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Biochem Spring > Chapter 16- Fatty Acids and Eicosanoids > Flashcards

Chapter 16- Fatty Acids and Eicosanoids Flashcards

1
Q

What is a positive modulator of lipolysis?

A

glucagon or epinephrine

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2
Q

What does CPTI do?

A

transport acyl-CoA into mitochondria

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3
Q

What is lipolysis?

A

hydrolysis of TAGs in adipocytes -> forms free FA

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4
Q

what is a negative modulator of CPTI?

A

malonyl-CoA

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5
Q

In ketogenesis Fatty acyl-CoA can be converted to

A

2 Acetyl-CoA or Acetoacetyl-CoA (beta-oxidation)

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6
Q

Acetoacetyl-CoA is synthesized from what?

A

2 acetyl-CoA catalyzed by thiolase in starvation

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7
Q

In fed state what is the fate of acetyl-CoA?

A

TCA cycle -> glucose via gluconeogenesis

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8
Q

In ketogenesis what is acetoacetyl-CoA converted to and by what enzyme?

A

HMG-CoA via HMG-CoA synthase

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9
Q

In ketogenesis what is HMG-CoA converted to and by what enzyme?

A

Acetoacetate via HMG-CoA lyase

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10
Q

In ketogenesis what is Acetoacetate converted to and by what?

A

spontaneously decarboxylated to acetone

converted to 3-hydroxybutyrate via 3-hydroxybutyrate dehydrogenase

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11
Q

Are ketones used by the liver?

A

No, the liver lacks succinyl-CoA-acetoacetate-CoA transferase so it cannot use ketone bodies

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12
Q

How does the body use ketone bodies?

A

when ketone bodies released from liver -> transported to muscle (major), kidney (major), brain (only in starvation) -> oxidized for energy

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13
Q

What is the rate limiting step in ketogenesis?

A

HMG-CoA reductase, release of FA from adipose and uptake of acyl-CoA into mitochondria (CPTI)

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14
Q

where does cholesterol synthesis occur?

A

liver cytosol

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15
Q

Where does ketogenesis occur

A

liver mitochondria

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16
Q

How is acetone excreted?

A

by lungs, expiration

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17
Q

How are ketone bodies excreted?

A

urine

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18
Q

Why does ketogenesis occur?

A

During gluconeogenesis acetyl-CoA uses oxaloacetate in the formation of citrate and eventually glucose. When oxaloacetate is depleted ketogenesis proceeds so acetyl-CoA can be utilized for energy.

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19
Q

Where is the major site of FA synthesis?

A

liver cytosol

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20
Q

Synthesis of long chain saturated FA is from?

A

Synthesized from dietary glucose via pyruvate

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21
Q

Where are enzymes for FA synthesis located?

A

The Es are localized in the cytosol, completely different from the mitochondrial Es for FA degradation

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22
Q

To synthesize palmitic acid, polymerization of initial 2 carbon units are from what

A

Acetyl-CoA, carbons 15, 16

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23
Q

What molecules are required for FA synthesis?

A

reduced NADPH, ATP, biotin, CO2, H2O

24
Q

What is the initial and controlling step of FA synthesis?

A

production of Malonyl-CoA, carboxylation reaction and requires biotin

25
Q

Describe FA synthase

A

a multi-enzyme complex, total of 8 reactions

26
Q

General concept of LCFA synthesis?

A

keep adding 2 carbon until C16 (palmitic acid) then enzyme no longer has affinity and releases FA

27
Q

How is acetyl-COa transported out of the mitochondria to be used for FA synthesis?

A

as citrate

28
Q

Where do the additional 2 carbons that add onto acetyl-CoA’s initial carbons come from?

A

malonyl-CoA, carbons 1-14

29
Q

What are 4 essential unsaturated FA

A

palmitoleic acid (16:1)
oleic acid (18:1)
linoleic (18:2)
alpha-linolenic (18:3)

30
Q

What do cis USFA provide?

A

fluidity of TG reserves, phospholipid membranes

Many serve as precursors of eicosanoids (prostaglandins, prostacyclins, thromboxanes, & leukotrienes)

31
Q

Where and how are double bonds introduced

A

In the ER, double bonds are introduced between carbons 9 and 10 by FA oxygenase, which require molecular oxygen (O2) and NADPH

32
Q

Arachidonic acid is the precursor of

A

PGs, TXs, PGIs, & LTs

33
Q

Essential fatty acids are stored almost completely as

A

esters of the 2-position of the glycerol backbone of cell membrane phospholipids

34
Q

essential fatty acids are released using what phospholipase in arachidonic acid synthesis?

A

phospholipase A2

35
Q

Activation of PLA2 and PLC

A

Stimuli -> intracellular Ca2+ with calmodulin -> activate membrane bound phospholipase A2 and C

36
Q

What drug inhibits phospholipase A2 activity?

A

glucocorticoids (i.e. cortisol)

37
Q

Phospholipase A1 cleaves

A

at SN-1, first acyl group on glycerol backbone

38
Q

Phospholipase A2 cleaves

A

at SN-2, first acyl group on glycerol backbone

39
Q

Phospholipase C cleaves

A

cleaves phospholipids just before phosphate group

40
Q

Phospholipase D cleaves

A

cleaves just after phosphate group freeing serine or choline or inositol or ethanol amine

41
Q

name two Cox-2 inhibitors

A

celecoxib

rofecoxib

42
Q

What is monteleukast used to treat?

A

treatment of allergen and exercise-induced asthma and allergic rhinitis

43
Q

MOA of Zarfirlukast or monteleukast

A

leukotriene receptor antagonist

44
Q

Biological activities of PGD2

A

inhibits platelet and leukocyte aggregation, decreases T-cell proliferation and lymphocyte migration and secretion of IL-1a and IL-2; induces vasodilation and production of cAMP

45
Q

Biological activities of PGE2

A

increases vasodilation and cAMP production, enhancement of the effects of bradykinin and histamine, induction of uterine contractions and of platelet aggregation, maintaining the open passageway of the fetal ductus arteriosus; decreases T-cell proliferation and lymphocyte migration and secretion of IL-1a and IL-2

46
Q

Biological activities of PGF2alpha

A

increases vasoconstriction, bronchoconstriction and smooth muscle contraction

47
Q

Biological activities of PGH2

A

precursor to thromboxanes A2 and B2, induction of platelet aggregation and vasoconstriction

48
Q

Biological activities of PGI2

A

inhibits platelet and leukocyte aggregation, decreases T-cell proliferation and lymphocyte migration and secretion of IL-1a and IL-2; induces vasodilation and production of cAMP

49
Q

Biological activities of TxA2

A

induces platelet aggregation, vasoconstriction, lymphocyte proliferation and bronchoconstriction

50
Q

Biological activities of TxB2

A

induces vasoconstriction

51
Q

Biological activities of LTB4

A

induces leukocyte chemotaxis and aggregation, vascular permeability, T-cell proliferation and secretion of INF-γ, IL-1 and IL-2

52
Q

Biological activities of LTC4

A

component of SRS-A, microvascular vasoconstrictor, vascular permeability and bronchoconstriction and secretion of INF-γ

53
Q

Biological activities of LTD4

A

predominant component of SRS-A, microvascular vasoconstrictor, vascular permeability and bronchoconstriction and secretion of INF-γ

54
Q

Biological activities of LTE4

A

component of SRS-A, microvascular vasoconstrictor and bronchoconstriction

55
Q

What is tested/detected in asthmatic reactions?

A

LTE4

Biochem Spring (8 decks)

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