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biochem > biochem lecture 3 pt 2 > Flashcards

biochem lecture 3 pt 2 Flashcards

1
Q

what enzyme carries out the modification/de-phosphorylation of glucose

A

glucose-6-phosphatase

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2
Q

what are phosphatases

A

enzymes that de-phosphorylates substrates

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3
Q

what is interesting about glucose-6-phosphatase

A

membrane associated protein that’s embedded within the membrane of ER in the cell

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4
Q

what is needed in order for glucose-6-phosphatase to dephosphorylate G6P

A

G6P has to be transported into the ER space (ER lumen) within the endoplasmic reticulum

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5
Q

what happens when G6P is transported to ER

A

phosphatase de-phosphorylates the glucose

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6
Q

what happens after the glucose is de-phosphorylated

A

glucose is transported back out of the ER lumen where it can be transported via a glucose transporter (GLUT2) into the bloodstream

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7
Q

what does GLUT2 do

A

glucose transporter, transports glucose into the bloodstream

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8
Q

where is glucose-6-phosphatase found

A

in liver, not muscles

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9
Q

why does it make sense that the liver has this enzyme as opposed to muscles etc.

A

liver needs to disseminate that glucose into the body, can’t do that without de-phosphorylating G6P

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10
Q

why does the muscle not need glucose-6-phosphatase

A

any glucose that’s released from glycogen stores in the muscle is gonna remain in the muscle cell, and used in muscle thru glycolysis

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11
Q

glycogen synthesis is called

A

glycogenesis

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12
Q

what is the enzyme that catalyzes the synthesis of the majority of glycogen

A

glycogen synthase

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13
Q

does glycogen synthase have the same function as glycogenin

A

no

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14
Q

what is necessary in order for glucose units to be added to the glycogen molecule

A

glucose has to be biochemically activated

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15
Q

how does the glucose get biochemically activated

A

process of uridylation (uridine diphosphate added to sugar –> UDP-sugar)

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16
Q

what is the process of uridylation

A

when uridine diphosphate is attached to the sugar (UDP-sugar)

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17
Q

describe the process of uridylation of glucose monomers

A

UTP has its 3rd phosphate group removed, and the remaining UDP molecule is attached to glucose

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18
Q

what is UDPG

A

uridine diphosphate glucose

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19
Q

what is UDP

A

an active donor of glucosyl units in growing polysaccharide chains

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20
Q

describe glycogen synthase

A

glycogen + UDPG –> (glycogen)n+1 + UDP

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21
Q

what is the point of tagging glucose w/ UDP

A

it’s a way of biochemically activating/targeting it for its incorporation into glycogen

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22
Q

what does glycogen synthase do

A

makes alpha-1,4 glycosidic bonds [catalyzes formation/extension of linear chains of glycogen by adding glucose units]

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23
Q

what does branching enzyme do

A

transplants a short chain, introduces a branch by forming an alpha-1,6 glycosidic bond [effectively creates the branch points within glycogen]

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24
Q

hexokinase

A

catalyzes the first step of glycolysis; helps w/ formation of glucose-6-phosphate from glucose

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25
Q

what are different ways to generate G6P

A

glycogen breakdown, glucose absorbed from diet; hexokinase forms glucose-6-phosphate from internalized glucose

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26
Q

where does glucose-6-phosphate go

A

glycolysis

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27
Q

what happens if you want to catalyze the synthesis of glycogen (instead of going to glycolysis)

A

glucose-6-phosphate needs to be isomerized into glucose-1-phosphate

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28
Q

what catalyzse the isomerization of G6P to G1P

A

phosphoglucomutase

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29
Q

what happens after G6P –> G1P

A

it creates UDP-glucose

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30
Q

how do you go from Glucose-1-phosphate to UDP-glucose

A

UDP-glucose pyrophosphorylase

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31
Q

what does UDP-glucose pyrophosphorylase do

A

uridylation of glucose to form UDP glucose (transfers phosphate from UTP, attaches UDP to glucose)

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32
Q

what’s up with UDP glucose

A

this is the form of glucose that’s going to be attached to glycogen and incorporated into glycogen’s structure

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33
Q

pyrophosphatase

A

removes or utilizse the pryophosphate generated in step 3 to generate free energy (useful for synthesis reactions)

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34
Q

how are these two opposing pathways regulated/controlled

A

hormones

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35
Q

insulin

A

hormone that lowers blood glucose levels

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36
Q

what does insulin inhibit

A

glycogen breakdown and gluconeogenesis

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37
Q

what does insulin promote

A

glycogen synthesis (to use up glucose in formation of glycogen to lower levels)

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38
Q

what are epinephrine and glucagon

A

hormones that raise blood glucose levels

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39
Q

what do epinephrine /glucagon stimulate/promote

A

glycogen breakdown and gluconeogenesis

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40
Q

what do epinephrine/glucagon inhibit

A

glycogen synthesis (to prevent glucose from being used up to make glycogen which will lower blood levels even more… we don’t want that)

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41
Q

what stimulates release of insulin

A

when you’ve ingested a carb rich meal

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42
Q

where does insulin come from/ is released from

A

pancreas

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43
Q

what is insulin involved in

A

major hormone involved in glucose uptake and storage

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44
Q

what does insulin do

A

stimulates the process that inhibits breakdown of glycogen, activates glycogen synthesis

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45
Q

what does insulin need to do in order to inhibit glycogen breakdown and activate glycogen synthesis

A

needs to be able to stimulate uptake of glucose into liver cells, muscle cells, etc.; and then stimulate process of glycogen synthesis

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46
Q

what is gluconeogenesis

A

synthesis of glucose from non-carbohydrate precursors (like lactate and pyruvate which provide carbon skeletons necessary for glucose synthesis)

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47
Q

what do epinephrine and glucagon do

A

stimulate breakdown of glycogen and stimulate gluconeogenesis

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47
Q

when does epinephrine/adrenaline work

A

fight or flight response; when you do this muscle needs energy to carry out a lot of muscle activity

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47
Q

where does that energy come from

A

need for available glucose is increased, comes in form of glycogenolysis stimulating glycogen breakdown

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47
Q

when does glucagon work

A

short-term starvation conditions

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47
Q

where does glucagon work

A

stimulates glycogen breakdown in liver

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47
Q

what is in liver

A

majro, predominant stores of glycogen

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47
Q

what does glucagon do

A

makes glucose available to brain and tissues under short-term starvation conditions

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47
Q

where does glucagon primarily work

A

in liver

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47
Q

what does converting G6P to glucose do

A

contribute to elevation of blood glucose

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47
Q

is there release of glucose into bloodstream in the liver?

A

no

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47
Q

what does liver have

A

glucose-6-phosphate which allows for release of glucose from liver (by converting G6P to glucose)

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48
Q

what does glycogenolyis generate

A

glucose-6-phosphate, gonna be used in glycolysis

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48
Q

what is there a lowering of in liver during glycogenolysis

A

lowering of glycolytic activity (glycolysis); b/c you don’t wanna use up glucose that’s released from glycogen; you wanna make it available to other body parts

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48
Q

what does liver favor

A

lowering of glycolysis

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49
Q

what does muscle favor

A

increase in glycolytic activity, b/c muscle will be metabolically active

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50
Q

what stimulates release of insulin from pancreas

A

ingesting carb-rich meal, hella glucose present in bloodstream (when you break down food, lots of carbs being released, many carbs are gonna be in form of glucose)

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51
Q

how do hormones work

A

binding of hormone to its receptor triggers activation of specific signal transduction pathway

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52
Q

what is the overall role of insulin

A

glucose uptake and storage; favors glycogen synthesis and inhibits glycogen breakdown

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53
Q

what does insulin do in the muscle (and liver???)

A

increases glycolysis

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54
Q

why does it make sense that insulin stimulates glycolysis

A

b/c if you’re gonna promote glycogen synthesis, you will need ATP to drive that synthesis/anabolic process

55
Q

why are you stimulating glycolysis as opposed to deriving energy from breakdown of glycogen

A

we have hella glucose around, some can be utilized for glycolysis (to make ATP to drive synthesis), but majority is used for glycogen synthesis

56
Q

so what two things is glucose being used

A

glycolysis AND glycogen synthesis

57
Q

what does insulin promote and inhibit

A

promotes glycogen synthesis AND inhibits glycogen breakdown

58
Q

how does insulin activate glycogen synthesis

A

insulin binds to its receptor, stimulates a kinase called PKB (upregulates it)

59
Q

what does PKB do

A

kinase, inhibits GSK3 (another kinase)

60
Q

what does GSK3 do when active

A

inhibits glycogen synthase

61
Q

what does PKB inhibiting GSK3 do

A

activates glycogen synthase

62
Q

what is glycogen synthase

A

enzyme that promotes/carries out glycogen synthesis

63
Q

what does inhibiting the inhibitor of glycogen synthase (GSK3) do

A

elevates glycogen synthase activity, and you get glycogen synthesis

64
Q

how does insulin inhibit glycogen breakdown?

A

insulin stimulates insulin sensitive protein kinase

65
Q

what does insulin sensitive protein kinase do

A

activates PP1 (protein phosphatase 1)

66
Q

what does PP1 do

A

de-phosphorylates a bunch of stuff

67
Q

what does blocking activity of GSK-3 while simultaneously activating PP1 do

A

de-phosphorylates any residues on glycogen synthase (anything that was phosphorylated earlier by GSK3, those phosphate groups are removed) –> elevates activity of synthase

68
Q

what does combined effects of inhibiting gGSK-3 while promoting de-phosphorylation of glycogen synthase (PP1) do

A

increases/elevates activity of synthase (remove any phosphate groups attached to AA residues on glycogen synthase polypeptide)

69
Q

what else does PP1 dephosphorylate

A

glycogen phosphorylase and phosphorylase kinase, decreasing activity of both

70
Q

does phosphorylating and de-phosphorylating always have the same outcome

A

no, depends on the specific protein

71
Q

what does phosphorylating/de-phosphorylating do to glycogen synthase

A

phosphorylating it inhibits it, de-phosphorylating it activates it

72
Q

what does phosphorylating/de-phosphorylating do to glycogen phosphorylase and phosphorylase kinase

A

phosphorylating it activates it, de-phosphorylating it inhibits it

73
Q

what is net effect of PP1 inhibiting the kinase that would normally activate the phosphorylase AND de-phosphorylating the glycogen phosphorylase

A

reducing activity of both enzymes, inhibiting glycogen breakdown

74
Q

what do you need to do when you have low blood glucose

A

stimulate breakdown of glycogen while also inhibiting glycogen synthesis

75
Q

what does releasing epinephrine/glucagon do

A

activates adenylyl cyclase which produces cAMP

76
Q

what is cAMP

A

allosteric effector

77
Q

what does cAMp activate

A

PKA (protein kinase A)

78
Q

what does PKA do

A

phosphorylates glycogen synthase and glycogen phosphorylase kinase

79
Q

what does phosphorylating glycogen synthase do

A

inhibits it

80
Q

what does PKA activation and activation of GSK3 (cuz its not being inhibited) do

A

inhibits glycogen synthase (phosphorylating glycogen synthase inhibits it)

81
Q

what else does PKA do in addition to phosphorylating glycogen phosphorylase kinase

A

phosphorylates the glycogen phosphorylase kinase

82
Q

what does activating phosphorylase kinase do

A

phosphorylates and activates phosphorylase

83
Q

what does activating phosphorylase do

A

favors activation of glycogen breakdown

84
Q

describe what happens in low blood glucose conditions

A

glucagon activates enzymes necessary to promote glycogen breakdown, and inhibits enzyme glycogen synthase

85
Q

what does hormonal control involve

A

activation of signal transduction pathways

86
Q

what do epinephrine and glucagon directly do

A

activate adenylyl cyclase

87
Q

how do they activate adenylyl cyclase

A

through G protein system

88
Q

what does adenylyl or adenylate cyclase do

A

takes ATP, lops off pyrophosphate, cyclizes remaining AMP

89
Q

what is cAMP a major allosteric regulator of

A

PKA

90
Q

what is another name of PKA

A

cyclic AMP dependent protein kinase A

91
Q

what does PKA do

A

phosphorylates and activates phosphorylase kinase

92
Q

what does activated phosphorylase kinase do

A

phosphorylates and activates glycogen phosphorylase

93
Q

what does activation of glycogen phosphorylase result in

A

breakdown of glycogen

94
Q

is insulin a G protein linked receptor

A

no

95
Q

what is cAMP

A

allosteric regulator

96
Q

where does cAMP bind to

A

regulatory site on PKA to bring about changes and increased activity of PKA

97
Q

what does adenylyl cyclase do

A

generates cAMP from ATP, PKA, serial phosphorylation or kinase cascade

98
Q

what does pKA do

A

PKA phosphorylates and activates the phosphorylase kinase, that being active now will phosphorylate and activate the glycogen phosphorylase, this is where you stimulate the breakdown of glycogen

99
Q

dose glucose have different fates in muscle vs liver?

A

yes

100
Q

what happens to glucose in muscle

A

glucose-1-phosphate monomers will be converted to glucose 6 phosphate –> glycolysis

101
Q

what does glycolysis help muscle do

A

muscle contraction, metabolic activity, increased muscle activity

102
Q

what happens to glucose in liver

A

glucose-1-phosphate –> glucose-6-phosphate, de-phosphorylated and released into blood

103
Q

covalent modification

A

phosphorylation/de-phosphorylation

104
Q

allosteric regulation

A

cAMP

105
Q

what kind of regulation is allosteric regulation

A

post-translational

106
Q

how does reciprocal control work

A

covalent modification AND allosteric regulation

107
Q

is phosphorylation reversible

A

yeah

108
Q

examples of allosteric effectors of glycogen phosphorylase

A

too much ATP or AMP etc.

109
Q

what does abundant ATP , high [ ] of G6P do

A

inhibits phosphorylase

110
Q

why does abundant ATP have effect of inhibiting

A

lot of glucose available to cell, won’t need more glycogen breakdown

111
Q

what does high AMP concentration indicate

A

hella ATP utilized, so less ATP; needs glycogen breakdown, so activates phosphorylase

112
Q

how does cell make decisions

A

based on relative concentration of allosteric effectors

113
Q

example of covalent modification of glycogen phosphorylase

A

serine residues on phosphorylase can be phosphorylated and de-phosphorylated

114
Q

what does de-phosphorylation favor

A

lowered activity

114
Q

what does phosphorylation favor

A

increased activity

115
Q

what regulates phosphorylase activity

A

both covalent and noncovalent control

116
Q

what is the active form of phosphorylase

A

a dimer

117
Q

T state

A

tense state; inactive form of enzyme

118
Q

R state

A

relaxed state, active form

119
Q

what do both covalent (phosphorylation) and non-covalent (allosteric) effects do

A

contribute to overall inactivity/activity of glycogen phosphorylase or synthase

120
Q

how is glycogen synthase covalently modified

A

by phosphorylating a serine residue by protein kinase A

121
Q

describe phosphorylated form of glycogen synthase

A

inactive

122
Q

describe phosphorylated form of phosphorylase

A

active

123
Q

is there reciprocal control of phosphorylase and glycogen synthase by covalent modification?

A

yes, because phosphorylation activates one and inactivates another [2 diametrically opposing effects of phosphorylation]

124
Q

what is another component of this system

A

glycogen targeting protein or GM

125
Q

what is GM

A

scaffolding or recruiter for various other players important for glycogen metabolism (phosphorylase, synthase etc.)

126
Q

how many sites are on GM

A

2 sites; GM site 1 and GM site 2

127
Q

do both sides have the same effect

A

no, depending on which site is phosphorylated it has different outcomes

128
Q

what does insulin do w/r to GM

A

stimulates phosphorylation of GM site 1, activates PP1 which de-phosphorylates glycogen phosphorylase kinase, glycogen phosphorylase, and glycogen synthase

129
Q

what does epinephrine do w/r to GM

A

stimulates phosphorylation of GM site 2, causes PP1 to dissociate from glycogen particle, prevents PP1 access to glycogen phosphorylase and glycogen synthase (this activates PKA)

130
Q

whaat activates PKA

A

epinephrine

131
Q

what does PKA do

A

phosphorylates an inhibitor protein of PP1

132
Q

net effect of epinephrine

A

breakdown of glycogen

133
Q

what does insulin pathway do

A

inhibits glycogen synthase kinase 3

134
Q

what does GSK3 do

A

phosphorylates and inactivates glycogen synthase

135
Q

what does insulin do

A

stimulates activity of PKB

136
Q

what does PKB do

A

phosphorylates GSK3, inhibiting it

137
Q

what happens if you inhibit GSK3

A

prevents phosphorylation of glycogen synthase and simultaneously activates PP1

138
Q

net effect of inhibiting GSK3

A

de-phosphorylation of glycogen synthase, means you’re gonna activate it

139
Q

effect of insulin

A

promoting glycogen synthase activation overall

140
Q

effect of insulin mediated inhibition of GSK3 and activation of PP1

A

favors activation of glycogen synthase

141
Q

what do insulin, G6P and glucose all do

A

favor activation of PP1

142
Q

what do glucagon/epinephrine do

A

favor inhibition of PP1 (through PKA pathway)

143
Q

what does insulin do to GSK3

A

inhibits it

144
Q

what does insulin do

A

stimulates glucose uptake, hexokinase activity, glycogen synthesis

145
Q

is there G6P in muscle

A

no

146
Q

what happens to glucose in muscle

A

G1P monomers or glucose absorbed into muscle from bloodstream is gonna be converted to G6P where it’s trapped and stays in muscle

147
Q

what happens if muscle needs a lot of ATP during strenuous activity

A

G6P is diverted to glycolysis, used for ATP production

148
Q

what happens when you have conditions that favor glycogen synthesis and storage in the muscle

A

G6P isomerized to G1P, converted to UDP glucose, used by glycogen synthase to produce more glucose

149
Q

what is the whole idea

A

glucose that enters muscle cell or released from glycogen in muscle cell stays in muscle

150
Q

is there release of glucose from muscle

A

no

biochem (15 decks)

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