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MIMS > Metabolism > Flashcards

Metabolism Flashcards

1
Q

What can entropy measure?

A

Wasted energy, degree of disorder, how widely energy is distributed

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2
Q

How can you cheat second law?

A

Couple reactions

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3
Q

What does ATP energy of hydrolysis depend on?

A

Concentrations of reaction and products, Mg2+, Ca2+ and H2O

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4
Q

Entropy change = ?

A

Standard entropy change + RTln ([products]/[reactants])

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5
Q

Why is ATP hydrolysis so exothermic?

A

Phosphate and ADP have more resonance stabilisation than ATP so can spread out -ve charge, electrostatic repulsion weakens POP bridge, stabilisation due to hydration because more water can bind to ADP and Pi than ATP

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6
Q

What is the phosphorylation potential?

A

Free energy of ATP hydrolysis is its phosphorylation potential

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7
Q

Which reactions is ATP coupled to?

A

Phosphorylates glucose to prime its breakdown to pyruvate, peptides more unstable than amino acids so use ATP to build them, joining two nucleic acids

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8
Q

What carries CO2?

A

Biotin

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9
Q

What carries glucose?

A

Uridine diphosphate glucose (ADP)

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10
Q

What is the redox system for energy reducing pathways?

A

NAD/NADH

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11
Q

What is the redox system for biosynthesis? Why?

A

NADP/NADPH - phosphate group allows enzymes to recognise this redox system

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12
Q

Why does acetyl CoA have lower delta G than ATP and why is it more exothermic?

A

Less stabilised by resonance

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13
Q

How is the acetyl group bonded in acetyl CoA?

A

As thioester (activated acetyl group)

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14
Q

What can the heart metabolise?

A

Fat, glucose, ketone bodies, lactate

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15
Q

How many ATP does glycolysis make?

A

2

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16
Q

How many ATP does Krebs make?

A

30

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17
Q

What controls entry of glucose into fat and muscle?

A

GluT4

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18
Q

What controls entry of glucose into liver cell?

A

GluT2

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19
Q

What are the three phases of glycolysis?

A

Chemical priming, cleavage, energy yielding

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20
Q

What is delta G like in glycolysis?

A

Only just favourable

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21
Q

What are interconvertible isomers during glycolysis?

A

G3P and DHAP

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22
Q

Why is glucose > G6P irreversible?

A

Large free energy change

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23
Q

What happens to the aldehyde in glyceraldehyde? Where does the oxygen come from and what is the reducing agent?

A

Converted to a carboxylic acid - oxygen from water, reducing agent is NAD

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24
Q

Where does the energy for the reaction catalysed by pyruvate kinase come from? What does the reaction need?

A

Replacing C=O and C=O to 2 x C=O, needs pyruvate kinase, Mg2+ and K+

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25
Q

What is a summary of glycolysis?

A

glucose + 2Pi + 2ADP + 2NAD > 2 pyruvate + 2ATP + 2NADH + 2H+ + 2H2O

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26
Q

What is the usual conc of lactate? Above what conc do you get hyperlactaemia?

A

1mM, 5mM

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27
Q

Why do you get hyperlactaemia?

A

Buffering capacity overpowered

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28
Q

How much ATP is produced in the liver? What does it produce instead?

A

Little, net producer of glucose

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29
Q

What is hexokinase inhibited by? Does this affect glucokinase?

A

G6P, no

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30
Q

What is a substrate and allosteric inhibitor of PFK-1? What assists with this?

A

ATP, citrate

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31
Q

What is inhibited in the inactive state of PFK-1? What overcomes this?

A

Glycolysis, AMP

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32
Q

Where is PFK-2 found? WHich hormone controls it?

A

Muscle, insulin and glucagon

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33
Q

What does the futile cycle between F6P and F-1,6-BisP control?

A

Balance between glycolysis and gluconeogenesis

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34
Q

WHat maintains the futile cycle between F6P and F-1,6-BisP in muscle?

A

AMP

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35
Q

WHat maintains the futile cycle between F6P and F-1,6-BisP in the liver?

A

F-2,6-BisP

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36
Q

Why does glucagon cause gluconeogenesis in the liver?

A

Decrease in F-2,6-BisP

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37
Q

What does fructose-1,6-bisP stimulate?

A

Pyruvate kinase

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38
Q

Why is glucose stored as glycogen?

A

Glucose would cause high osmotic potential which would damage cells and also avoids glycosylation of proteins

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39
Q

What is one end of glycogen joined to?

A

Glycogenin

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40
Q

WHy is UDP good?

A

Good leaving group

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41
Q

Why is UTP needed?

A

G1P not a powerful enough glucose donor for G-G bond so needs energy from UTP

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42
Q

Why glycogen enzymes are active during exercise?

A

Phosphorylase active, synthase inactive

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43
Q

What activates protein kinase A?

A

cAMP

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44
Q

How does PKA activate glycogen phosphorylase?

A

Activates phosphorylase kinase which activates glycogen phosphorylase

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45
Q

Which enzyme inactivates glycogen phosphorylase?

A

Protein phosphatase

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46
Q

What activates phosphorylase kinase for normal muscle action?

A

Ca2+ and also 5’AMP

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47
Q

What happens to glycogen phosphorylase once fed?

A

cAMP goes to 5’AMP and protein phosphatase deactivates it

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48
Q

How does insulin affect glycogen synthase?

A

Inhibits GSK3 so glycogen synthase no longer inhibited

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49
Q

What are the three irreversible reactions in glycolysis?

A

Glucose to G6P, F6P to F-1,6-BisP, and PEP to pyruvate

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50
Q

How many ATP does pyrivate kinase forwards produce?

A

1

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51
Q

How many ATP does pyruvate to PEP produce?

A

Two

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52
Q

What does increased AMP cause in muscle?

A

Increased glycolysis

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53
Q

What increases glycolysis and decreases gluconeogenesis in the liver?

A

F-2,6-BisP

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54
Q

What controls PFK-2 in cardiac muscle and liver?

A

Adrenaline in cardiac muscle, glucagon and insulin in liver

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55
Q

What regulates PFK-2 in skeletal muscle?

A

No hormonal control, regulated by F6P availability

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56
Q

How much glucose is produced from fat?

A

None

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57
Q

How does pyruvate get into the matrix?

A

Symported with a proton

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58
Q

How many NADH, FADH2, GTP and CO2 per Krebs turn?

A

3NADH, 1FADH2, GTP, 2CO2

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59
Q

Which TCA intermediates are symmetrical?

A

Fumarate and succinate

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60
Q

What is link reaction coupled to?

A

Losing CO2 means acetyl CoA is generated

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61
Q

What does lipoamide do?

A

Flexible arm, tethers acetyl group between two sites and moves reducing potential to a third site

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62
Q

Where is succinate dehydrogenase?

A

Inner mitochondrial membrane

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63
Q

What takes place in the cytosol?

A

Glycolysis, pentose phosphate, FA synthesis

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64
Q

What takes place in the mitochondria?

A

Krebs, beta oxidation, ETC

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65
Q

How much oxaloacetate is usually in the cell?

A

Small amounts

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66
Q

Why is an anapleurotic pathway needed?

A

If you keep removing compounds you lose carbon so need a pathway with intermediates

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67
Q

How many ATP from NADH?

A

2.5

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68
Q

How many ATP from FADH2?

A

1.5

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69
Q

In cytosol what is ratio of [NAD]:[NADH]?

A

1000

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70
Q

In mitochondrion what is ratio of [NAD]:[NADH]?

A

8

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71
Q

What does PDH phosphatase deficiency cause?

A

Lactic acidosis

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72
Q

What does the PDH complex contain?

A

PDH kinase and PDH phosphatase

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73
Q

What do PDH kinase and PDH phosphatase do?

A

PDH kinase deactivates PDH and PDH phosphatase activates it

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74
Q

What inhibits PDH kinase?

A

Inhibited by pyruvate

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75
Q

What activates PDH phosphatase?

A

Ca2+ for exercise and insulin in adipocytes for lipid synthesis

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76
Q

What else regulates PDH?

A
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77
Q

What inhibits isocitrate dehydrogenase?

A

The NADH/NAD ratio found in the fed state and ATP

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78
Q

What stimulates isocitrate DH?

A

ADP

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79
Q

What stimulates and inhibits alphaKG DH?

A

Inhibited by its own products, stimulated by Ca2+

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80
Q

What is limiting when there’s lots of acetyl CoA?

A

Oxaloacetate

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81
Q

What does the purine nucleotide cycle do?

A

ATP breakdown can produce fumarate to produce more oxaloacetate

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82
Q

What do purine nucelotide cycle deficiencies cause?

A

Muscle cramps

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83
Q

How can you measure the Krebs cycle?

A

Oxygen or carbon “chase the label”

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84
Q

How can you use fMRI in the Krebs cycle?

A

Deoxyhaem is paramagentic and haem is diamagnetic so alters signal

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85
Q

What converts triacylglycerols/triglycerides into glycerol and fatty acids?

A

Lipases

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86
Q

What activates lipases?

A

Phosphorylation by PKA

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87
Q

What activates protein kinase?

A

cAMP from glucagon, adrenaline, noradrenaline

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88
Q

What breaks down the cAMP which activates protein kinase? How?

A

Insulin, activates phosphodiesterase

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89
Q

What does beta oxidation do?

A

COnverts aliphatic fat to acetyl CoA units

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90
Q

What happens to the fatty acids to make acyl-CoA?

A

Activated by CoA

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91
Q

Why is beta oxidation bond favourable?

A

High energy bond converting ATP to AMP, the PPi formed makes 2 x Pi

92
Q

Where does beta oxidation occur?

A

Inner membrane

93
Q

What are the enzymes for short, medium and long chain beta oxidation?

A

Very long chain acyl CoA dehydrogenase = VLCDH, long chain = LCDH, medium = MCDH, short = SCAD

94
Q

What catalyses beta oxidation?

A

Carnitine acyltransferase I

95
Q

How does carnitine acyltransferase I travel?

A

Attached to carnitine

96
Q

What happens once enzyme is inside the cell in beta oxidation?

A

Passed back to CoA again by carnitine acyltransferase II

97
Q

Why are fats good for storage?

A

Don’t need hydration, unlimited storage, highly reduced, bound to albumin in blood to prevent capillary damage

98
Q

What is the process of beta oxidation?

A

Oxidise to introduce double bond, hydrate to introduce an alcohol, oxidise the alcohol to a ketone, add CoA and you get acetyl CoA and a chain two carbons shorter

99
Q

What does beta oxidation produce?

A

FADH2, NADH and acetyl CoA

100
Q

Can you get glucose from fat derived acetyl CoA?

A

No

101
Q

What happens if the liver produces more acetyl CoA than it’s possible to use during starvation or diabetes?

A

Ketone bodies will be formed

102
Q

What does the feta heart use for fuel?

A

Uses glucose then switches to fatty acids after birth

103
Q

What is MCAD deficiency?

A

Babies can’t oxidise fatty acids and die when glycogen is depleted

104
Q

What causes Jamaican vomiting sickness?

A

Unripe ackee contains acetyl CoA dehydrogenase inhibitor so glycogen reserves are depleted

105
Q

What are the three ketone bodies?

A

acetoacetate, B hydroxybutyrate and acetone

106
Q

What happens to acetoacetate in muscle mitochondria?

A

Cleaved to make 2 x acetyl CoA to enter Krebs

107
Q

Why can’t liver do succinyl-CoA to acetoacetate CoA?

A

Doesn’t have transferases needed

108
Q

How does acetoacetate make acetyl CoA in mitochondria?

A

Two acetyl CoAs form acetoacetyl CoA, add another acetyl CoA then get something complicated but then produces acetoacetate and acetyl CoA which starts again

109
Q

How can the glycerol from fatty acids produce glucose?

A

Goes to DHAP using glycerol kinase and then G3P dehydrogenase

110
Q

Why must glycerol > glucose be done in the liver?

A

Adipose tissue doesn’t have the enzymes

111
Q

What happens to long chain fatty acids in mitochondria?

A

Oxidised in peroxisomes, to supply mitochondria with shorter chains

112
Q

What controls peroxisome synthesis?

A

A transcription factor

113
Q

What inhibits the carnitine shuttle? Why?

A

Malonyl CoA so synthesis and degradation can’t occur together

114
Q

What regulates fatty acid oxidation?

A

Lipolysis of triglycerides, carnitine huttle inhibition, competition with Krebs for NAD and FAD

115
Q

If there’s no GluT4 why are more fatty caids released from adipose cells?

A

No GluT4 so no glucose in fat cell so free fatty acids can’t reform triglycerides so more fatty acids released

116
Q

Why is fat easier to store than glycogen?

A

Needs less water adn more energy rich

117
Q

Where does fat synthesis and oxidation happen?

A

Synthesis in cytoplasm, oxidation in mitochondria

118
Q

Process of malonyl CoA production? What is the enzyme?

A

acetyl CoA + CO2 + ATP > malonyl CoA + ADP + Pi using acetyl CoA carboxylase

119
Q

How does acetyl CoA get to the cytosol?

A

Carried there as citrate

120
Q

What provides the reducing potential for fatty acid synthesis?

A

NADPH

121
Q

What supplies NADPH?

A

G6P oxidation

122
Q

What does fatty acid synthase do?

A

Adds acetyl CoA to a fatty acid strand

123
Q

What does malonyl CoA do?

A

Removes CO2 to drive the reaction

124
Q

What residue of fatty acid synthase does the fatty acid attach to?

A

Cysteine

125
Q

After 16 carbons what happens to the fatty acid?

A

Detached by hydrolysis, either elongates further or made into triglyceride or phospholipid

126
Q

How does citrate make neutral fat?

A

citrate to acyl-CoA to malonyl CoA to free fatty acid to neutral fat

127
Q

What is the acetyl CoA carboxylase in liver and adipose?

A

Acc1

128
Q

What is the acetyl CoA carboxylase in heart and skeletal muscle?

A

Acc2

129
Q

Where does the acetyl CoA attach to the membrane?

A

Near carnitine acyltransferase so the malonyl CoA will inhibit FA oxidation

130
Q

What does insulin activate to make more acetyl CoA?

A

Pyruvate DH

131
Q

What does insulin activate to increase malonyl-CoA supply?

A

acetyl CoA carboxylase

132
Q

What does a high carb diet do?

A

Lots insulin so lots of fat synthesis enzymes, directly stimulates PFK and ACC and indirectly increases NAPDH production and acetyl CoA transport into cytoplasm

133
Q

Where do TAGs go after production in the liver?

A

Into a VLDL and exported into blood then adipose

134
Q

How is TAG removed from blood?

A

Lipoprotein lipase binds VLDL and chylomicrons by releasing apoproteins, hydrolyses at tissue surface and the fatty acids are released into cells

135
Q

In adipose tissue, what does PKA do?

A

TAG lipase activate phosphorylation

136
Q

What increase cAMP concentration?

A

Glucagon, adrenaline and noradrenaline

137
Q

What breaks down cAMP?

A

Insulin

138
Q

How do glucogenic amino acids enter the Krebs cycle?

A

Directly

139
Q

What happens to ketogenic amino acids?

A

Must be metabolized as ketoacids

140
Q

Why is amino acid metabolism most intensive in liver?

A

Urea cycle here, serum protein synthesis occurs here, specialist biosynthesis

141
Q

What does muscle tissue do to branched amino acids?

A

Oxidises them and glutamate/glutamine produced in exported to liver

142
Q

What do 2-oxo acids do?

A

Transfer amino groups between amino acids courtesy of amino transferases

143
Q

AlphaKG + amino acid = ?

A

Glutamate + 2-oxo acid

144
Q

What does B6 do?

A

PYRIDOXAL PHOSPHATE Prosthetic group of amino transferase, acts as temporary parking spot for amino group and transfers to glutamate, alanine and aspartate

145
Q

What does alanine do at the interface of Cori cycle and amino acid synthesis?

A

Carries ammonia and carbon of pyruvate to the liver where the ammonia is excreted and the pyruvate makes glucose

146
Q

What happens to excess ammonia + glutamate? Which enzyme does this?

A

Makes glutamine using glutamine synthase

147
Q

In the liver what happens to glutamine?

A

Produces glutamate and ammonium ion in the mitochondria using glutaminase

148
Q

In the liver what happens to glutamate?

A

Makes ammonia and alpha KG using glutamate dehydrogenase

149
Q

How does glutamate DH work?

A

Oxidative deamination, either NAD or NADP cofactor, allosterically regulated by GTP and ADP

150
Q

How is nitrogen introduced to the urea cycle?

A

In form of aspartate and ammonia

151
Q

What is the connection between the Krebs and urea cycle called?

A

Krebs bicycle, links fate of amino groups with their carbon skeletons

152
Q

What can excess ammonia do to brain?

A

Accumulate and cause it to swell

153
Q

Which neurones relase glutamate derived from alpha KG?

A

Excitatory

154
Q

WHich cells take uo the glutamate and what do they do with it?

A

Glial cells and recycle it to glutamine to replenish lost carbon

155
Q

What activates methionine’s methyl group?

A

ATP - called SAM or AdoMEt

156
Q

What are donors for pathways which only need one carbon?

A

Folic acid or methionine

157
Q

Where does folic acid collect the 1C fragment from?

A

Serine

158
Q

What do ubiquinone and cytochrome c do?

A

Shuttle electrons between complexes

159
Q

Which ETC complex is irreversible?

A

IV - control here

160
Q

What do FMN and FAD have for redox? Which complexes are they found in?

A

Isoalloxazine ring in complex I and II

161
Q

What do Fe-S complexes do?

A

Transfer single electrons and carry out redox of flavins and UQ

162
Q

What do cytochromes do?

A

Transfer electrons between Fe2+ and Fe3+

163
Q

Which complex uses Cu not Fe-S?

A

IV

164
Q

What is complex I?

A

NADH-Q reductase

165
Q

What is complex 2?

A

Succinate dehydrogenase/succinate-Q reductase

166
Q

What is complex III?

A

Q-cytochrome c oxidoreductase

167
Q

What is complex IV?

A

Cytochrome c oxidase

168
Q

Why is ubiquinone membrane-soluble?

A

Lipophilic side chain

169
Q

How many H+ for each 2e-?

A

10

170
Q

How many H+ for Complex I, Q and complex 4?

A

4, 4, 2

171
Q

How many haems does cytochrome b have?

A

Two at opposite ends = one high potential, one low potential

172
Q

What is experimental evidence for transport chain order?

A

Monitor redox state using spectroscopy (visible for cytochromes, UV for UQ, e- sping resonance for Fe and Cu), no O2 = all components reduced, introduce O2 and oxidation goes backwards, can electrochemically measure redox potential

173
Q

What are the 4 redox centres?

A

Cyt a, a3, CuA and CuB

174
Q

How many subunits does F0 have?

A

10

175
Q

What are the subunits in F1?

A

3 alpha-beta twins and one gamma rotor

176
Q

What determines how many protons are needed to make ATP in the F0?

A

C units

177
Q

How do ATP and ADP exchange in and out of the mitochondria?

A

Due to charge

178
Q

How does phosphate enter the mitochondria?

A

Due to charge

179
Q

What are the three F1 states?

A

Loose (bind ADP and Pi), tight (H2O released) and Open (ATP produced, low affinity for ADP and Pi)

180
Q

What happens if there are more electrons in than electrons out?

A

Get QH. making O2- making aconitase making Fe2+ which makes .OH

181
Q

When and why is gluathione produced?

A

When you produce lots of NAD to protect against free radical damage making peroxide and H2O

182
Q

Why does muscle respond only to adrenaline?

A

No glucagon receptors

183
Q

How much fatty acid is released during exercise?

A

A small amount from muscle triglycerides

184
Q

What happens to the Pi produced from ATP breakdown during exercise?

A

Makes G1P from glycogen then makes G6P then glycolysis

185
Q

What forms AMP?

A

Adenylate kinase

186
Q

What is AMP deaminated to?

A

IMP

187
Q

How does IMP allow glycolysis use for longer?

A

Makes adenosin which stimulates vasodilation, also stimulates glycolysis

188
Q

How does cell make more succinyl CoA during exercise?

A

Makes it from isoleucine and valine

189
Q

What happens to GluT4 during insulin resistance?

A

Won’t be recruited to sarcolemma so excess glucose doesn’t enter muscle so glycogen synthesis impaired and glycogen breakdown increases

190
Q

What happens when the pancreas can’t maintain increased insulin production from insulin resistance?

A

Type II diabetes

191
Q

How does lack of insulin sensitivity affect lipoprotein lipase activity?

A

Decreases it, prevents VLDL upake, hormone sensitive lipase is acitvated from cAMP accumulation to produce circulating fatty acids and glycerol and further impairs glucose metabolism

192
Q

What happens when muscles and adipocytes can’t take up excess glucose?

A

Non-esterified fatty acids elevated, further inibits glucose uptake, promotes VLDL-triacylglycerol secretion

193
Q

What happens following low glycolysis rate from no GluT4 during diabetes?

A

Worsens hyperglycaemia, worsened by fatty acid oxidation, B oxidation produces acetyl CoA and NADH which inhibits PDH and turns off Krebs, muscle produces lactate and alanine so get gluceoneogenesis

194
Q

How do you get lipotoxicity?

A

Overfeeding > lots of malonyl CoA > fatty acid synthesis inhibits carnitine acyltransferase > increased gluconeogenesis, lipid synthesis and restricted B oxidation

195
Q

What does fatty acid influx promote in muscke?

A

B oxidation but no coordinated Krebs increasee

196
Q

What do products of increased fat oxidation cause in mitochondria?

A

Accumulate and might activate Ser kinases that impede insulin signalling and GluT4 translocation

197
Q

What does the Guthrie test look for?

A

Phenylketonuria - deficiency is PAH (phenylalanine hydroxylase)

198
Q

What inhibits citrate synthase?

A

ATP (allosterically)

199
Q

Why is citrate synthase regulation important for gluconeogenesis?

A

Oxaloacetate is using at the start of gluconeogenesis but if ATP is high then citrate synthase inhibition diverts oxaloacetate to gluconeogenesis whilst the acetyl CoA is used to generate ketone bodies

200
Q

What phosphorylates ADP?

A

Phosphoenolpyruvate and phosphocreatine

201
Q

What buffers ATP in many tissues?

A

Phosphocreatine

202
Q

How can you measure PCr?

A

31P nmr spectroscopy

203
Q

Where does oxygen for oxidation of G3P come from?

A

Water

204
Q

What activates PKA?

A

cAMP

205
Q

What inhibits gluconeogenesis?

A

Ethanol

206
Q

What does alanine do in the glucose-alanine cycle?

A

Carries NH3 and the carbon skeleton of pyruvate from muscle > liver

207
Q

WHat happens to excess ammonia?

A

Added to glutamate to form glutamine by glutamine synthetase

208
Q

What happens to glutamine in the liver?

A

NH4+ liberated by glutaminase

209
Q

How does liver release collected nitrogen from glutamate?

A

As NH3 via oxidative deamination using glutamate dehydrogenase in the mitochondria

210
Q

What does glutamate dehydrogenase use as a cofactor? What regulates it?

A

NAD+ or NADP+, allosterically regulated by GTP and ADP

211
Q

What happens in the urea cycle?

A

Nitrogen input as aspartate and ammonia, plus ATP then NH3 reacts with bicarbonate to form carbamoylphosphate, this is added to ornithine to make citrulline, aspartate condenses with it +ATP to form argininosuccinate, this is cleaved to form fumarate and arginine, this is hydrolysed by arginase to release urea and ornithine to start again

212
Q

What do ost excitatory neurones release?

A

Glutamate from alphaKG so must be replaced in TCA

213
Q

How do glial cells replace carbon lost from TCA?

A

Take up the glutamate and recycle it back to glutamine

214
Q

Why does excess ammonia in the brain deplete TCA of alphaKG?

A

Converts it to glutamate then glutamine

215
Q

What do folic acid and methionine do?

A

The main 1C donors for a range of biosynthetic pathways inc DNA and RNA synthesis

216
Q

How does folic acid collect 1C fragments?

A

Via serine hydroxymethyltransferase

217
Q

WHat is the first reserve used during a sprint?

A

PCr

218
Q

WHat is the phosphate from ATP breakdown used for? What stimulates this?

A

By phosphorylase to make G1P from glycogen - stimulated by Ca2+ from muscle contraction and adrenaline

219
Q

What forms AMP?

A

Adenylate kinase

220
Q

What happens to AMP?

A

Deaminated to inosine monophosphate which stimulates glycogenolysis, then degraded to adenosine which stimulates vasodilation

221
Q

What happens during long term exercise?

A

Glycogen and fatty acids oxidised, fatty acids released from adipose due to hormone sensitive lipase, some fatty acid released from muscle triglyceride breakdown, fatty acids and glycogen-derived pyruvate make acetyl CoA

222
Q

What happens if run out of oxaloacetate?

A

Convert isoleucine and valine to succinyl-CoA

223
Q

Why do raised FFA levels cause insulin sensitivity?

A

Prevent GluT4 from reaching cell surface because FFAs inhibit IRS-1 (part of the signalling pathway)

224
Q

Why is there decreased glycolysis and Krebs cycle if no insulin signalling?

A

Insulin signalling would normally increase it

225
Q

What does higher FFAs increasing beta oxidation do?

A

Produces acetyl CoA and NADH which inhibit TCA, also makes alanine and lactate which causes gluconeogenesis in the liver

226
Q

How do you get metabolic overload in skeletal muscle?

A

Fatty acid influx during overnutrition, beta oxidation with no coordinated TCA increase, by products e.g. ROS and acetylcarnitines accumulate, may activate Ser kinases which impede insulin signalling and GluT4 translocation

MIMS (8 decks)

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