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MCB II Block 2 > Energy and Glycolysis > Flashcards

Energy and Glycolysis Flashcards

1
Q

what is gibb’s free energy

A

energy capable of doing work

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2
Q

what is enthalpy

A

the heat content of the reacting system

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3
Q

what is entropy

A

quantitative expression of the randomness or disorder in the system

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4
Q

deltaG=

A

deltaH - TdeltaS

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5
Q

if delta G is negative

A

net loss of free energy
spontaneous
exergonic

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6
Q

it is exergonic if

A

delta G is negative

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7
Q

if delta G is positive

A

Net Gain of Free Energy
Not Spontaneous
Endergonic

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8
Q

if it is endergonic

A

delta G is positive

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9
Q

draw graph of negative delta G

A

pg 6

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10
Q

draw graph of positive delta G

A

pg 6

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11
Q

what does H stand for

A

enthalpy

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12
Q

what does S stand for

A

entropy

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13
Q

the more positive S, the more

A

thermodynamically favorable rxn will be

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14
Q

how does positive S make rxn more favorable

A

Ie a positive ΔS tends to make ΔG more negative or exergonic. This is why an ice cube will melt spontaneously at room temperature (the water molecules are becoming more disordered or gaining entropy) even though ice melting is an endothermic reaction (absorbs heat energy).

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15
Q

what does delta G tell us about the reaction

A

if it will take place, but can only tell based on initial and final states

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16
Q

standard delta G is energy change when reactants and products are at concenctrations of

A

1 mol/L

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17
Q

biochemical standard for delta G is energy change at what pH

A

7

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18
Q

look up delta G in my biochem book

A

lda;lfkj

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19
Q

do practice problems from my biochem gbook for delta G

A

fa;slkdf

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20
Q

delta G 0 =

A

-RT ln Keq

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21
Q

delta G = delta G0 +

A

RT ln [B]/[A]

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22
Q

negative delta G

A

favor product

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23
Q

log 1 =

A

0

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24
Q

what is so important about ATP

A

high energy phosphate bonds

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25
Q

draw ATP

A

pg 9

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26
Q

in the process of breaking phosphate bonds in ATP

A

energy is released

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27
Q

ATP reaction is highly

A

exergonic

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28
Q

when glucose is in tissues, tissues like the liver will do what with glucose

A

produce a polymer of glucose: glycogen

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29
Q

where does energy come from to turn glucose to glycogen

A

ATP

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30
Q

glucose to glucose 6 P is what kind of rxn

A

endergonic - need ATP

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31
Q

UTP is similar to

A

ATP - it has two high energy bonds

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32
Q

draw full chain for glucose to glycogen

A

pg 11

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33
Q

UDP glucose to glycogen is what kind of rxn

A

endergonic

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34
Q

UTP is used to

A

combine sugars

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35
Q

CTP is used for

A

lipid synthesis

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36
Q

GTP is used for

A

protein synthesis

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37
Q

ATP can be used to repair

A

UTP, CDP, GTP

it sacrifices itself to repair the other guys

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38
Q

cleavage of high energy bonds release energy b/c products are more

A

stable

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39
Q

2 ADP =

A

ATP + AMP

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40
Q

draw out glycolysis

A

pg 14

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41
Q

breaking of carbon bonds in foods yields

A

energy

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42
Q

glucose linked to another glucose via what bond

A

glycosidic bonds

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43
Q

when break glycosidic bonds what is delta G

A

negative - it is a spontaneous rxn

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44
Q

carbs contain how much energy

A

4 kcal/g

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45
Q

protein contains how much energy

A

4 kcal/g

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46
Q

fat contains how much energy

A

9 kcal/g

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47
Q

EtOH contains how much energy

A

7 kcal/g

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48
Q

how do we store energy

A

adipose triacylglycerol → fat
glycogen
protein

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49
Q

how much of body weight is fat

A

20%

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50
Q

how much of our calories is stored in fat

A

85%

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51
Q

the polymers in fat are highly

A

reduced

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52
Q

when you oxidize fat

A

you get energy

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53
Q

glycogen polymer used to release

A

glucose

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54
Q

what are the two kinds of glyogen energy used

A

liver glycogen

muscle glycogen

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55
Q

ribose 5-phosphate is needed to produce

A

nucleic acids

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56
Q

glucose used to do what

A

lots of things
extracellular matrix and cell wall
glycogen, starrch, sucrose s(storage)
(look on pg 19)

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57
Q

draw out alpha d glucopyranose

A

pg 19

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58
Q

draw out D-glucose

A

pg 19

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59
Q

draw out and Beta D glucospyranose

A

pg 19

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60
Q

glucose metabolism depends on what two hormones

A

insulin and glucagon

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61
Q

insulin and glucagon are produced by

A

pancreas

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62
Q

insulin is a hormone that when secreted body is teling tissue

A

“we have just eaten, we are going to put this away, produce glycogen, fat, and do protein synthesis”

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63
Q

glucagon does what

A

reverses with insulin does. mobilizes fuels, maintains blood glucose levels during fasting.

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64
Q

what cells in pancreas produce glucagon

A

alpha cells

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65
Q

as glucose levels rise what happens to insulin

A

rises

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66
Q

as glucose levels rise hat happens to glucagon

A

fall

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67
Q

alpha cells do what

A

secrete glucagon

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68
Q

beta cells do what

A

secrete insulin

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69
Q

alpha and beta cells are from

A

pancreas

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70
Q

draw out pathway of glucose regulation of insulin **

A

pg 25

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71
Q

what phosphorylates glucose to glucose 6 phosphate

A

glucokinase

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72
Q

what does it mean that glucokinase has high Km

A

low affinity for glucose - it’s good b/c you only want it to work when glucose levels are high

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73
Q

draw out pathway of glucose regulation of insulin know this well!!!

A

pg 25

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74
Q

polymers of carbohydrates

A

amylose & amylopectin

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75
Q

look at and understand difference b/w different sugar rings

A

pg 28

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76
Q

is sucrose reducing sugar

A

no

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77
Q

reducing sugar contains

A

3 anomeric carbon

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78
Q

fiber traps

A

water

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79
Q

by trapping water, fiber

A

softens stool

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80
Q

fiber can also inhibit

A

absorption of cholesterol

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81
Q

fructose, galactose, glucose are all

A

monomers from sugars

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82
Q

monomer sugars get in through what protein

A

SGLT1

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83
Q

glucose is taken against

A

concentration gradient (secondary transport)

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84
Q

Fructose absorbed by

A

GLUT5

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85
Q

GLUT5 is in

A

endothelial cells

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86
Q

all 3 monomer sugars can be transfered by

A

GLUT2

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87
Q

if there are mutations in gene for SGLT1 what will happen

A

severe diahhrea and dehydration

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88
Q

GLUT4

A

insulin-sensitive transporter.

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89
Q

in presence of insulin, number of what transporter increases

A

GLUT4

90
Q

is glucose transport into RB rate limiting

A

no

91
Q

what happens when GLUT2 doesn’t work

A

Fanconi-Bickel syndrome

92
Q

GLUT2 where is it located

A

liver

93
Q

if GLUT2 doesn’t work what happens with liver

A

glucose is accumulated in it

liver is too large

94
Q

what happens to kidney if GLUT2 doesn’t work correctly

A

kidney doesn’t function correctly

too much glucose in kidney

95
Q

what does pancreas do regarding glucose

A

enses glucose level

96
Q

baby pts with GLUT2 deficiency, what happens with pancreas

A

impairment

if glucose cannot get in pancreas, insulin not released, have hyperglyemia → diabetes

97
Q

GLUT1 deficiency affects

explain

A

brain
the brain needs a lot of glucose, if you impair glucose getting to BBB, you are affecting brain. all symptoms are brain impairment

98
Q

RBC depend on what for energy

A

glucose

99
Q

why does pt not die if they have GLUT1 deficiency

A

redundancy mechanisms, if something doesn’t work there is plan B.
sometimes these mechanisms compensate to normality, sometimes they don’t.

100
Q

what is the only GLUT stimulated by insulin

A

GLUT4

101
Q

if GLUT4 isn’t working right what develops

A

hyperglycemia

102
Q

glucose passes into CSF via

A

GLUT1

103
Q

neural cells take up glucose via

A

GLUT3

104
Q

Sugar + O2 what is waste product

A

CO2 + H2O

105
Q

why is sugar and O2 eneergy released in steps

A

to conserve the energy, and the intermediates can also be used for other things

106
Q

glycolysis is taking glucose to

A

pyruvate

107
Q

first five steps known as

A

priming the pump

108
Q

what is priming the pump

A

making glucose more reactive

109
Q

glycolysis takes place where

A

in all cells in the cytoplasm

110
Q

glucose is catabolized to yield

A

pyruvate

111
Q

pyruvate is oxidized in

A

TCA

112
Q

when pyruvate is oxidized in TCA it produces

A

CO2 and NADH

113
Q

in absence of O2, pyruvate is

A

reduced to lactate

114
Q

how many regulatory steps in glycolysis

A

3

115
Q

draw out glycolysis

A

pg 39

116
Q

what is first step of glycolysis

A

phosphorylation of glucose

117
Q

what is first regulatory step of glycolysis

A

1st one! glucose → phosphorylated

118
Q

is step one reversible? in glycolysis

A

no, it is irreversible

119
Q

rxns far from equilibrium are common points of

A

regulation

120
Q

what two enzymes help us out with phosphorylating glucose

A

hexokinase (muscular tissues)

glucokinase

121
Q

what is concentration of glucose

A

5 mm

122
Q

is hexokinase or glucokinase usually used

A

hexokinase

123
Q

when is glucokinase used

A

when we eat and glucose is increased - affinity for substrate is low but once it gets going the velocity takes off

124
Q

glucokinae affinity for substrate

A

low

but has high capacity

125
Q

what is Km for glucokinase

A

high (low affinity)

126
Q

what is Vmax for glucokinase

A

high

127
Q

glucokinase is inhibited by

A

fructose 6-P

128
Q

hexokinase is inhibited by

A

G6p

129
Q

the liver only uses glucokinase when

A

glucose levels are high

130
Q

if glucose is interalized and processed to produce G6P and you accumulate F6P it does what

A

inhibits glucokinase - signals liver to stop glycolysis

131
Q

mutation of glucokinase leads to

A

MODY and gestational diabetes

132
Q

what is step two of glycolysis

A

G6P isomerised into fructose 6 P by PGI

133
Q

what is PGI stand for

A

phosphoglucose isomerase

134
Q

what is step 3 of glycolysis

A

F6P to Fructose 1,6-biphosphate by FPK-1

want it to have more energy

135
Q

Is ATP needed for step 3

A

yes

136
Q

what is the main regulatory point of glycolsysi

A

step 3

137
Q

is step 3 reversible

A

no it is irreverislbe, it is a rate limiting step

138
Q

ATP at low concentration in glycolysis (specifically step 3) is a

A

substrate

139
Q

ATP at high concentration in glycolysis (specifically step 3) is a

A

inhibitor

140
Q

why do cells use ATP as energy

A

in normal concentration it is 5 mm

it only has 10% change

141
Q

why is AMP used as sensor

A

when anything changes it changes by 600%, it is very sensitive

142
Q

PFK1 if mutations will have

A

rare form of glycogen storage disease: GSD-VII

143
Q

what will accumulate if there is mutation in PFK1

A

fructose 6 P
glucose 6 P
glycogen

144
Q

glucose 6 P is inhibitor of

A

glycogen

145
Q

so ultimately if there is mutation in PFK1, what will ultimately happen

A

interfere with glycogen degradation, sp pt has accumulation of glycogen, splenomegaly

146
Q

PFK1 is tightly

A

regulated

147
Q

what increaes Fructose 2,6 bisP

A

insulin

148
Q

go through glucose regulation in liver

A

pg 52

149
Q

what is step 4 & 5 of glycolysis

A

cleavage of fructose 1,6-bisphosphate and isomerization

150
Q

what does aldolase do

A

cleave fructose 1,6bisP into DHAP and glyceraldehyde 3-P

151
Q

DHAP is isomerised into

A

glyceraldehyde 3-P

152
Q

aldolase there are many

A

isozymes

each of two or more enzymes with identical function but different structure

153
Q

aldolase A expressed where

A

embryo,skeletal muscle, RBC

154
Q

GSD stand for

A

glycogen storage disease

155
Q

Aldolae B is expressed where

A

liver

156
Q

mutation in Aldolase B have

A

fructose intolerance

157
Q

mutation in Aldolase A have

A

GSD

158
Q

where is Aldolase C found

A

brain

159
Q

what is step 6 in glycolysis

A

Glyceraldehyde 3-phosphate dehydrogenase (GAPDH)

160
Q

step 6 is what kind of reaction

A

oxidation reduction

161
Q

write out Glyceraldehyde 3-phosphate dehydrogenase mechanism

A

pg 56

162
Q

arsenic toxicity is primariliy due to

A

inhibition of pyruvate dehydrogenase – see TCA Cycle.

163
Q

what are steps 7-9 in glycolysis

A

phophoglycerate kinase, phosphoglycero mutase and enolase

164
Q

pyruvate kinase is allosterically inhibited by

A

by ATP, acetyl-CoA, and long-chain fatty acids (all signs of an abundant energy supply),

165
Q

what triggers activation of pyruvate kinase

A

and the accumulation of fructose 1,6-bisphosphate triggers its activation.

166
Q

pyruvate kinase deficiency causes

A

hemolytic anemia

167
Q

any defect of glycolytic pathway leads to

A

hemolytic anemia

168
Q

when pyruvate kinase if not functioning well what is a cell that will esp. have issues

A

RBC - all ATP comes from glycolysis

169
Q

pyruvate kinase deficiency increases levels of

A

2,3 bisphosphoglycerate

170
Q

1,3bisphosphoglycerate is precurser fo

A

2,3bisphosphoglycerate

171
Q

if there are high levels of 2,3bisphosphoglycerate what happens to delivery of oxygen

A

delivery of oxygen improves, so it is compensating. so the hemoglboin pt does have works better.

172
Q

if there is a problem with the enzymes leading to 1,3bisphoshpoglycerate what happens to delivery of oxygen

A

2,3bisphophoglycerate decreases so delivery of oxygen decreases. so if they also have pyruvate kianse defiicency they don’t have enough oxygen and they have anemia, and they also dont have compensatory mechanism

173
Q

lactic acid normally produced by

A

RBC

174
Q

name three points of regulation for glycolysis

A

hexokinase
PFK1
PK

175
Q

hexokinase has feedback control by

A

glucose 6-P

176
Q

PFK1 activated by

A

AMP & fructose 2,6 bisP

177
Q

PFK1 inhibited by

A

ATP & citrate

178
Q

PK is activated by

A

fructose 1,6-bisP

179
Q

PK is inhibited by

A

ATP

180
Q

net aerobic glycolysis

A

2 pyruvate
2 ATP
2NADH

181
Q

does the brain ever use anaerobic glycolysis

A

no

182
Q

anaerobic metablism produces low amoutn of

A

ATP but its fast help

183
Q

aerobic metb

A

help

184
Q

what are three possible fates of pyruvate

A

lactate
Acetyl CoA
ethanol

185
Q

high level NADH low levels NAD cells produce

A

lactate

186
Q

lactic acid pKa

A

3.85

187
Q

lactic acid is completely

A

dissociated - physiological pH of 7.4

188
Q

in absense of mitochondria or O2 what happens to NADH

A

it is oxidized to NAD+ by reduction of pyruvate to lactate catalysed by lactate dehydrogenase (LDH)

189
Q

aerobic metbolism fast or slow?

A

slow

190
Q

anaerobic metabolism fast or slow?

A

fast

191
Q

bottom line: : if you have any problems with organelles that use O2 (mitochondria) you induce the formation

A

lactic acid

192
Q

what kind of glycolysis in tumor cells

A

anaerobic

193
Q

how does PET test work

A

basically light up the glucose in the body

pt ingests the modified glucose, tmor cells take a lot of it, and then can view in pet scan

194
Q

tryglycerol becomes

A

glycerol & palmitate

pg 16

195
Q

describe the glucoregulation process in α cells

A

increase in plasma glucose → cell generates ATP → ATP closes K+ channels → depolarization → Ca2+ and Na+ channels activated → blocks exocytosis (which would contain glucagon)
pg 27

196
Q

describe the glucoregulation process in ß cells

A

increase in plasma glucose → cell generates ATP → ATP closes K+ channels → depolarization → Ca2+ channels activated → release insulin via exocytosis

197
Q

starch is digested by

A

amylase

198
Q

when starch is digested what does it yield

A

oligosaccharides, maltose & isomaltose

199
Q

describe structure of amylose

A

linear glucose chains connected by α1→4 linkages*

200
Q

describe the structure of amylopectin

A

branched glucose chains. linear glucose chains connected by α1→4 linkages, branch points are α1→6 linkages*

201
Q

sucrose is mono or disaccharide

A

disaccharide*

202
Q

sucrose is made up of

A

fructose & glucose*

203
Q

what kind of bond connects fructose & glucose in sucrose

A

disaccharide*

204
Q

is sacrose a reducing sugar? why or why not?

A

no
Sucrose is non reducing sugar because the anomeric carbon from fructose and glucose are used to form a glycosidic bond
*

205
Q

is lactose a reducing sugar? why or why not?

A

yes
since only one anomeric carbon is used to form a glycosidic bond. The other anomeric carbon can open and close giving rise the reducing properties.*

206
Q

are mono or disaccharides taken up by cells

A

only mono*

207
Q

describe structure of maltose

A

Maltose – a glucose-glucose disaccharide connected by α1→4 linkages (ie. fragments of the linear chains of starch – either amylose or amylopectin)*

208
Q

describe structure of Isomaltose*

A

glucose-glucose disaccharide connected by α1→6 linkages (ie. fragments of starch from the branch points of amylopectin only)

209
Q

where is GLUT1 expressed

A

cell types with barrier functions

think BBB, and all the other barriers

210
Q

where is GLUT2 expressed

A

high-capacity, low-affinity transporter

think liver, pancreas, intestine

211
Q

what is the most important regulated step of glycolysis?

A

step 3, Fructose-6-phoshate to fructose 1,6-bisphosphate by FPK-1

212
Q

PFK1 is allosterically inhibited by

A

ATP

213
Q

PFK1 is allosterically activated by

A

AMP

214
Q

draw mechanism of high glucagon and low insulin and how it affects PFK-2 and FBP-2

A

pg 52

215
Q

draw mechanism of high insulin and low glucagon and how it affects PFK-2 and FBP-2

A

pg 52

216
Q

arsenic poisioning starts where

A

cytosol

217
Q

Arsenic toxicity is primarily due to the inhibition

A

pyruvate dehydrogenase

218
Q

high NADH/NAD+ ration favors production of what

A

lactate

219
Q

in the heart and liver the low NADH/NAD+ ratio favor production of what

A

oxidation of lactate to pyruvate

220
Q

anaerobic glycolysis (like if O2 isn’t getting to tissues) produces

A

lactate→lactic acidosis

221
Q

under low oxygen conditions, describes what happens with HIF (esp. in regards to tumor)

A

if low oxygen, more HIF. HIF is TF.

increases production of glucose transporters.

MCB II Block 2 (10 decks)

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