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GI > Fatty Acid Metabolism > Flashcards

Fatty Acid Metabolism Flashcards

1
Q

A heterogeneous group of water-­insoluble (hydrophobic) organic molecules that can be extracted from tissues by nonpolar solvents

A

Lipids

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2
Q

Serve not only as a major source of energy for the body, but they also provide the means for separating cells and subcellular structures into distinct compartments

A

Lipids

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3
Q

The digestion of triacylglycerol is initiated in the stomach by an acid-­stable lipase called

A

Lingual Lipase

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4
Q

Also produced that can hydrolyze triacylglycerol molecules containing fatty acids of short or medium chain length

A

Gastric Lipase

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5
Q

More useful in the neonate, with a less acidified stomach and a diet of breast milk abundant in medium and short chain length TAGs

A

Gastric Lipase

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6
Q

Activates a pancreatic, phosphatidylinositol triphosphate pathway

A

CCK

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7
Q

Dietary triacylglycerol is degraded by pancreatic lipase which preferentially removes the fatty acids at carbons #1 and #3, leaving a

A

2-monoacylglycerol

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8
Q

Binds to both the water-­lipid interface and to pancreatic lipase, thereby anchoring and activating the enzyme

-a small pancreatic enzyme

A

Colipase

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9
Q

This enzyme acts on cholesterol esters, monoacylglycerol, or other lipid esters such as esters of vitamin A

-found in pancreatic juice

A

Esterase

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10
Q

Phospholipids are degraded by a two-­step process. Pancreatic juice is rich in the proenzyme

A

Phospholipase A2

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11
Q

This enzyme removes the fatty acid at carbon #2 of the phopholipid, leaving a lysophospholipid

A

Phospholipase A2

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12
Q

The remaining fatty acid at carbon #1 is removed by lysophospholipase, leaving a

A

Glycerylphosphorycholine

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13
Q

Free fatty acids, free cholesterol, and 2-­

monoacylglycerol are the major products of dietary lipid degradation in the

A

Jejunum

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14
Q

The double bonds in human fatty acids are almost always of the

A

Cis configuration

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15
Q

Glucose that is not utilized in glycolysis, glycogen synthesis, the HMP pathway, are readily converted to

A

Fatty acids (stored as TAGs)

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16
Q

Occurs in the cytoplasm of cells of liver, adipose, intestine, lactating mammary glands and to a lesser extent, kidney

A

Fatty acid synthesis

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17
Q

The process of FA synthesis incorporates carbons from acetyl CoA into the growing fatty acid chain, utilizing

A

ATP and NADPH as cofactors

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18
Q

Prior to the first catalytic step in fatty acid synthesis, we need to see the transfer of

A

Acetate units from mitochondrial acetyl CoA to cytoplasm

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19
Q

This transfer is performed via a

A

Citrate intermediate

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20
Q

This process of translocation across the inner mitochondrial membrane occurs when the matrix-­side citrate concentration is

A

High

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21
Q

The first enzyme of the faty acid synthesis pathyway is

-the site of regulation

A

Acetyl CoA carboxylase

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22
Q

The remaining several reactions in fatty acid synthesis are catalyzed by a multienzyme complex called

A

Fatty acid synthase (FAS)

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23
Q

In humans, this enzyme complex consists of a dimer, each monomer of which has

A

7 enzymatic domains

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24
Q

The FAS also has a domain that covalently binds a molecule of

A

Phospantetheine

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25
Q

In prokaryotes the phosphopantetheine-

containing domain is a separate peptide, and is referred to as the

A

Acyl Carrier Protein (ACP)

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26
Q

The product of fatty acid synthase is the 16-­carbon saturated fatty acid

A

Palmitic Acid

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27
Q

Fatty acids can be elongated in the

A

Mitochondria or ER

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28
Q

Chain desaturation occurs in the

A

ER

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29
Q

Requires biotin as a cofactor

A

Acetyl CoA Carboxylase (also PK and propionyl carboxylase)

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30
Q

What is the committed step of FA synthesis?

A

Acetyl CoA Carboxylase

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31
Q

Short-­term control by allosteric modifiers includes

A

Citrate

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32
Q

Allosterically activates the enzyme by promoting formation of large polymers

A

Citrate

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33
Q

Inhibit acetyl CoA carboxylase by breaking down those polymers

A

Palmitoyl CoA (and malonyl CoA)

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34
Q

Inhibits acetyl CoA carboxylase through cAMP-mediated phosphorylation

A

Glucagon

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35
Q

Stimultes acetyl CoA carboxylase by dephosphorylation

A

Insulin

36
Q

Long-­term control of FA synthesis is exerted via diet, by way of

A

Insulin and Glucagon

37
Q

Both a high-­carbohydrate diet or a fat-­free diet stimulate fatty acid synthesis through increased synthesis of

A

Acetyl CoA Carboxylase

38
Q

In contrast, a high-­fat diet or fasting (causing increased glucagon levels) results in

A

Inhibition of FA synthesis

39
Q

Glucose also contributes to the synthesis of fatty acids and, therefore, to TAG production, by the diversion of

A

Pyruvate derived acetyl CoA to the enzymes of FA synthesis

40
Q

Synthesis of glycerol phosphate occurs in both the

A

Adipose and the liver

41
Q

Activates fatty acids to their ‘CoA’ form

A

FA synthetase (thiokinase)

42
Q

Attaches the fatty acid moieties to the glycerol phosphate “backbone” in a process that also requires a phosphotase

A

Acyltransferase

43
Q

Removes the phosphate prior to the addition of the third fatty acid

A

The Phosphotase

44
Q

Stored in the cytosol as “depot” fat

A

Adipose derived TAG

45
Q

On the other hand, liver-

derived triacylglycerol is packaged in the lipoprotein

A

VLDL

46
Q

Fatty acids stored in adipose tissue in the form of neutral triacylglycerol serve as a major

A

Fuel storage depot

47
Q

Depot fat mobilization is characterized by the release of free fatty acids from their triacylglycerol parent. The release is initiated by the enzyme

A

Hormone sensitive lipase

48
Q

Removes a fatty acid from either C1 or C3 of the triacylglycerol

A

Hormone sensitive lipase

49
Q

Next, additional lipases specific for mono-­ or diacylglycerol degradation remove the remaining

A

Fatty acids

50
Q

Following their release, they exit the adipose cell and are transported in the circulation bound to

A

Albumin

51
Q

The glycerol molecule may be taken up by liver for

A

Gluconeogenesis or FA synthesis

52
Q

The major pathway for catabolism of saturated fatty acids is called

A

B-oxidation

53
Q

Two-­carbon units are successively removed from the carboxyl end of the fatty acid, in the form of acetyl-­CoA

A

B-oxidation

54
Q

Subsequently can enter the TCA cycle for additional oxidation and energy generation via the electron transport chain and ATP synthase

A

Acetyl CoA

55
Q

The first step of B-oxidation is the conversion of the fatty acid to its activated form called

A

Fatty Acyl CoA

56
Q

Because b-­oxidation occurs in the mitochondria, the fatty acid must be transported across the mitochondrial membrane. This requires the carrier

A

Carnitine

57
Q

Consists of two enzymes, carnitine acyl transferase (CAT) I and II

A

Carnitine Shuttle

58
Q

Step one of B-oxidation is the transport of fatty acyl CoA across the outer mitochondrial membrane by

A

CAT I

59
Q

Step 2 of B-oxidation takes place on the inner mitochondrial membrane and is catalyzed by

A

CAT-II

60
Q

Congenital absence of a member of the carnitine system in skeletal muscle results in diminished ability to use

A

Long-chain FA’s as fuel

61
Q

This often takes the form of

A

Exercise intolerance

62
Q

Inhibits carnitine palmitoyltransferase I, thus preventing the entry of acyl groups into the mitochondria

A

Malonyl CoA

63
Q

Transferred from the Matrix into the intermembrane space to be resused

A

Carnitine

64
Q

The steps in B-­oxidation are a recurring sequence of four reactions that result in the shortening of the carbon chain by

A

2 carbons per sequence

65
Q

These four steps are repeated for fatty acids of even-­numbered carbon chains (n/2 -­ 1) times, each cycle producing

A

1 acetyl CoA, 1 ADH, and 1 FADH2

66
Q

The final cleavage in B-oxidation releases

A

2 acetyl CoAs

67
Q

The three activities present in the mitochondrial “tri functional protein.” are the

A

Hydratase, dehydrogenase, and acyltransferase (thiolase)

68
Q

The B-­oxidation of a saturated fatty acid with an uneven number of carbon atoms proceeds by the same reaction steps as that of fatty acids with an even number of carbons until the

A

Final 3 carbons (propionyl CoA) are reached

69
Q

The processing of propionyl CoA requires which three things?

A

Biotin, Vitamin B12, and the enzyme medium-chain acyl-CoA dehydrogenase

70
Q

The processing of propionyl CoA results in

-can be used in the TCA cycle

A

Succinyl-CoA

71
Q

The liver has the enzymatic capacity to divert acetyl CoA derived from fatty acid or pyruvate oxidation into

A

Ketone Body Synthesis

72
Q

Exit the liver and are transported via the blood to peripheral tissues where they can be reconverted to acetyl CoA and then oxidized via the TCA cycle

A

Ketone Bodies

73
Q

Can the liver utilize ketone bodies for energy?

A

No

74
Q

Can occur by:

  1. ) The incomplete breakdown of fatty acids, or…
  2. ) The reversal of the thiolase reaction of fatty acid oxidation.
A

The first step of ketone body synthesis

75
Q

Next, a third molecule of acetyl CoA condenses with acetoacetyl CoA to produce

A

HMG CoA

76
Q

The formation of HMG CoA is catalyzed by

A

HMG CoA synthase

77
Q

Finally, HMG CoA is cleaved by

A

HMG CoA Lyase

78
Q

This cleavage releases

A

Acetyl CoA and acetoacetate

79
Q

Can be reduced to form 3-­hydroxybutyrate or can spontaneously decarboxylate to produce acetone

A

Acetoacetate

80
Q

In peripheral tissues, 3-

hydroxybutyrate is reoxidized to acetoacetate, which is then converted to

A

Acetoacetyl CoA

81
Q

Provided by succinyl CoA via 3-­ketoacyl-­CoA transferase

A

The Coenzyme A for this reaction

82
Q

Missing in the liver, thus preventing it from metabolizing ketones for energy

A

3-ketoacetyl-CoA Transferase

83
Q

Then, the acetoacetyl CoA is rapidly removed by

A

Thiolase

84
Q

Soluble derivatives
of fatty acids that can be used by peripheral organs to preserve glucose supplies for
glucose-­demaning organs

A

Ketone bodies

85
Q

Can metabolize ketone bodies in the later stages of a fast

A

The brain

86
Q

There’s a sharp edge to this, however, in that as ketone body levels increase, there is also increased strain on the system that regulates

A

Blood pH

87
Q

The term applied to this advanced state of starvation, and may be detected by the odor of acetone on the breath

A

Ketoacidosis

GI (59 decks)

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