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BDS Stage 1 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

What is metabolism ?

A

the sum of all chemical reactions in a cell needed to survive , grow and reproduce

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2
Q

How do enzymes catalyse reactions that happen at higher temperatures ?

A

they lower the activation energy

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3
Q

What happens during catabolic reactions ?

A

breakdown foodstuffs into smaller molecules

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4
Q

How does catabolism play a dual role ?

A

energy is released as well as small molecules being released

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5
Q

What happens during anabolic reactions ?

A

the energy released from catabolism is used to produce new molecules

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6
Q

What is the thermic effect of food ?

A

a high amount of energy is needed to process the food that the net amount of energy released is small

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7
Q

What is the units for the energy released from food ?

A

kCal per gram

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8
Q

How do organisms extract energy from food ?

A

oxidation

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9
Q

What is oxidation ?

A

the removal of electrons

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10
Q

What is reduction ?

A

the addition of electrons

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11
Q

In chemical reactions how do reduction and oxidation occur ?

A

simultaneously

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12
Q

How is energy conserved in reactions ?

A

the number of electrons is conserved

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13
Q

What can activated carriers store ?

A

chemical groups

electrons

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14
Q

What do activated carriers do ?

A

they act as the link between catabolism and anabolism

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15
Q

Energetically favourable reactions ….

A

… can drive unfavourable reactions

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16
Q

How does NAD store energy ?

A

in the from of 2 high energy electrons and H atoms

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17
Q

What is the precursor of NAD ?

A

niacin vit B3

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18
Q

What does NAD deficiency cause ?

A

pellagra - magneta tongue

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19
Q

What does FAD deficiency cause ?

A

angular stomatitis

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20
Q

During oxidation what happens to ATP

A

ADP is turned to ATP

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21
Q

During reduction what happens to ATP ?

A

ATP is turned to ADP

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22
Q

How is ATP generated ?

A

in the ETC of substrate level phosphorylation

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23
Q

Which chemical groups can activated carriers hold ?

A

acetyl
methyl
carboxyl groups

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24
Q

What are the 4 types of enzymatic control ?

A

allosteric
hormonal
rate limiting step
substrate supply

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25
Q

What is the rate limiting step ?

A

an irreversible reaction

the enzymes that catalyse the reaction are strictly regulated

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26
Q

What are allosteric effectors ?

A

they bind away from the active site

they can inhibit/activate enzyme activity

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27
Q

What is product feedback inhibition ?

A

when the product of the reaction can act on an earlier component to diminish the response

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28
Q

What is hormonal control of enzymes ?

A

phosphorylation of enzymes that is hormone mediated

enzyme induction - producing more enzyme - transcription and translation levels are effected

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29
Q

Which amino acids are phosphorylated when proteins are phosphorylated ?

A

serine
tyrosine
threonine

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30
Q

`Which enzyme controls protein phosphorylation ?

A

protein kinase

protein phosphatase

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31
Q

What does compartmentalisation allow ?

A

metabolic reactions to be controlled separately

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32
Q

Where does glycogenesis occur ?

A

cytosol

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33
Q

What are the 3 steps of glycogenesis ?

A

donor formation
elongation
branching

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34
Q

What enzymes are involved in glycogenesis ?

A

glycogen synthase

Branching enzyme

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35
Q

What is the activated donor in glycogenesis ?

A

UDP-glucose

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36
Q

What activates glycogen synthase ?

A

Glucose 6 Phosphate

ATP

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37
Q

What inhibits glycogen synthase ?

A

Glucagon
Adrenaline
they phosphorylate glycogen synthase inactivating it

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38
Q

Where does glycogenolysis occur ?

A

cytosol

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39
Q

What is the first step of glycogenolysis ?

A

removal of glucose units from glycogen

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40
Q

What happens after glucose 6 phosphate is made ?

A

in the liver it is converted to glucose by glucose 6 phosphatase

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41
Q

How does debranching happen ?

A

debranching enzyme removes the distal 3 units
amylo alpha 1,6 glucosidase removes the alpha 1,6 link
this releases free glucose
can be phosphorylated by hexokianse

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42
Q

What are the enzymes involved in glycogenolysis ?

A

glycogen phosphorylase
glucose 6 phosphatase
debranching enzyme
amylo alpha 1,6 glucosidase

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43
Q

What stimulates glycogen phosphorylase ?

A

glucagon and adrenaline

they phosphorylate

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44
Q

Describe a phosphorylation cascade ?

A

the presence of adrenaline or glucagon in tge blood can cause ATP to be converted to cAMP
cAMP activates protein kinase
protein kinase inhibits Glycogen Synthase
protein kinase phosphorylates phosphorylase kinase
phosphorylase kinase activates Glycogen phosphorylase

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45
Q

What are the 2 phases of glycolysis ?

A

energy investment

energy generation

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46
Q

What are the steps in the energy investment phase ?

A

Glucose is phosphorylated by hexakinase to glucose 6 phosphate
this isomerises to fructose 6 phosphate
this is converted to fructose 1,6 bisphosphate by phosphofructokinase
this splits into an equilibrium of dihydorxyacetone phosphate and glyceraldehyde 3 phosphate

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47
Q

What are the steps in the energy generation phase ?

A

glyceraldehyde 3 phosphate changes into 1,3 bisphosphoglycerate
this changes into 3 phosphoglycerate
this then changes into 2 phosphoglycerate
this then turns into phosphoenoylpyruvate in dehydration
this is the turned into pyruvate by pyruvate kinase

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48
Q

What is the yield of glycolysis per every molecule of glucose ?

A

2 pyruvate
2 net ATP
2 G3P

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49
Q

Where is glucokinase found ?

A

in the liver

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50
Q

What is the cori cycle for ?

A

What happens to glucose under anaerobic conditions

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51
Q

What are the steps of the cori cycle ?

A

Glucose 6 phosphate is converted to Pyruvate (glycolysis)
pyruvate is converted to lactate by lactate dehydrogenase
the lactate is taken to the liver
converted back to Pyruvate
made into the glucose in gluconeogenesis

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52
Q

The glucose made in the cori cycle can be used for what ?

A

glycolysis

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53
Q

Where does the link reaction happen ?

A

mitochondrial matrix

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54
Q

What conditions does the link reaction happen under ?

A

Aerobic

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55
Q

What is the link reaction ?

A

pyruvate is converted to acetyl coA in an irreverisble oxidative decarboxylation
catbon dioxide comes off
coA comes in

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56
Q

What catalyses the link reaction ?

A

pyruvate dehydrogenase complex

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57
Q

What is also made in the link reaction ?

A

NADPH - for biosynthesis

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58
Q

What is substrate level phosphorylation ?

A

Direct formation of ATP from the phosphorylation of ADP

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59
Q

What is oxidative phosphorylation ?

A

ATP is formed in the ETC as electrons are transferred from electron carriers to molecular oxygen

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60
Q

Where does the TCA cycle occur ?

A

mitochondrial matrix

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61
Q

What are the steps in the TCA cycle ?

A 
Acetyl coA condenses with oxaloacetate to form citrate
citrate to isocitrate 
isocitrate to alpha-ketoglutarate 
alpha- ketoglutarate to succinyl coA
succinyl coA to succinate 
succinate to fumarate 
fumarate to Malate.
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62
Q

What are the 3 enzymes in the TCA cycle ?

A

Citrate synthase
isocitrate dehydrogenase
alpha-ketoglutarate dehydrogenase complex

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63
Q

What is also produced in the TCA cycle ?

A

GDP-GTP-ATP
FAD-FADH2
NAD-NADH
CO2

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64
Q

What are the 2 steps of the pentose phosphate pathway ?

A

irreversible oxidative phase

reversible non oxidative phase

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65
Q

What is the irreversible oxidative phase ?

A

glucose 6 P combines with water and 2x NADP

makes ribulose 5 phosphate carbon dioxide and 2xNADPH

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66
Q

What catalyses the irreversible oxidative phase ?

A

glucose 6 phosphate dehydrogenase

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67
Q

Where does the pentose phosphate pathway occur ?

A

cytosol
liver
adrenal cortex
mammary glands

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68
Q

What is the reversible non oxidative phase ?

A

ribulose 5 phosphate can be turned into Glyceraldehyde 3 phosphate
Ribose phosphate to make nucleic acids
fructose 6 phosphate which can isomerise back to glucose 6 phosphate

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69
Q

Where does the pyruvate in gluconeogenesis come from ?

A

lactate

alanine

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70
Q

What are the steps in gluconeogenesis ?

A 
2 x pyruvate 
2 x Oxaloacetate
2 x phosphoenoylpyruvate 
equlibrium of dihydroxyacetone phosphate and glyceraldehyde 3 phosphate 
fructose 1,6 bisphosphate 
furctose 6 phosphate 
glucose 6 phosphate 
glucose
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71
Q

What enzymes are involved in gluconeogenesis ?

A

pyruvate carboxylase
PEP carboxykinase
Fructose 1,6 bisphosphotase
glucose 6 phosphatase

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72
Q

What do amino acids consist of ?

A

carbon skeletons - ketoacids

to which an amino group can be attached

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73
Q

What is transamination ?

A

the formation of one amino acid from another by transfer of an alpha amino group

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74
Q

Which enzymes catalyse transamination ?

A

aminotransferase

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75
Q

Where are aminotransferase enzymes found ?

A

in the cytosol and the mitochondria

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76
Q

What do aminotransferase enzymes catalyse specifically ?

A

transfer of an alpha amino group to an alpha ketoacid

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77
Q

What does transamiantion require ?

A

vitamin b6 - pyridoxine

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78
Q

How is glutamate made via transamination ?

A

from alpha ketoglutarate which receives an alpha amino group to become glutamate

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79
Q

How can aspartate be made from glutamate ?

A

glutamate transfers its alpha amino group to become alpha ketoglutarate
the group is recived by oxaolacetate (a ketoacid) which becomes aspartate

80
Q

How are aminotransferases subject to product feedback inhibition ?

A

high amounts of aspartate (the product) can turn off the enzyme

81
Q

As the demand for amino acids increases what can happen ?

A

enzyme induction in the liver as demand for specific amino acids increases

82
Q

How is tyrosine made ?

A

from the essential amino acid phenylalanine by

phenylalanine hydrolase

83
Q

What does a build up of phenyalanine lead to ?

A

formation of phenyl ketones
leads to CNS damage
can saturate transporters in the blood brain barrier so that other molecules cant enter the brain

84
Q

what are the consequences of phenylketonuria ?

A

they have to stop protein break down and therefore require high energy foods (fat/sugar)

85
Q

How can phenylketonuria occur ?

A

no phenylalanine hydrolase - tyrosine cant be made and therefore phenylalanine builds up

86
Q

Which amino acids are described as being glucogenic ?

A

amino acid that end up as TCA cycle intermediates - they ultimately end up as oxaloacetate

87
Q

Which amino acids are described as being ketogenic ?

A

amino acids that become intermediates in ketogenesis (acetoacetate production)

88
Q

What does it mean to be solely ketogenic ?

A

they make acetoacetate only

89
Q

what does 3 phosphoglycerate turn into ?

A

pyruvate via glycolysis

90
Q

What does pyruvate get converted into ?

A

acetyl coA

91
Q

what does acetylcoA get converted into ?

A

acetoacetate - a ketone body

92
Q

Which amino acids are purely ketogenic ?

A

leucine
lysine
tryptophan
they enter at acetoacetate

93
Q

How is ammonia formed ?

A

protein turnover
inactivation of neurotransmitters
exercise
protein brekadown

94
Q

Why must ammonia be removed from the tissues ?

A

it is toxic

95
Q

How is ammonia removed from cells ?

A

it is converted to urea in the liver

removed from cells that cant make urea

96
Q

How is ammonia removed from the brain ?

A

alpha ketoglutarate is converted to glutamate by glutamate dehydrogenase
this uses up one ammoium ion
the glutamate is then converted to glutamine by glutamine synthase - this used another ammonium ion
this is taken to liver where glutamine is converted back to glutamate by glutaminase , this releases another ammonium ion
the second ion is removed via oxidative deamination

97
Q

How is ammonia removed from the muscles ?

A

alpha ketoglutarate is converted to glutamate using an ammonium ion and glutamate dehydrogenase
glutamate is transaminated to alanine using pyruvate
alanine is taken to the liver
in the liver alanine is converted back to glutamate

98
Q

Which enzyme catalyses the conversion of glutamate tioalanine via transamination ?

A

alanine amino transferase

99
Q

What is oxidative deamination ?

A

glutamate is converted alpha ketoglutarate via glutamate dehydrogenase to release another ammonium ion

100
Q

What happens to the ammonium ions released in the liver ?

A

they enter the urea cycle

101
Q

What happens in the urea cycle ?

A

toxic ammonia is converted to the urea in the liver

102
Q

For every molecule of urea how many ammonium ions are removed ?

A

2

103
Q

What is citrulline ?

A

it is formed when carbamoyl phosphate combines with ornithine

104
Q

How is ornithine formed ?

A

arginase catalyses the reaction by which arginine is converted into ornithine releasing urea

105
Q

Where does the urea cycle happen ?

A

in the liver

partly in cytosol and partly in mitochondria

106
Q

What happens in the urea cycle ?

A

carbon dioxide and ammonium combine to form carbamoyl phosphate - this is catalysed by carbamoyl phosphate synthase
carbamoyl phosphate is transferred to ornithine to form citrulline
exits mitochondria on a carrier
citrulline and aspartate combine to make arginosuccinate
arginosuccinate is converted to arginine relasing fumarate
arginate is converted to ornothine again by arginase which releases the urea

107
Q

What is the rate limiting step in the urea cycle ?

A

carbon dioxide + ammonium to give carbamoyl phosphate catalysed by carbamoyl phosphate synthase

108
Q

What is the source of aspartate ?

A

the fumarate released from the conversion of arginosuccinate to arginine
fumarate is converted to malate
malate is oxidised to oxaoloacetate
oxaloacetate is transaminated to form aspartate using glutamate.

109
Q

What happens in the lipolysis of triglycerides ?

A

triglycerides are converted into fatty acids and glycerol by lipase

110
Q

What happens to the glycerol ?

A

it is taken to the liver where
glycerol is phosphorylated to glycerol phosphate by glycerol kinase
glycerol phosphate is converted to dihydroxyacetone phosphate
this splits into an equilibrium with glyceraldehyde 3 phosphate
glyceraldehyde 3 phosphate is converted to glucose in gluconeogenesis

111
Q

What happens during the activation of fatty acids ?

A

fatty acids + coA gives fatty acyl coA

catalysed by fatty acyl coA synthase

112
Q

How is fatty acyl coA transported into the mitochondria ?

A

the CAT shuttle

113
Q

What is the CAT shuttle ?

A

acyl coA changes into coA
at the same time acyl carnitine is made from carnitine
acyl carnitine is taken into the mitochondria on a translocase carrier
acyl carnitine becomes carnitine as the coA becomes acyl coA for oxidation

114
Q

Describe beta oxidation of fatty acetyl coA ?

A

acetyl coA is oxidised to transenoyl coA
transenoyl coA is hydrated to betahydroxyacyl coA
this is oxidised to betaketoacylcoA
this is thiolysed into acetyl coA and an acycl CoA which is now 2 carbons shorter

115
Q

Where does beta oxidation take place ?

A

mitochondria

116
Q

Describe ketogenesis ?

A

acetyl coA is compressed with another molecule of acetyl coA to make acetoacetyl coA
this is converted to HMG-coA via HMG-coA synthase
this is converted back to acetyl coA and acetoacetate is given off and this turns into B-hydroxybutarate.

117
Q

What is the first step in fatty acid synthesis ?

A

transport from the mitochondria into the cytosol

118
Q

How is citrate transported into the cytosol ?

A

citrate breaks down into acetylcoA and oxaloacetate
acetylcoA is used for fatty acid synthesis
oxaloacetate breaks into malate
malate is made into pyruvate
pyruvate enters the mitochondria
pyruvate turns into oxaloacetate
this turns back into cirate

119
Q

What happens in the activation of acetyl coA ?

A

acetyl coA is converted into malonyl coA via acetyl coA carboxylase using carbon dioxide

120
Q

What is fatty acid synthase ?

A

it is a dimer of acyl carrier proteins

they accept malonyl coA and acetyl coA when the coA is released

121
Q

What are the 4 steps of reaction in adding 2 carbon units ?

A

condensation
reduction
dehydration
condensation

122
Q

What happens in condensation ?

A

the malonyl ACP and the acetyl ACP combine to form acetoacyl ACP which is 2C

123
Q

7 cycles of these reactions leads to what being formed ?

A

16 acyl chain - palmitate when cleaved off the ACP

124
Q

How many ATP are produced in the oxidation of palmitoyl coA ?

A 
there are 7 cycles of Beta oxidation 
this makes 7 FADH2   7NADH and 8 acetyl coA 
each NADH makes 2.5 ATP
Each FADH2 makes 1.5 ATP 
in the TCA cycle - 7.5 ATP 
1.5 ATP 
1 ATP 
multiply by 8 - 108 ATP
125
Q

What is the yield of one round of the TCA cycle ?

A

1 FADH2
3 NADH
1 GTP

126
Q

What is the yield of one beta oxidation ?

A

1 FADH2
1 NADH
1 acetyl co A - at the end get 2 as they both are acetyl coA

127
Q

How are unsaturated fatty acids made ?

A

elongation beyond 16 carbons requires oxidases which introduce double bonds

128
Q

What is cholesterol ?

A

a 27 carbon steroid molecule made from acetyl coA

129
Q

How is cholesterol synthesised ?

A

formation og HMG by HMG coA reductase

HMG is converted to squalene which is made into cholesterol

130
Q

What stimulates HMG-coA Reductase ?

A

high insulin: glucagon as phosphorylation inactivates the enzyme

131
Q

How are fatty acids transported

A

by being attached to albumin

132
Q

How are triglycerides transported ?

A

lipoproteins

133
Q

how is cholesterol transported ?

A

lipoproteins

134
Q

What does a lipoprotein do ?

A 
phospholipid bilayer 
unesterified cholesterol 
esterified cholesterol 
hydrophobic core 
apo proteins
135
Q

What chylomicrons do ?

A

transport triglycerides from ingested fats to the rest of the body

136
Q

What do chylomicrons contain ?

A

triglyceride
cholesterol
apo protein B48

137
Q

What is the action of chylomicrons ?

A

they steal Apo protein CII and Apo protein E from HDL
this activates lipoprotein lipase in the endothelial surface of vasculature
hydrolyses the triglycerides

138
Q

What happens to the chylomicrons when the triglycerides have been depleted ?

A

they return the apo protein CII to HDL

139
Q

What happens to the Apo B48 and Apo E ?

A

they return to the liver for degradation

140
Q

What do VDL and IDL do ?

A

transport lipids from the liver to the rest of the body

141
Q

Where are VDL and IDL made ?

A

hepatocytes

142
Q

What do VLDL and IDL contain ?

A

triglycerides
cholesterol
Apo 100

143
Q

What do VLDL and IDL do when released into circulation ?

A

steal apo CII and Apo E from HDL

allows lipoprotein lipase to hydrolyse the triglycerides

144
Q

What happens as the TAG is removed from the VDL ?

A

the apo CII is returned to HDL

VLDL becomes IDL

145
Q

What do IDL remnants do ?

A

go back the the liver

146
Q

What happens to IDL remaining in circulation ?

A

receives cholesterol from HDL

donates phospholipids and TAG to HDL

147
Q

What does LDL do ?

A

transports cholesterol to peripheral tissues

148
Q

What does Apo E do ?

A

binds to LDL receptors on peripheral cell
LDL enters the cell by endocytosis
in the cell LDL fuses with lysosomes - cholesterol released

149
Q

Where is HDL made ?

A

in the liver

150
Q

What does HDL contain ?

A

phospholipid and Apo proteins

151
Q

What does HDL do ?

A

accepts free cholesterol from the peripheral cells

passes it onto VLDL./IDL to become LDL

152
Q

What are the other roles of HDL ?

A

source of apo proteins for chylomicrons and VLDL

can carry cholesterol back to the liver

153
Q

What are genetic dyslipidameias ?

A

elevated blood triglyceride or cholesterol due to abnormal lipid metabolism
could be due to faulty lipoprotein lipase

154
Q

What is the hormonal response to a food deficit ?

A 
blood glucsoe decreases 
so insulin decreases
glucagon decreases 
noradrenlaine increases
cortisol increases 
overall -     insulin:glucagon decreases
155
Q

What food stores are metabolised for energy ?

A

glycogen
adipose tissue
muscle amino acids

156
Q

What is the mechansim for topping up blood glucose between meals ?

A

blood glucose decreases
glucagon/ noradrenaline decrease
liver glycogenolysis - glucose released into the blood

157
Q

What does the release of glucagon and noradrenaline do to key enzymes ?

A

glycogen synthase is inhibited

glycogen phosphorylase activated

158
Q

How long do liver glycogen stores last ?

A

12 hours

159
Q

What happens to top up blood glucose after ?

A

gluconeogenesis
muscle amino acids are transmaminated to alanine
this goes to the liver
alanine is transaminated back to pyruvate
this is converted to glucose in gluconeogenesis

160
Q

How is alanine converted to pyruvate ?

A

transamination
alanine donated alpha amino group to alpha ketoglutarate - become glutamate
the alanine becomes pyruvate
the glutamate can be used in the removal of ammonia in the urea cycle

161
Q

What does glucagon do to key enzymes ?

A

pyruvate kinase is inhibited - glycolysis inhibited

Fructose 1,6 BPase is stimulated - gluconeogenesis

162
Q

What does acetyl coA do to key enzymes ?

A

inhibits pyruvate dehydrogenase complex - stop production of more acetyl coA
pyruvate carboxylase activated by acetyl coA - gluconeogenesis

163
Q

What is the consequence of using ,muscle amino acids for gluconeogenesis ?

A

decreased protein synthesis

increased production of urea in urea cycle

164
Q

After depletion of liver glycogen how much protein and urea is lost daily ?

A

12-14 g N

80g of protein

165
Q

What activates lipase ?

A

a decrease in insulin

166
Q

What does lipase do ?

A

lipolysis - break down of lipids to fatty acids and glycerol

167
Q

What can glycerol be used for ?

A

gluconeogenesis

168
Q

What happens to the fatty acids ?

A

they can undergo Beta oxidation in the liver or the muscle to make acetyl coA

169
Q

What is the consequence of rapid fat break down ?

A

not enough oxaloacetate to combine with acetyl coA to enter the TCA cycle
acetyl coA is redirected to ketogenesis in the HMG-coA cycle - in the liver

170
Q

How long after initial food deficit are ketone bodies produced ?

A

3 days

171
Q

What can ketone bodies be used for ?

A

they are a source of fuel for brain and cardiac muscle

enzyme induction occurs in the brain and cardiac muscle - utilise the ketone bodies for energy

172
Q

What is adaptation ?

A

when the brain can get 50% of its energy frome ketone bodies and there isnt a need fro glucose

173
Q

What does adaptation include ?

A 
no requirement for glucose
rate of gluconeogenesis decreases 
less amino acids sued 
decreased nitrogen loss 
less than 5g a day loss
174
Q

In trauma how is information conducted to the brain ?

A

baroreceptors
pain receptors
sensory receptors

175
Q

What happens once trauma is detected by the brain ?

A

There is a change in the hormone profile -
glucagon , NA and cortisol are increased
reduced insulin to glucagon ratio

176
Q

What is starvation ?

A

hypoglycaemia
increased ketogenesis
small protein losses when adapted

177
Q

What is trauma ?

A

Hyperglycaemia due to increased cori cycle activity
blunted ketone body formation
marked protein loss - no adaptation

178
Q

Why is their hyperglycaemia in trauma ?

A

insulin resistance due to high levels of catabolic hormones
increased cori cycle activity
increased gluconeogenesis due to raised glucagon and cortisol

179
Q

Describe the cori cycle ?

A 
glucose 6 phosphate 
converted to pyruvate 
converted to lactate 
taken to the liver 
made into pyruvate
glucose via gluconeogenesis 
the glucose cant et in due to the high insulin resistance - contributes to hyperglycaemia
180
Q

Why is their marked protein loss in trauma ?

A

increased protein loss because less ketone bodies to use as fuel

181
Q

What fuels the immune system in trauma ?

A

glutamine
reduced rate of protein synthesis
increased cytokine activity results in catabolism

182
Q

What are the traits of DM ?

A

hyperglycaemia and ketoacidosis

183
Q

What does insulin promote in a non-diabetic ?

A

GLUT-4 transporter which transports glucose into cells

this promotes glycogenesis

184
Q

Why does blood glucose increase due to DM ?

A

blood glucose increases due to more catabolic hormones
cells are deficient in glucose because no GLUT-4
glycogenolysis and gluconeogenesis occur

185
Q

What happens to amino acids in DM ?

A

the amino acids are lost from the muscle to fuel gluconeogenesis
insulin would have uptaken it for anabolic reactions

186
Q

What does decreased insulin mean ?

A

lipase is active

high rate of lipolysis and therefore high amount of fatty acids in the blood

187
Q

What happnes to the fatty acids ?

A

they are oxidised in the muscle or the liver
by beta oxidation to form acetyl coA
the acetly coA can also be used to mske ketone bodies

188
Q

What happens in a non diabetic to control lipolysis ?

A

acetoacetate - a ketone body stimulates insulin which will turn lipase off

189
Q

Why does lipolysis continue in diabetics ?

A

there is no insulin for acetoacetate to stimulate hence lipase remains active and lipolysis will continue

190
Q

What is the diabetic diet ?

A

low in sugars and fat

high in fibre , fruit and veg

191
Q

What is the diabetic diet associated with ?

A

low rates of dental caries

192
Q

What can type 2 diabetes lead to an increased risk of ?

A

periodontal disease

193
Q

How is fructose metabolised ?

A

the slow muscle route - Glucose 6 phosphate isomerising to fructose 6 phosphate and then fructose 1,6 BP which splits into the equilibrium of DHAP and G3P

the fast hepatic route - fructose is phosphorylated by hepatic fructokinase into fructose 1 phosphate and then converted unto DHAP by fructose 1 phosphate aldolase

194
Q

What is fructosuria ?

A

absence of hepatic fructokinase
this mean the hepatic fast route cant be taken for fructose metabolism
instead the slow muscle route is taken and this leads to a build up of fructose in the blood which spills into the urine

195
Q

What us hereditary fructose intolerance ?

A

absence of fructose 1 phosphate aldolase
the fructose 1 phosphate cant be converted to DHAP
inorganic phosphate is trapped
phosphate is needed to phosphorylate glycogen phosphorylase and fructose 1,6 BPase
this means glycogenolysis and gluconeogenesis cant occur
results in hypoglycaemia

196
Q

What are the sources of fructose ?

A

sucrose
avoid anything with sucrose
people with HFI have a low sugar diet - therefreo good DMFT

BDS Stage 1 (39 decks)

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