Apos

A

high protein and phospholipid content
ApoA-I
ApoE
ApoC-II

83
Q

Chylomicron processing

A
  1. nascent chylomicrons are synthesized in the liver and transported via lymphatics to the bloodstream
  2. mature chylomicron is produced when HDL adds ApoC -II and ApoE
  3. Chylomicron ApoC-II is recognized by CLPL, which hydrolyzes TGs into glycerol and FAs: ApoC is released back to HDL
  4. FAs and glycerol are endocytosed by binding ApoE
84
Q

abetalipoproteinemia

A

lack of ApoB’s

85
Q

VLDL, IDL, LDL prcoessing

A
  1. VLDL is released by the liver. ApoCII is recognized by CLPL, breaks down VLDL. ApoCII released back to HDL.
  2. The remaining molecule is IDL. Cholesterol in the IDL is released via the receptor recognition of ApoE.
  3. IDL loses more TGs and via hepatic lipoprotein lipase s well as ApoE —> becomes LDL
  4. LDL delivers cholesterol to the liver and peripheral tissues via binding of ApoB-100 to LDL receptors on targets cells etc.
86
Q

HDL processing

A
  1. HDL is produced in the liver
  2. it is released and picks up cholesterol from tissues
  3. is esterfies cholesterol
  4. it exchanges estrified cholesterol with VLDL, IDL, LDL for TGs and phospholipids
  5. it exchanges and receives ApoE and ApoC-II with VLDL, IDL, LDL
  6. VLDL, IDL, LDL deliver cholesterol to liver
87
Q

Type I Hyperlipoproteinemia

Cause, Effect

A

Deficiency in ApoC or LPLs

Surge of TGs and Chylomicrons

88
Q

Type II Hyperlipoproteinemia

Cause Effect

A

Deficiency in LDL receptor

Surge in Cholesterol, TGs, LDL, VLDL

89
Q

Type III hyperlipoproteinemia

A

AKA familial dysbetalipoproteinemia

Defect in ApoE

Surge in cholesterol, Chylomicon remnants, TGs, IDL

90
Q

Type IV hyperlipoproteinemia

A

aka familial hypertriglyceridemia

Reduction in catabolism of VLDLs or increase in their synthesis

Surge in cholesterols (slightly), TGs, VLDL

91
Q

Type V hyperlipoproteinemia

A

combination of I and IV

surge in chylomicrons, VLDL, TGs but normal LDL

92
Q

Tangier disease

A

defect in transporter that supports cholesterol pickup by nascent HDL

93
Q

abetalipoprotenmia

A

Lack of ApoB’s

decrease in chylomicrons and VLDL, IDL, LDL

94
Q

hpoalphaliporproteinemia

A

accelerated catabolism of ApoA I an II

decrease in HDL

95
Q

HDL’s beneficial effects

A

because of its ability to receive cholesterol from peripheral tissues, HDL increase is considered to confer benefits like reduced CAD.

HDL is increased by exercise, smoking cessation, moderate alcohol consumption, and antihyercholestermic drugs and weight loss

96
Q

HDL levels are low in

A

smoking, progestin, androgens, beta blockers, and high intake of PUFA (omega-6)

97
Q

Statins

A

statins mimic the structure of HMG CoA and Mevalonate (substrate and product of HMG Co-A Reductase

98
Q

HMG CoA Reductase

A

rate limiting enzyme in cholesterol biosynthesis
Statins are competitive inhibitors of HMG CoA Reductase
enhance transcription of LDL receptor
more uptake into hepatocytes, lowering plasma levels w

99
Q

Lovastatin

A

targets HMG CoA Reductase

100
Q

what is the rate limiting step in cholesterol biosynthesis?

A

HMG-CoA reductase converting HMG-CoA along with NADPH reducing HMG-CoA into Mevalonic Acid. Mev is eventually converted into cholesterol

Cardiopulmonary Exam 1 (21 decks)

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