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Gluconeogenesis Flashcards

1
Q

Mobilization of liver glycogen stores helps to maintain adequate glucose supply, but these storescan
be fully depleted in

A

24 hours

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2
Q

The synthesis of new glucose from simple carbon-­skeleton precursors,
also helps maintain bloodglucose levels, and can serve this function for up to several weeks

A

Gluconeogenesis

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3
Q

Occurs not only during periods of extended fasting/starvation, but at all times

A

Gluconeogenesis

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4
Q

Critical for the clearance of blood lactate produced by tissues and cells performing anaerobic glycolysis, such as rapidly exercising muscle and RBCs

A

Gluconeogenesis

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5
Q

Most of the bodies gluconeogenesis occurs in the

A

Liver

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6
Q

Can contribute up to 10% of the body’s gluconeogenesis but only in the later stages of a fast

A

Kidneys

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7
Q

Not able to perform gluconeogenesis, though it provides important substrates for this process

A

Muscle

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8
Q

Requires chemical energy in the form of ATP and NADH

A

Gluconeogenesis

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9
Q

Are able to perform gluconeogenesis even during the lean times of an extended fast because they are simultaneously also able to oxidize fatty acids for the production of ATP and NADH

A

Liver and Kidney

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10
Q

The metabolic conditions that call for accelerated gluconeogenesis include the mobilization of fatty acids for

A

Catabolism

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11
Q

Several compounds may contribute their carbon skeletons to glucose synthesis. These include all the glycolytic and TCA cycle intermediates with the significant exception of

A

Acetyl CoA

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12
Q

18 of the 20 amino acids, as well as a few other compounds such as propionate and glycerol can also contribute their carbon skeletons to

A

Gluconeogenesis

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13
Q

The product of anaerobic glycolysis, produced in tissues during periods of high energy demand but low oxygen supply

A

Lactate

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14
Q

Also produced in specialized cells which lack mitochondria, such as RBCs

A

Lactate

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15
Q

Summarizes the principal means by which lactate is cleared from the body

A

The Cori Cycle

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16
Q

Reversible depending on the concentration of pyruvate and lactate, and the NADH/NAD+ ratio

A

The lactate dehydrogenase reaction

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17
Q

The oxidation of lactate occurs in the cytoplasm and produces

A

Pyruvate and NADH/H+

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18
Q

Two moles of lactate are recruited for the formation of

A

One mole of glucose

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19
Q

Pyruvate is then transported into mitochondria where we see the first reaction unique to

A

Gluconeogenesis

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20
Q

Our goal is the production of

-can not be produced by reversing the pyruvate kinase reaction

A

Phosphoenolpyruvate (PEP)

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21
Q

The first gluconeogenic ‘detour’ is a two-­step process, beginning with the conversion of pyruvate to the TCA cycle intermediate oxaloacetate (OAA) by

A

Pyruvate carboxylase

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22
Q

CO2 and ATP are required in this reaction, and a critical cofactor for pyruvate carboxylase is

A

Biotin

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23
Q

The conversion of pyruvate to oxaloacetate by pyruvate carboxylase is stimulated by high levels of

A

Mitochondrial acetyl CoA

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24
Q

Muscle tissues lack the enzyme

A

Pyruvate carboxylase

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25
Q

Oxaloacetate cannot be transported across the mitochondrial membrane, so,it is carried across the mitochondrial membrane by either

A

Malate or aspartate

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26
Q

Conversion of malate to OAA produces NADH, therefore whether OAA uses malate or aspartate shuttle depends on the need for reducing equivalents in the

A

Cytosol

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27
Q

Used to convert 1,3-

bisphosphoglycerate to glyceraldehydes 3-­phosphate during gluconeogenesis

A

NADH

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28
Q

Cytoplasmic oxaloacetate is then converted to PEP by

A

PEP-carboxykinase

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29
Q

The formation of PEP-carboxykinase

  1. ) Consumes 1?
  2. ) Releases 1?
A
  1. ) GTP

2. ) CO2

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30
Q

Each of the first two reactions unique to gluconeogenesis are driven energetically by the hydrolysis of a high energy

A

Phosphodiester bond

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31
Q

This makes these reactions

A

Irreversible

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32
Q

We now take advantage of five consecutive reversible reactions of glycolysis to convert two moles of PEP into one mole of

A

Fructose 1,6-bisphosphate

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33
Q

Along the way we consume another pair of ATP molecules with the conversion of two moles of 3-­phosphoglycerate to

A

1,3-bisphosphoglycerate

34
Q

The conversion of two moles of 3-phosphoglycerate to 1,3-bisphosphoglycerate consumes another pair of ATP molecules. This reaction is catalyzed by

A

3-phosphoglycerate kinase

35
Q

In the next reaction, catalyzed by glyceraldehyde 3-phosphate dehydrogenase, we oxidize the

-produced in the original oxidation of lactate

A

NADH/H+

36
Q

With fructose 1,6-bisphosphate we return to a familiar area in glycolysis, and to the highly regulated enzyme

A

PFK-1

37
Q

That reaction, with the consumption of an ATP, is irreversible, so a second detour is taken with the gluconeogenic enzyme

A

Fructose 1,6-bisphosphatase-1 (FBP-1)

38
Q

This enzyme removes the phosphate on carbon #1 of fructose 1,6-­bisphosphate to produce fructose 6-phosphate

A

FBP-1

39
Q

Are an enzyme pair for glycolysis/gluconeogenesis in the same way that glycogen synthase and phosphorylase are for glycogen metabolism

A

PFK-1 and FBP-1

40
Q

Allosteric regulation of fructose 1,6-­bisphosphatase is effected by

A

AMP and Fructose 2,6-bisphosphate

41
Q

Serves as a local signal of energy need

A

AMP

42
Q

Gluconeogenesis is an energy requiring process, so AMP inhibits the

A

FBP-1

43
Q

Fructose 2,6-­bisphosphate allosterically inhibits

A

FBP-1

44
Q

The principal regulatory site in the glycolysis/gluconeogenesis story

A

PFK-1/FBP-1

45
Q

Remember that insulin and glucagon also regulate

A

Pyruvate kinase

46
Q

Glucagon-­mediated phosphorylation of this enzyme prevents the conversion of

-conserves it for gluconeogenesis

A

PEP

47
Q

The final step in gluconeogenesis is the conversion of glucose 6-phosphate to free glucose, but we are unable to use the ATP-­consuming enzyme

A

Glucokinase

48
Q

Instead, a membrane-­bound complex of proteins catalyzes this step. This complex of proteins includes the enzyme

A

Glucose-6-phosphatase

49
Q

This reaction takes place in the

A

ER

50
Q

Glucose 6-­phosphate is transported into the ER, where it reacts with the membrane-­bound

A

Phosphatase

51
Q

Genetic deficiency for glucose 6-­phosphatase in liver has been characterized extensively and is referred to as

A

Von Gierke’s Disease, also called Type 1 Glycogen Storage Disease)

52
Q

Gluconeogenesis is an energy consuming process. In order to convert lactate to glucose, the liver (and kidney) must consume the equivalent of

A

6 ATPs (4 ATP and 2 GTP)

53
Q

While ATP has no direct allosteric effect on gluconeogenic enzymes, it inhibits two

A

Rate-limiting glycolytic enzymes

54
Q

In this way, high levels of ATP help to stimulate net

A

Gluconeogenesis

55
Q

In this way, high levels of ATP help to stimulate net gluconeogenesis by ensuring the inhibition of the counter directional enzymes

A

Pyruvate kinase and PFK-1

56
Q

An intermediate of the TCA cycle that inhibits PFK-1

A

Citrate

57
Q

It is principally at the fructose 6-­phosphate/fructose 1,6-bisphosphate stage of things that we see control via

A

Glucagon and insulin

58
Q

Liver interprets high insulin/glucagon ratios as a sign of carbohydrate energy abundance, and inhibits

A

Gluconeogenesis

59
Q

Conversely, it treats low insulin/glucagon ratios as a signal of carbohydrate energy deficiency, and therefore throttles up

A

Gluconeogenesis

60
Q

Functions to clear the lactate that is produced by anaerobic glycolysis

A

The Cori Cycle

61
Q

Has one end point and many potential start points

A

Gluconeogenesis

62
Q

Eighteen of the twenty common amino acids are able to donate their carbon
skeletons to

A

Gluconeogenesis

63
Q

Integral to this is the disposal of the amine nitrogen on amino acids, tightly linking gluconeogenesis via amino acids to the process of

A

Urea Production (I.e. The Urea Cycle)

64
Q

The use of substantial quantities of amino acids for gluconeogenesis is reserved, in large part, to the circumstance of an

A

Extended fast

65
Q

What are the only two amino acids that are unable to participate in gluconeogenesis?

A

Leucine and Lysine

66
Q

Leucine and lysine are “ketogenic”, meaning their catabolism leads only to

A

Acetyl CoA

67
Q

Similarly, fatty acids composed of an even number of carbons produce only

  • Via the process of B-oxidation
  • Cannot participate in gluconeogenesis
A

Acetyl CoA

68
Q

Not a tenable source of carbon atoms for gluconeogenesis

A

Acetyl CoA

69
Q

Acetyl CoA and OAA combine to produce

A

Citrate

70
Q

Acetyl CoA doesn’t contribute net carbon atoms to the ensemble of

-Thus why it can not contribute to gluconeogenesis

A

TCA cycle intermediates

71
Q

Contrasting this, those 18 glucogenic amino acids are able to contribute to the pools of TCA cycle intermediates without consuming a TCA cycle intermediate. Such a contribution is referred to as an

A

Anapleurotic reaction

72
Q

When there is net production of a TCA cycle intermediate, there is no problem in feeding OAA into

A

Gluconeogenesis

73
Q

Free glycerol, produced when the three fatty acids of a TAG are released, is taken up by the liver and in two reactions, catalyzed by

A

Glycerol Kinase and Glycerol-3-phosphate dehydrogenase

74
Q

In this process, glycerol is converted into

A

Dihydroxyacetone phosphate

75
Q

Has a number of metabolic sources, including catabolism of valine and isoleucine, and the conversion of cholesterol to bile salts

A

Propionate

76
Q

Also derives from fatty acids with branch structures and from fatty acids with an odd number of carbons

A

Propionate

77
Q

Following a carboxylation reaction, propionate donates its carbons to the synthesis of

-another example of an anapleurotic reaction

A

Succinyl CoA

78
Q

The neonate’s liver glycogen stores are typically

A

Modest

79
Q

Its ability to metabolize certain types of fatty acids for energy is also markedly reduced, compared to even slightly older babies

A

Neonates

80
Q

Also, the neonate’s brain to body ratio is the largest it will ever be and hence the brain places a disproportionate demand on the child’s

A

Glucose supply

81
Q

The matter is compounded by the fact that in the newborn, a critical liver enzyme in gluconeogenesis is in very low levels. This enzyme is

A

PEP carboxykinase (PEPCK)

82
Q

As limited glycogen stores are depleted in the first few hours after birth, gluconeogenesis must step in to fill the gap. In the absence of adequate levels of PEP carboxykinase, we may see

A

Hypoglycemia

GI (59 decks)

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