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Biochem Loyola > Gluconeogenesis > Flashcards

Gluconeogenesis Flashcards

1
Q

Increased NADH leads to _______ lactate formation

A

Increased

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2
Q

Decreased NADH leads to _______ lactate formation

A

Decreased

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3
Q

What is the effect of ethanol metabolism on the NADH/NAD ratio?

A

Increases it

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4
Q

When you consume ethanol, you become hyper/hypoglycemic?

A

Hypoglycemic

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5
Q

When consuming ethanol, oxaloacetate is depleted as a precursor and instead converted into ________

A

Malate

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6
Q

When consuming alcohol, pyruvate is depleted as a precursor and instead converted to ___________

A

Lactate

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7
Q

What enzyme is needed for the following reaction?

Glucose 6-phosphate –> glucose

A

Glucose 6-phosphatase

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8
Q

What enzyme is needed for the following reaction? Fructose 1,6-bisphosphate –> Fructose 6-phosphate

A

Fructose 1,6-bisphosphatase

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9
Q

What enzyme is needed for the following reaction? Oxaloacetate –> phosphoenolpyruvate

A

Phosphoenolpyruvate carboxykinase

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10
Q

What enzyme is needed for the following reaction?

pyruvate –> oxaloacetate

A

Pyruvate carboxylase

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11
Q

What is the sum of the reaction of mixing pyruvate with ethanol?

A

Ethanol + Pyruvate –> Acetaldehyde + lactate

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12
Q

What is the sum of the reaction of oxaloacetate and ethanol?

A

Ethanol + oxaloacetate –> acetaldehyde + malate

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13
Q

High NADH _________ gluconeogenesis

A

Opposes

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14
Q

Removal of pyruvate and OAA from the pool of gluconeogenic precursors during alcohol metabolism contributes to what condition?

A

Hypoglycemia

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15
Q

What are the irreversible enzymes of glycolysis?

A

Glucokinase, PFK1, and pyruvate kinase

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16
Q

What hormone increase the synthesis of glycolytic enzymes

A

Insulin

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17
Q

What hormones increase the synthesis of gluconeogenic enzymes?

A

Glucagon and epinephrine

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18
Q

What are the 4 irreversible enzymes of gluconeogenesis?

A

Glucose-6-phosphatase, Fructose 1,6-bisphosphatase, Phosphoenolpyruvate carboxykinase, and pyruvate carboxylase

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19
Q

What is an example of glucagon altering gene expression?

A

PEPCK

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20
Q

How does glucagon alter gene transcription?

A

Glucagon acts on a GPCR glucagon receptor, and Gs stimulates adenylate cyclase to produce cAMP. cAMP activate PKA, which facilitates the conversion of CREB to CREB-P. CREB-P turns on CRE, promoting PEPCK transcription

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21
Q

Which state, fed or fasted, would increase synthesis of gluconeogenic enzymes?

A

Starvation/Fasted states

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22
Q

What is the effect of increased cAMP on gluconeogenic enzymes

A

Increased synthesis

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23
Q

What is the effect of insulin and glucose on gluconeogenic enzymes

A

Decreased synthesis

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24
Q

What is the effect of insulin and glucose on glycolytic enzymes

A

increased synthesis

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25
Q

What is the effect of decreased cAMP on glycolytic enzymes?

A

Increased synthesis

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26
Q

What is the effect of elevated acetyl coA on pyruvate carboxylase and subsequently gluconeogenesis

A

Activator, increases pyruvate –> phosphoenolpyruvate, increases gluconeogenesis

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27
Q

What is the effect of increased glucagon on PEPCK?

A

Activator, increases phosphoenolpyruvate –> oxaloacetate

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28
Q

What is the effect of insulin on PEPCK?

A

Inhibits it (since you must be fed if you have insulin circulating)

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29
Q

What are the activators of pyruvate kinase in glycolysis?

A

F-1,6-BP, glucose

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30
Q

What are the inhibitors of pyruvate kinase in glycolysis?

A

Glucagon and ATP

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31
Q

What is the reaction catalyzed by F16BPase?

A

Fructose 1,6-bisphosphate to fructose 6-Phosphate

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32
Q

What are the inhibitors of F16BPase

A

F26BP and AMP

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33
Q

What are the inhibitors of phosphofructokinase in glycolysis

A

ATP and citrate

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34
Q

What are the activators of PFK in glycolysis

A

F26BP and AMP

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35
Q

What are the effects of each of the following on G6Pase

  1. insulin
  2. glucagon
  3. Glucose
A
  1. inhibits
  2. promotes
  3. inhibits
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36
Q

What are the effects of insulin and glucose on glucokinase

A

Promote

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37
Q

What is the reaction catalyzed by Glucose-6-phosphatase

A

G6P to glucose

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38
Q

Is G6Pase deficiency dominant or recessive?

A

Autosomal recessive

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39
Q

What is another term for G6Pase deficiency

A

GSD type 1, or Von Gierke disease

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40
Q

What are the characteristics of G6Pase deficiency

A

poor tolerance to fasting, growth retardation, hepatomegaly due to accumulation of glycogen and fat in the liver, elevated serum uric acid, and elevated serum lactate

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41
Q

What processes are inhibited by a G6Pase deficiency?

A

Gluconeogenesis and glycogenolysis

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42
Q

What step is inhibited by a G6Pase deficiency

A

Conversion of G6P to glucose

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43
Q

What enzyme is only found in the liver, kidney, and intestines that is important for gluconeogenesis and glycogenolysis

A

G6Pase

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44
Q

Which side of the ER does the catalytic surface of G6Pase face?

A

Lumen

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45
Q

What transporter does glucose 6 phosphate enter the ER through?

A

ubiquitous transporter

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46
Q

What are the steps to get from F16BP and water to Glucose and Pi

A

F16bp+H20 –F16BPase–> F6P+Pi G6P+H20 –G6Pase–> Glucose+Pi

47
Q

What reaction is inhibited by F26BP and AMP

A

F16BPase (F16BP -> F6P +Pi)

48
Q

What energy-carrying molecule is required by PEPCK?

A

GTP

49
Q

What reaction is catalyzed by PEPCK?

A

Oxaloacetate + GTP –> PEP + CO2 + GDP

50
Q

Why would PC (pyruvate carboxylase) deficiency cause acidosis?

A

Elevated lactic acid levels

51
Q

What are symptoms of someone who has PC deficiency?

A

failure to thrive, developmental delay, recurrent seizures, metabolic acidoses

52
Q

What accumulates in PC deficiency?

A

Pyruvate in the plasma, which converts to lactate by LDH, causing elevated plasma lactic acid

53
Q

What is found in the serum of someone with PC deficiency?

A

High alanine

54
Q

Why would gluconeogenesis and urea cycle both be inhibited as a result of PC deficiency?

A

Because

  1. pyruvate would not convert to OAA
  2. OAA is a precursor for aspartate, which is a precursor for both urea cycle and gluconeogenesis
55
Q

Is PC a mitochondrial enzyme or a cytoplasmic enzyme?

A

Mitochondrial

56
Q

What cofactor does PC require?

A

biotin

57
Q

What molecule activates PC?

A

Acetyl CoA

58
Q

What reaction does pyruvate carboxylase catalyze?

A

Pyruvate –> OAA

59
Q

What high-energy molecule does PC need to work?

A

ATP

60
Q

What are the 4 control points of gluconeogenesis

A

G6Pase, F16BPase, PEPCK, and PC

61
Q

What are the 3 control points of glycolysis?

A

Hexokinase, PFK, pyruvate kinase

62
Q

What are the mitochondrial enzymes required to reverse the irreversible steps of glycolysis?

A

PC

63
Q

What are the cytoplasmic enzymes required to reverse the irreversible steps of glycolysis?

A

F16BPase, PEPCK, and G6Pase

64
Q

Propionyl CoA is a good precursor for ______

A

Gluconeogenesis

65
Q

What does propionyl CoA form as a result of?

A

B-oxidation of odd-chain FA, isoleucine, valine, and alpha-ketoburytuc acid

66
Q

How much glucose is produced from 1 propionyl CoA?

A

1/2

67
Q

What gluconeogenic precursor does propionate form?

A

Oxaloacetate

68
Q

Glycerol is a precursor for the synthesis of _____ and _____ in the liver and adipose tissue

A

TAGs and phospholipids

69
Q

What reaction is catalyzed by glycerol kinase

A

Glycerol –> glycerol 3-phosphate (which goes into fat)

70
Q

What reaction is catalyzed by glycerol 3-phosphate dehydrogenase?

A

Glycerol 3-phosphate –> Dihydroxyacetone phosphate

71
Q

What can be made from dihydroxyacetone phosphate?

A

1/2 glucose molecule or lactate

72
Q

What high energy molecule is needed by glycerol kinase

A

ATP

73
Q

What high energy molecule is needed for glycerol 3-phosphate dehydrogenase?

A

NAD+ (gets reduced to NADH)

74
Q

What gluconeogenic precursor does glycerol form?

A

triose phosphate

75
Q

Can acetyl-CoA be used to make glucose?

A

No. It is committed to either FA synthesis or Krebs cycle

76
Q

What forms Acetyl CoA?

A

Breakdown of FA and pyruvate via PDH

77
Q

Gluconeogenesis from all precursors requires ____

A

ATP

78
Q

Gluconeogenesis from amino acids requires ____ ATP, which is used for ___

A

additional; ureagenesis

79
Q

What is the major source of ATP for gluconeogenesis during an overnight fast?

A

Oxidation of FAs

80
Q

What reaction does galactokinase catalyze?

A

Galactose –> Galactose-1-phosphate

81
Q

What reaction does UDP-Glc:Gal-1-P Uridyltransferase catalyze?

A

Galactose-1-phosphate –> glucose-1-phosphate

82
Q

What reaction does phosphoglucomutase catalyze?

A

Glucose-1-P –> Glucose-6-P

83
Q

What reaction does glucose-6-phosphatase catalyze

A

G6P –> Glucose

84
Q

Which step of the process from galactose to glucose requires ATP?

A

Galactokinase (galactose –> galactose-1-P)

85
Q

Which precursor can be used to directly synthesize glucose?

A

Galactose

86
Q

Define fructolysis

A

Conversion of fructose into lactate

87
Q

What reaction does fructokinase catalyze?

A

Fructose –> F1P

88
Q

What reaction does aldolase B catalyze?

A

F1P –> glyceraldehyde + dihydroxyacetone phosphate

89
Q

What reaction does triose kinase catalyze?

A

Glyceraldehyde –> lactate

90
Q

Which steps of fructolysis require ATP?

A

Fructokinase (fructose –> F1P) and triose kinase (glyceraldehyde –> Glyceraldehyde 3P)

91
Q

What gluconeogenic intermediate is formed from fructose?

A

triose phosphate

92
Q

What is the cori cycle?

A

Using glucose to make lactate

93
Q

What are the steps of the Cori cycle starting from glucose in the liver

A

Glucose enters RBC, glycolysis happens, 2ATP and 2 Lactate are produced, the 2 lactate can return to the liver to be used for gluconeogenesis

94
Q

How many ATP does 2 Lactate –> Glucose require?

A

6

95
Q

How does pyruvate become alanine in the skeletal muscle during the alanine cycle?

A

It is transaminated

96
Q

What is the fate of alanine entering the liver?

A

Ureagenesis and deamination to produce pyruvate for gluconeogenesis

97
Q

How many ATP are required to go from 2 pyruvate to glucose?

A

6

98
Q

What gluconeogenic intermediate is formed by amino acids like alanine and by lactate?

A

Pyruvate

99
Q

Where does lactate for pyruvate generation for gluconeogenesis come from?

A

Glycolysis in other tissues

100
Q

Where does the aspartic acid for OAA comes from for gluconeogenesis?

A

Breakdown of muscle protein

101
Q

Where does the glycerol for dihydroxyacetone phosphate for gluconeogenesis come from?

A

TAG

102
Q

What do trioses get converted into in gluconeogenesis?

A

F16BP

103
Q

Why are neonates at risk for hypoglycemia?

A

Because it takes hours to induce PEPCK to make glucose from lactate or alanine

104
Q

Neonate’s brain is very dependent on glucose from ____ and _____

A

glycogen degradation and gluconeogenesis

105
Q

What are the 3 major gluconeogenic precursors

A

Lactate, glucogenic AAs like alanine, and glycerol

106
Q

Where do we get lactate as a gluconeogenic precursor?

A

general metabolism, RBC metabolism, muscle metabolism

107
Q

Where do we get glucogenic AAs like alanine as precursors for gluconeogenesis?

A

Overnight degradation of muscle AAs

108
Q

Where do we get glycerol as a precursor for gluconeogenesis

A

degradation of adipose tissue triacylglycerols

109
Q

Oxaloacetate can be viewed as an _______ form of pyruvate

A

activated

110
Q

The two mechanisms of maintaining glucose levels are _________

A

gluconeogenesis and glycogen

111
Q

Glucagon and epinephrine have 3 effects during starvation, what are they?

A
  1. promote gluconeogenesis
  2. increase gene transcription of gluconeogenic enzymes
  3. promote mobilization of glucose via glycogen degradation
112
Q

How do glucagon/epinephrine block glycolysis?

A

Inhibit PFK2 to inhibit PFK1

113
Q

What three genes do glucagon and epinephrine decrease gene transcription of?

A

Glucokinase, PFK1, and pyruvate kinase

Biochem Loyola (14 decks)

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