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biochemistry > glycolysis and gluconeogenesis > Flashcards

glycolysis and gluconeogenesis Flashcards

1
Q

what process is occuring when pyruvate is converted to OOA?

A

carboxylation

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2
Q

what does PEP carboxylase do?

A

carboxylates (adds carbon dioxide ) to form OOA and and inorganic phosphate

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3
Q

what is the fate of pyruvate when using pyruvate carboxylase?

A

adds a carbon to pyruvate forming OOA

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4
Q

what is the fate of OOA when using PEP carboxykinase?

A

PEP- helps reverse pyruvate kinases effect and decarboxylates and phosphorylates PEP when GTP is present

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5
Q

Is pyruvate kinase a reversible or irreversible reaction?

A

irreversible

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6
Q

does pyruvate kinase phosphorylate pyruvate?

A

no it is a substrate level phosphorylation enzyme that produces ATP/ makes ATP. so it takes the phosphate from PEP and gives it to ADP and cannot be reversed

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7
Q

why is pyruvate kinase a irreversible reaction?

A

because it has a large negative free energy charge

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8
Q

when pyruvate kinase is phosphorylated what happens to pyruvate?

A

pyruvate kinase is inhibited when it is phosphorylated to allow gluconeogenisis to occur and pyruvate will not be formed

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9
Q

what enzyme cleave fructose 1,6 bisphosphate, which is the second/ regulating step in gluconeogenesis?

A

fructose 1,6 bisphosphatASE, which inhibits glycolysis by inhibiting PFK-1 from making fructose 1,6 bisphosphotase

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10
Q

what is the enzyme used in the main regulated step in glycolysis?

A

phosphofructokinase 1- phosphorylates fructose 1,6 bisphosphosphate

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11
Q

where is the phosphate group added when using phosphofructokinase 1?

A

position 1 on the fructose (fructose 1,6 bisphosphate)

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12
Q

in gluconeogenes, since pyruvate is an irreversible reaction, what are the 2 enzymes that allow an alternate pathway to reverse the effect of pyruvate kinase/ irreversible step?

A

pyruvate carboxylase and pep carboxykinase

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13
Q

what molecule do we need alot of in the first step of gluconeogenesis for gluconeogenesis which is an unfavorable reaction to become favorable?

A

alot of OOA from the kreb cycle needs to be produced so PEP carboxylase/ pyruvate carboxylase is used to add a carbon to pyruvate to make OOA, after we have OOA, the second enzyme PEP carbokinase convertes OOA to PEP known as the alternate step in gluconeogenesis

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14
Q

what is the difference between bisphosphate and diphosphate?

A

For a diphosphate, the 2 phosphate groups in the compound are directly attached to one another.

For a bisphosphate, the 2 phosphate groups in the compound are attached to different atoms on the compound, meaning that they are not attached to one another.

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15
Q

why does phosphoaditylinistol bispohospahate have three phosphates?

A

because it needs to form IP3

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16
Q

what is the fourth enzyme used in gluconeogensis to make glucose 6 phosphate to glucose?

A

glucose 6 phosphotASE

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17
Q

what are the 4 regulated steps gluconeogenesis?

A

pyruvate carboxylASE, PEP carboxykinase, Fructose 6 bisphosphotASE, glucose 6 phosphotASE

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18
Q

what is the purpose of gluconeogensis?

A

because we have cells that do produce there own energy/fuel such as the renal medulla, the brain, and the RBC gluconeogensis helps keep and maintain there energy when the energy level is low(fasting when gylcogen stores are done)

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19
Q

when does gluconeogensis/ glucagon happen?

A

when the glycogen store( are limited) are low/depleted, fasting, or fight or flight

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20
Q

what does the urea cycle do?

A

gets rid of nitrogen

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21
Q

does glycogen degradation and gluconeogenesis occur at the same time?

A

yes but glycogen degradation is the main source out of the two until all of the stored glycogen is depleted

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22
Q

what 2 organs allow gluconeogenesis to occur?

A

liver and the kidney

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23
Q

if have ethanol abuse to the liver, (being mean to the liver), then it will not be able to do what?

A

gluconeogenesis or glycolysis

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24
Q

does the kidney/renal medulla form or use glucose?

A

uses glucose

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25
Q

does the renal cortex form or use glucose?

A

forms glucose

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26
Q

if have a overnight fasting where will gluconeogenesis occur?

A

90% in the liver and 10% in the renal cortex(kidney)

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27
Q

if have a prolonged fasting 10-40 days, where will gluconeogenesis occur?

A

60: in the liver and 40% in the renal cortex(kidney), so there is an increase of gluconeogenesis in the kidney and and less of gluconeogenesis in the liver

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28
Q

At the cellular level, is gluconeogenesis found only in the cytoplasm?

A

no it is needed in the liver and the mitochondria (puruvate carboxylase-kreb cycle)

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29
Q

what substrates does the mitochondria need when in the fasting state?

A

lactate, pyruvate and glycogenic amino acids

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30
Q

where is PEP carboxykinase found at the cellular level?

A

in the mitochondria and cytosol

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31
Q

why would lactate be needed in gluconeogenesis?

A

to make pyruvate so that pyruvate can be carboxylated by pyruvate carboxylase to be converted into OOA so that OOA can be converted into PEP by using PEP carboxykinase

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32
Q

so is having a high level of lactate in the cell during the fasting state bad?

A

no because we use and convert lactate so that it can form glucose to produce energy

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33
Q

where is pyruvate carboxylase located at the cellular level?

A

mitochondria

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34
Q

what are the two main amino acids that the liver pick up from the blood?

A

alanine and glutamate( this is used for the urea cycle and this is how nitrogen is trasported to the urea cycle)

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35
Q

what does glucogenic amino acid mean?

A

amino acids can be used for gluconeogenesis (alanine and glutamate)

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36
Q

can the carbon skeleton be used for gluconeogenesis?

A

yes when the liver wants to do it

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37
Q

when the liver chooses to do glycolysis and it is in affect, what happens to alanine and glutamate?

A

they are degraded

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38
Q

when the liver chooses to do gluconeogenesis and it is in affect, what happens to alanine and glutamate?

A

they are used, and the urea cycle gets its nitrogen this way to make ammonia and the carbon skeleton is used as well

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39
Q

is gluconeogenesis a reversal of glycolysis?

A

no, it just uses the same enzymes

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40
Q

why cant glycolysis and gluconeogenesis happen at the same time?

A

tight hormonal regulation ensures that they do not happen simultaneously

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41
Q

what hormones favors gluconeogenesis?

A

Glucagon and cortisol

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42
Q

what hormones inhibit gluconeogenesis?

A

Insulin

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43
Q

what hormones favor glycolysis?

A

insulin

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44
Q

what enzyme enzyme allow PFK-1 to be activated and at the same time inhibits fructose 6 bisphosphotase?

A

fructose 2, 6 bisphosphate

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45
Q

what inhibits fructose 1,6 bisphophotASE?

A

fructose 2, 6 bisphosphate

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46
Q

where is fructose 6 phosphatASE bound?

A

the ER toward the ER lumen

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47
Q

what is T1?

A

glucose 6-P translocase

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48
Q

what is T2?

A

transports Pi

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49
Q

what is T3?

A

GLUT-7 transports glucose from ER lumen into cytosol

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50
Q

what is SP?

A

stabilizing protein

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51
Q

where is the generated glucose released into the blood?

A

GLUT-2 in the plasma membrane

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52
Q

where is glucose 6 phosphotase found?

A

in the kidney and liver

53
Q

why is glucose 6 phosphotase needed?

A

to allow for free glucose molecules to leave the liver to go to the blood stream

54
Q

when does TAG degradation take place?

A

TAG degradation takes place in fat cells only during fight or flight situation—releases free fatty acids and free glycerol to the liver

55
Q

what is hormone sensitive lipase?

A

it is the enzyme that helps with degradation of TAGs

56
Q

what describes the interactions between muscle and the hepatocytes during fasting?

A

the cori cycle and the alanine glucose cycle

57
Q

when the TAGs are released from the adiopose tissue what are they then cleaved into ?

A

free glycerol backbone and fatty acids

58
Q

in gluconeogenesis , where is lactate given off of in the body ?

A

in the muscles ( RBC) to the liver for conversion into glucose

59
Q

in gluconeogenesis, where is alanine and glutamine given off of in the body?

A

in the muscles (and other cells) to the liver

60
Q

there is a high abundance of alanine and glutamine in the body, what has the patient not done in a day or so?

A

eaten a meal, so his body is in the fasting state and gluconeogenesis is occuring and glycogen degradation occurs simutaneously until it runs out then gluconeogenesis takes over

61
Q

what metabolism is used when lactate is produced?

A

anaerobic metabolism in the muscles

62
Q

what does the formation of lactate from pyruvate need?

A

needs lactate dehydrogenase and NAD+ as a coenzyme

63
Q

when lactate is produced what is it taken up by?

A

the blood

64
Q

are red blood cells independent of a nutritional state?

A

yes, meaning if your in your fast or fed state then you are still going to get energy to the RBC regaurdless

65
Q

when alanine makes pyruvate, what is the name of this process?

A

transamination

66
Q

when alanine is elevated what state are we in?

A

fasting

67
Q

when alanine is in the blood what cells take them up, so that they can create pyruvate?

A

hepatocytes- liver cells

68
Q

in order for alanine to make pyruvate what is needed ?

A

alpha keto glutarate and alanine aminotransferase

69
Q

what is the coenzyme needed when making pyruvate out of alanine?

A

PLP (pyridoxal phosphate)

70
Q

what cycle are alanine and glutamine transported to in the liver?

A

the urea cycle

71
Q

where is alanine and gluatmine released from?

A

the muscles

72
Q

when there is an increase of alanine and glutamine, what hormone is low?

A

insulin

73
Q

during muscle protein degradation are alanine and glutamine high or low levels?

A

high, proteins are being degraded

74
Q

what is the cori cycle?

A

the metabolic pathway in which lactate produced by anaerobic glycolysis in the muscles moves to the liver and is converted to glucose, which then returns to the muscles and is metabolized back to lactate.

75
Q

at the cellular level, where is alanine converted to pyruvate?

A

cytosol

76
Q

why is alanine aminotransferase special?

A

it is a injury marker for the liver

77
Q

what is used for pyruvate carboxylase to fucntion?

A

carbon dioxide and botin(prosthetic group)

78
Q

is ATP cleaved or produced in the process of pyruvate carboxylase making OOA?

A

it is cleaved and the phosphate is absorbed and used

79
Q

in the mitochondria, pyruvate carboxylase needs this as a allosteric activator?

A

it needs acetyl CoA

80
Q

when carbon dioxide is activated, pyruvate carboxylase carries it to what?

A

biotin its prosthetic group

81
Q

after pyruvate carboxylase transfers carbon dioxide to biotin, what does it generate?

A

OOA

82
Q

when OOA is formed, and cannot cross the membrane, what has to happen?

A

it has to change into malate to cross the mitochondrial membrane and then it is converted back to OOA in the cytosol

83
Q

do we need biotin (a vitamin), for all carboxylases?

A

yes except vitamin K( gamma carboxylation)

84
Q

how is malate converted back to OOA in the cytosol?

A

it is reoxidized to OOA , which is oxidatively decarboxylated to PEP by PEP carboxykinase

85
Q

What does PEP carboxykinase need as substrates to form PEP ?

A

it needs OOA and GTP—->PEP, GDP, CO2

86
Q

what is used to form OOA?

A

NAD+( so that it can be oxidized) and malate to form OOA which is the substrate for the cystolic form of PEP carboxykinase

87
Q

what does PEP carboxykinase uses as its energy?

A

GTP, does not care about ATP

88
Q

is PEP carboxykinase a G protein?

A

yes, it uses GTP

89
Q

what does UTP activate? (ATP CAN MAKE-USED UP and then make another fuel currency GTP)

A

sugar

90
Q

what does CTP activate?

A

lipids

91
Q

what does GTP activate?

A

liver,translation, g protein(PEP carboxykinase)

92
Q

when does the liver switch glycolysis to gluconeogenesis?

A

when glucagon is abundant

93
Q

what is special about the isozyme of pyruvate kinase?

A

protein kinase A can phosphorylate and inactivate it,

94
Q

what is the puropse of the isozyme (aka as the short form dependent cyclic AMP(cAMP) protein kinase) of pyruvate kinase to be phosphorylated and inactivated?

A

it assures that PEP is saved for gluconeogenesis

95
Q

can gluconeogenesis happen when there is no fatty acid degradation going on at the same time in the mitochondria?

A

no, gluconeogenesis can only perform gluconeogenesis when it degrades at the SAME time fatty acids in the mitochondria degrade

96
Q

What leads to degradation of TAGS in fat cells?

A

when gluconeogenesis takes place during fasting and low insulin/glucagon ratio in the blood

97
Q

after TAGS in fat cell are degraded what happens?

A

free fatty acids are then released from adipocytes into the blood, bound to albumin and taken up into hepatocytes and other tissue

98
Q

when does TAG degradation take place?

A

TAG degradation takes place in fat cells only during fight or flight situation—releases free fatty acids and free glyserol to the liver

99
Q

what is hormone sensitive lipase?

A

it is the enzyme that helps with degradation of lipids

100
Q

what do low insulin levels activate to be released from the muscles in the adipose tissue?

A

TAGs- glycerol storage

101
Q

when the TAGs are released from the adiopose tissue what are they then cleaved into from the hormone sensitive lipase ?

A

free glycerol bacbone and fatty acids

102
Q

is citrate synthase regualated in humans or bacteria by NADH?

A

in bacteria.

In humans, citrate synthase is inhibited by the product citrate

103
Q

in the citric acid cycle, in humans, what is the first enyzme that is inhibited by NADH?

A

isocitrate dehydrogenase

104
Q

what is the second enzyme inhibited by NADH in the kreb cycle?

A

alpha keto glutarate dehydrgenase

105
Q

Does gluconeogenesis and mitochondrial beta oxidation of fatty acids take place at the same time during fasting in the hepatocytes?

A

yes

106
Q

when the liver degrades the fatty acids in the mitochondria using beta oxidation what is generated?

A

NADH and acetyl CoA

107
Q

what is NADH and acetyl CoA used to regulate?

A

PDH complex, TCA cycle and gluconeogenesis

108
Q

what happens when the acetyl CoA and NADH are newly generated?

A

they inhibit the pyruvate dehydrogenase complex(PDH)directly by product inhibition and also indirectly by activation of PDH kinase

109
Q

what does acetyl CoA allostrically activate?

A

pyruvate carboxylase

110
Q

what is used during fasting for hepatic ketone body formation?

A

acetyl CoA

111
Q

What does NADH inhibit in the TCA cycle?

A

isocitrate dehydrogenase, alpha keto glutarate dehydrogenase complex and the formation of malate from OOA is favored(gluconeogenesis)

112
Q

what is the ultimately regulated enzyme in the hepatic gluconeogenesis?

A

fructose1,6 bisphosphotase

113
Q

what inhibits fructose 1,6 bisphosphotase?

A

AMP and fructose 2,6-bisphosphotase

114
Q

what does high AMP levels signal?

A

low ATP levels so we do not need gluconeogenesis, instead we need to reserve energy for other liver functions and even perform glycolysis to generate ATP

115
Q

can low ATP levels cause liver damage?

A

yes, high ATP levels are always high in the liver, so this could indicate liver damage(low ATP levels and can not do gluconeogenesis so glycolysis kicks in to make more ATP)

116
Q

what does phosphofructokinase 2 do?

A

activates glycoylsis by activating fructose 2,6 bisphosphate which helps activate PFK1

117
Q

which part of the bifunctional enzyme is activated when ther are high levels of insulin?

A

PFK1

118
Q

during fasting and low insulin levels, what happens to muscle protein?

A

muscle protein is degraded and more alanine is released by muscle and activated the alanine glucose cycle in the liver

119
Q

what is glycerol kinase?

A

Glycerol kinase is a phosphotransferase enzyme involved in triglycerides and glycerophospholipids synthesis. Glycerol kinase catalyzes the transfer of a phosphate from ATP to glycerol thus forming glycerol phosphate (ATP + glycerol ADP + sn-glycerol 3-phosphate).

120
Q

what is the energy requirment for gluconeogenesis?

A

from 2 pyruvates.. you need 4 ATP and 2 GTP in additon 2 NADH are used

121
Q

what is taken up in the blood during the fasting state?

A

alanine, glutamine, lactate, glycerol, free fatty acids

122
Q

when there is a uptake of fatty acids and beta oxidation what is formed?

A

acetyl CoA and generate energy in the form of NADH and FADH2 from the ETC=energy

123
Q

what does pyruvate carboxylase need as an activator?

A

acetyl CoA

124
Q

when insulin dephosphorylates and enzyme or molecule will the enzyme be active or inactive?

A

the enzyme is activated and vice versa for glucagon

125
Q

what does cyclic dependent AMP proetin kinase A do?

A

it affects the bifunction enzyme by phosphorylation( insulin does not like phosphates so it does not like protein kinase A) and cutting off PFK2 which activates glyclyisis and turns on Fructose 2,-bisphosphotase which promotes gluconeogenesis

126
Q

what does phosphoprotein phosphotase favor?

A

it favors insulin(dephosphorylation) and activated PFK2 by cleaving the phosphate group and activating it

127
Q

when PFK2 is on what will elevate in concentration?

A

fructose 2,6 nisphosphate which increase glycolysis

128
Q

when fructose bisphosphotase 2 is activated what happens to glycolysis?

A

it does not happen, gluconeogenesis happens

129
Q

T/F beta oxidation of fatty acids has to be going on when gluconeogenesis is occuring?

A

true

biochemistry (28 decks)

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