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MCB II Block 3 > Gluconeogenesis > Flashcards

Gluconeogenesis Flashcards

1
Q

gluconeogenesis is the biosynthesis of new

A

glucose

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2
Q

where does gluconeogenesis occur

A

mostly liver

a little bit kidney

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3
Q

when is kidney involved in gluconeogenesis

A

after llong starvartion, more than 48 hours

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4
Q

what provides the liver energy to fuel gluconeogenesis

A

ß oxidation of fatty acids

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5
Q

the high rate of a.a. metabolism in liver generates

A

urea

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6
Q

what happens to the urea the liver generates

A

mvoes to kidney for excretion

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7
Q

draw out the chart of effects of gluconeogenesis

A

pg 3

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8
Q

the _____ realeased from adipose tissue is used by the liver for gluconeogenesis

A

glycerol

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9
Q

skeletal mucsle does not have what enzyme

A

glucose 6 phosphatase

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10
Q

because skeletal muscle does not have glucose 6 phosphatase, what does it do with gluconeogenesis

A

it cannot deliver free glucose to blood, so it just does gluconeogenesis to generate glucose for storage as glycogen

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11
Q

draw out gluconeogenesis

A

pg 4

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12
Q

name three starter compounds for gluconeogensis

A

lactate
glycerol
alanine

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13
Q

lactate and alanine are turned into what to be used for gluconeogenesis

A

pyruvate

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14
Q

how is lactate turned into pyruvate

A

oxidized

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15
Q

how is alanine turned into pyruvate

A

transaminated

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16
Q

pyruvate is converted to what to be used for gluconegoenesis

A

oxaloacetate

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17
Q

oxaloacetate is converted to what to be used for gluconegenesis

A

phosphoenol pyruvate

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18
Q

what sugars can be used as precurser for gluconeogenesis

A

pyruvate
lactate
oxaloacetate

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19
Q

what protein can be used as precurser for gluconeogenesis

A

alanine - can be converted to TCA intermediates

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20
Q

animals cannot produce glucose from

A

fatty acids

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21
Q

what catalyses pyuvate → oxaloacetate

A

pyruvate carboxylase

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22
Q

what is needed in the reaction of converting pyruvate to oxaloacetate

A

ATP

biotin

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23
Q

what catalyzes the reaction of oxaloacetate to phosphoenolpyruvate

A

PEP carboxylase

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24
Q

inhibition of what is essential when turning pyruvate into oxaloacetate

A

pyruvate dehydrogenase

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25
Q

biotin helps trap

A

HCO3-

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26
Q

biotin trapping HCO3- is helpful for what kind of reactions

A

carboxylation

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27
Q

how is biotin attached to pyruvate carboxylase

A

amide bond to lysine residue

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28
Q

where does pyruvate → oxaloacetate occur

A

in mitochondria

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29
Q

deficiencies of biotin affect mainly

A

fatty acid biosynthesis

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30
Q

the first gluconeogenic step stravels through

A

mitochondria

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31
Q

oxaloacetate can be converted to what in mitochondria and what does this allow?

A

malate

malate can travel through the mitochondria into cytosol for gluconeogenesis

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32
Q

besides malate what else can travel through mitochondria

A

PEP

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33
Q

besides turning into malate what else can oxaloacetate turn into

A

PEP

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34
Q

draw out the two pathways for oxaloacetate turning into malate & PEP

A

pg 10

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35
Q

ethanol inhibits

A

gluconeogenesis

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36
Q

how does ethanol inhibit gluconeogenesis

A

alters NAD+/NADH ratio

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37
Q

alcohol consumption results in high levels of

A

NADH/NAD+

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38
Q

with high levels of NADH/NAD+ what happens to pyruvate

A

reduced to lactate

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39
Q

what is final result of ethanol making high NADH/NAD+ ratio

A

lactic acidosis

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40
Q

high acetyl CoA reflects high

A

energy charge

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41
Q

acetyl CoA can allosterically activate

A

pyruvate carboxylase

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42
Q

acetyl CoA promotes

A

gluconeogesnsis

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43
Q

not only does Acetyl CoA activate pyruvate carboxylse, it inhibits

A

PDH

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44
Q

what inhibits PDH

A

Acetyl CoA

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45
Q

Acety CoA is produced by

A

ß oxidation

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46
Q

basically if there is high Acetyl CoA it is a signal that

A

cell has enough energy to fuel gluconeognesis

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47
Q

what two functions arise in starving state

A

urea synthesis
ketogenesis
(pg 12)

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48
Q

draw out acetyl coA affect on gluconeogenesis (on oxaloacetate and pyruvate)

A

pg 13

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49
Q

what does PDH stand for

A

pyruvate dehydrogenase

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50
Q

what inhibits PDH

A

ATP
NADH
Actyl CoA

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51
Q

absolute control of glucose oxidation is mediated by availability of what

A

NAD+

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52
Q

when is NADH converted back to NAD+

A

ox phos

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53
Q

Oxidation of glucose is diminished when ketoacids in the brain or fatty acids in skeletal muscle are oxidized
why is this?

A

when they are oxidized it steals NAD+ so NAD+ isn’t available for oxidation of glucose

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54
Q

what is the cost of going through gluconeogenesis

A

4 ATP
2GTP
2NADH

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55
Q

why is gluconeogenesis necessary

A

brain
RBC
nervous system
they all NEED glucose for energy

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56
Q

gluconeognesis can generate glucose from a.a. but NOT

A

fatty acids

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57
Q

how is glucose 6 phosphate transported out of liver

A

dephosphorylated

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58
Q

where is glucose 6 phosphatase

A

ER lumen

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59
Q

glucose production in liver requires two proteins only found in gluconeogenic tissue:

A

glucose 6 phosphate translocase

glucose 6 phosphatase

60
Q

what point connects glycolysis and gluconeogenesis

A

glucose 6 phosphate translocase

glucose 6 phosphatase

61
Q

draw out G6P leaving liver

A

pg 15

62
Q

pyruvate kinase is inactivated by phosphorylation by

A

PKA

glucagon signaling

63
Q

what is enzyme for Fructose 1,6-bisphosphate → fructose 6-phosphate

A

fructose bisphosphatase-1

64
Q

does Fructose 1,6-bisphosphate → fructose 6-phosphate

make TP?

A

no

65
Q

what is enzyme for Glucose 6-phosphate → glucose

A

glucose 6 phosphatase

66
Q

does Glucose 6-phosphate → glucose

make ATP?

A

no

67
Q

glucagon effects gluconeognesis by what three mechanisms

A

Changes in allosteric effectors (2,6-bisphophoglyceate)

Covalent modification of enzyme activity (pyruvate kinase)

Induction of enzyme synthesis (PEPCK)

68
Q

what controls the amount of F26BP

A

insulin & glucagon

69
Q

what does insulin do to F26BP

A

promotes

70
Q

what does insulin promote

A

glycolysis

71
Q

what does insulin inhibit

A

gluconeognessi

72
Q

what does glucagon do to F26BP

A

decreases it

73
Q

glucagon promotes

A

gluconeogenesis

74
Q

glucagon inhibits

A

glycolysis

75
Q

draw out the regulation of glucagon and insulin and glycolysis/gluconeogenesis

A

pg 18

you drew this last block too. don’t forget PFK -2 and FBP 2

76
Q

F26BP activates PFK-1 by

A

increasing its affinity for fructose 6 phosphate

77
Q

FBPase-1 is inhibited by

A

F26Bp

78
Q

PEP is only used for production of

A

glucose

79
Q

glucagon via PKA inactivates

A

pyruvate kinase

80
Q

draw out glucagon affect on pyruvate kinase

A

pg 20

81
Q

FOX01 is a

A

transcription factor

82
Q

what does insulin do to FOX01

A

turns it off

83
Q

in the cytosol FOX01 is phosphorylated by

A

PKB

84
Q

phosphorylated FOX01 is then tagged

A

by ubiquitin → degradation in proteasome

85
Q

what does FOX01 transcribe

A

PEP carboxykinase

Glucose 6 phosphatase

86
Q

draw out insulin effect on FOX01

A

pg 21

87
Q

what is the ultimate effect of insulin on FOX01

A

turns off transcription of PEP carboxykinase and glucose 6 phosphatase

88
Q

during prolonged fasting, gluconeogenesis is induced. what key enzymes are activated during this time

A

glucose 6 phosphatase (G6Pase), fructose 1,6-bisphosphatase (Fbpase), pyruvate carboxylase (PC), and phosphoenolpyruvate carboxykinase (PEPCK)

89
Q

the expression of enzymes for gluconeogenesis is activated by

A

glucagon

stress hormone cortisol

90
Q

glucagon and cortisol act on what key transcription factors

A

cAMP response element binding protein (CREB)

FoxOs

91
Q

list the steps for glucagon to induce PEPCK

A

Glucagon → PKA → CREB → PGC-1α → Fox01 → PEPCK

92
Q

what decreases expression of PGC-1α

A

insulin

93
Q

what does PGC-1α do

A

upregulates ALA synthase

94
Q

draw out insulin and glucagon, fasting vs. feeding and the TF they alter

A

pg 22

95
Q

why can we produce glucose from so many a.a. intermediates? (see pg 7)

A

they are all intermediates of TCA cycle, so can all get to oxaloacetate

96
Q

compare and contrast a meal of glucose vs. meal of protein and how they affect glucose insulin and glucagon

A

after glucose meal: insulin and glucose levels rise, glucaon levels fall. after about two hours the insulin and glucose levels drop off
after protein meal: glucose levels dont change. insulin level rise slightly and remain constant, don’t drop off after 2 hours. glucagon rise slightly and remain constant.

97
Q

exercise leads to the production of what two things that activates liver gluconeogenesis

A

alanine & lactate

98
Q

draw out the glucose alanine cycle

A

pg 25

99
Q

draw out the glucose lactate cycle

A

pg 25

100
Q

the glucose alanine cycle is used primarily for what purpose

A

for skeletal muscle to eliminate nitrogen during exercise and replenish the energy supply

101
Q

glucose lactate cycle is used for what purpsoe

A

recycles lactate produced by muscle during anaerobic metabolism
produces glucose via gluconeogenesis in liver

102
Q

glucose oxidation produces

A

pyruvate

103
Q

pyruvate can undergo transamination and become

A

alanine

104
Q

pyruvate to alanine is catalyzed by

A

alanine transaminase

105
Q

what is 100% needed to turn lactate to glucose

A

gluconeogenesis

106
Q

in type II diabetes, what is difference in mellitus gluconeogenesis

A

it is 3x faster than in non-diabetic pt

107
Q

list the two main functions of gluconeogenesis

A

maintain glucose levels

remove lactate from tissues, esp the ones that are constantly producing lactate like RBC

108
Q

what drugs have been used to inhibit gluconeogenesis, lowering glucose for pts with diabetes mellitus type I and II

A

Metformin & phenformin

109
Q

what does ALT stand for

A

alanine transaminase

110
Q

glucose and glutamine go to what intestinal cell from teh blood supply

A

intestinal enterocytes

111
Q

what serves as the major substrate for intestinal gluconeogenesis

A

carbon atoms of glutamine

112
Q

draw out the pathway once glucose and glutaine enter intestinal enterocyte

A

pg 27

113
Q

what happens to 2-oxoglutarate, made from glutamine

A

it is turned into oxaloacetate

114
Q

in small intestine ,after 2-oxoglutarate is turned into oxaloacetate what happens

A

converted to PEP (phosphoenolpyruvate)

115
Q

PEP stands for

A

phosphoenolpyruvate

116
Q

in small intestine, PEP is diverted to

A

gluconeogenic pathway

117
Q

when glucose enters enterocyte, what happens

A

glycolsysis → pyruvate → reduced to lactate or transaminated to alanine → gluconeogenic substrate in liver

118
Q

what serves as the major precursor of glucose in small intestine

A

glutamine

119
Q

the presence of G6Pase in SI plays a role in export of

A

glucose to portal circulation

120
Q

gluconeogenesis in the kidney allows disposal of

A

acid in metabolic acidosis

121
Q

Increased renal catabolism of glutamine is facilitated by increased expression of

A 
genes that encode glutaminase (GA)
glutamate dehydrogenase (GDH)
phosphoenolpyruvate carboxykinase (PEPCK)
apical Na+/H+exchanger (NHE3)
SNAT3
122
Q

increased expression of NHE3 contributes to transport of

A

ammonium ions

123
Q

Increased expression of NHE3 contributes to acidification of

A

luminal fluid

124
Q

The combined increases in renal ammonium ion excretion and gluconeogenesis result in a net synthesis of

A

HCO3−ions

125
Q

HCO3−ions are transported across basolateral membrane by what

A

Na+/3HCO3−cotransporter

126
Q

in diabetes type 2 what is out of control

A

gluconeogenesis

127
Q

what is happening to liver in type 2 diabetes

A

1) Fatty liver (steatosis)
2) Inflammation
3) Insulin resistance
4) ↑Fatty acid biosynthesis
5) ↑ gluconeogenesis

128
Q

what is happening to muscle in type 2 diabetes

A

insulin resistance

glucose uptake and utilization

129
Q

the increased gluconeogenesis and insulin resistance results in what in type 2 diabetes

A

hyperglycemia & hyperinsulinemia

130
Q

what does metformin do

A

lowers liver gluconeogenesis

131
Q

draw out metformin affect on gluconeogenesis

A

pg 30

132
Q

why do we need 2 pyrvate to do gluconeogenesis

A

glucose is 6 carbon and pyruvate is 3 carbon

133
Q

pyruvate kinase is activated by

A

F16BP

134
Q

pyruvate kinase is inhibited by

A

ATP, alanine, glucagon & epinephrine, PKA

135
Q

phosphofructokinase is activated by

A

F26BP

136
Q

phosphofructokinase is inhibited by

A

ATP

Citrate

137
Q

describe the role of fructose 2,6 bisphosphate in regulating glycolysis and gluconeogenesis

A

pg 19

138
Q

gluckinase is induced by

A

insulin

139
Q

describe glucose and glucokinase km

A

very high (so not high binding affinity)

140
Q

pyruvate carboxylase is activated by

A

Acetyl-CoA

141
Q

phosphoenolpyruvate kinase is induced by

A

glucagon
epinephrine
glucocorticoids

142
Q

phosphoenolpyruvate kinase is repressed by

A

insulin

143
Q

Glucose 6 phosphatase is induced during

A

fasting

144
Q

what inhibits glucose 6 phosphatase

A

F 2,6 BP

AMP

145
Q

what does adenylate kinase do

A

converts ADP to ATP + AMP

MCB II Block 3 (6 decks)

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