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GI > Liver - metabolism > Flashcards

Liver - metabolism Flashcards

1
Q

which enzyme converts glucose to glycogen?

A

glycogen synthase

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2
Q

In which organs does AMP-activated protein kinase phosphorylate key enzymes?

A

liver, heart, muscle, adipose tissue

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3
Q

what are the effects of AMP-activated kinase phosphorylating key enzymes?

A

AMP = signal of low energy state
increase in energy providing pathways
inhibit anabolic/ synthetic pathways

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4
Q

does glucagon stimulate or inhibit glycogen breakdown and how?

A

stimulates by phosphorylation of a protein that activate glycogen phosphorylase

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5
Q

which enzyme converts acetyl CoA to malonyl CoA?

A

acetyl coA carboxylase

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6
Q

what stimulates acteyl coA carboxylase?

A

insulin (high insulin levels –> store fats)

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7
Q

Which 3 compounds inhibit the conversion of acetyl coA to malonyl coA?

A

AMPK, glucagon, adrenaline

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8
Q

when are carbohydrates converted to fatty acids?

A

excess carbohydrates

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9
Q

where does fatty acid and lipid synthesis occur?

A

mainly in the liver
also in adipose tissue
breast tissue during lactation to decrease the strain on the body

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10
Q

where does the link reaction take place?

A

mitochondria

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11
Q

what is pyruvate converted into in anaerobic conditions?

A

lactate

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12
Q

which compound from the krebs cycle is converted into acetyl CoA in the cytoplasm?

A

citrate

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13
Q

where does fatty acid synthesis take place in the cell?

A

cytoplasm

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14
Q

what is the key control point for fatty acid synthesis?

A

acteyl coA carboxylase (acetyl coA –> malonyl coA)

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15
Q

what are fatty acids combined with to form triacylglycerols?

A

glycerol 3-phosphate

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16
Q

how is acetyl coA converted into malonyl coA?

A

ATP and CO2 required

enzyme = acetyl coA carboxylase

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17
Q

which enzyme combines C4 chains with more malonyl coa?

A

fatty acid synthase

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18
Q

how many carbons in palmitate?

A

16

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19
Q

where are fatty acids modified and stored?

A

endoplasmic reticulum

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20
Q

where are triacyclglyerides made?

A

endoplasmic reticulum

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21
Q

what happens to lipids in adipose tissue?

A

stored in cytosol

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22
Q

what happens to lipids in the liver?

A

packaged into VLDLs –> blood –> adipose tissue for storage or peripheral tissue for energy

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23
Q

which happens to lipids in peripheral tissues?

A

used as an energy source

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24
Q

what are the 2 steps involved in fatty acid metabolism?

A
  1. carrier needed to transport fatty acyl CoA from cytosol into matrix
  2. B oxidation
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25
Q

where does B oxidation of fatty acids occur?

A

mitochondrial matrix of liver hepatocytes

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26
Q

which fatty acids can diffuse across the cell membrane without a carrier?

A

those with fewer than 12C chains

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27
Q

what products are produced from fatty acid metabolism?

A

ATP, NADH, FADH, acetyl coA

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28
Q

which cofactors are involved in B oxidation and what happens to them?

A

FAD and NAD get reduced to FADH and NADH

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29
Q

how are fatty acids activated before they are transported across the cell membrane?

A

ATP required to activate them to fatty acyl coA

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30
Q

what controls fatty acid oxidation?

A

the transport of fatty acids across cell membranes by carnitine carriers

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31
Q

when is breakdown of fatty acids inhibited?

A

when high levels of malonyl coA (signalling high energy state)
high levels inhibit acyl-transferase -1 so fatty acids are not transferred to carnitine carriers

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32
Q

which enzyme is required for fatty acid synthesis?

A

acetyl coA carboxylase

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33
Q

overall how many ATP molecules are produced per palmitoyl coA molecule?

A

108

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34
Q

what is produced with each turn of b oxidation?

A

1 acetyl coA (NADH, FADH)

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35
Q

Is fatty acid oxidation aerobic or anaerobic and why?

A

aerobic because NADH and FADH are oxidised by the krebs cycle etc. which are aerobic processes

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36
Q

when does ketone body formation occur?

A

excess acetyl coA for example when the body breaks down fats for energy when fasting or in uncontrolled diabetes

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37
Q

why can acetyl coA not be metabolised via the krebs cycle?

A

starvation state so krebs cycle intermediates are depleted

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38
Q

what are the steps in ketone body formation?

A

2 acteyl coA –> acetoacetyl coA –> HMGcoA –> acetoacetate –> acetone and 3-hydroxybutyrate

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39
Q

where does ketone body formation occur?

A

mitochondria of liver cells

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40
Q

what are the 3 ketone bodies?

A

acetoacetate, acetone, 3-hydroxybutyrate

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41
Q

which organ can use ketone bodies for energy?

A

brain oxidises ketone bodies for energy

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42
Q

what is cholesterol used for?

A

component of cell membranes

synthesis of hormones, bile, vitamin D etc

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43
Q

what are the 2 sources of cholesterol?

A 
from the diet (egg yolk, liver, meat)
and synthesis (75%)
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44
Q

where is cholesterol synthesised?

A

in almost all tissues but mainly the liver

to some extent in the small intestine

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45
Q

how do plant sterols and stanols helps to lower plasma cholesterol levels?

A

they inhibit cholesterol uptake from the gut

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46
Q

how many stages are there to cholesterol biosynthesis?

A

4

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47
Q

which is the most important step?

A

1st stage

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48
Q

where do statins inhibit cholesterol synthesis?

A

inhibit HMG coA reductase enzyme

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49
Q

what is required for cholesterol synthesis?

A

ATP

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50
Q

what happens during the 1st stage of cholesterol synthesis?

A

acetyl coA –> mevalonate (C6)

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51
Q

what happens during the second stage of cholesterol synthesis?

A

mevalonate –> phosphorylated isoprene units (C5) = activation

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52
Q

what happens in the 3rd stage of cholesterol synthesis?

A

6 isoprene units polymerised –> C30 chain (squalene)

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53
Q

what happens in the final stage of cholesterol synthesis?

A

cyclisation –> ring structure (lanosterol) –> cholesterol

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54
Q

which 3 compounds are isoprenoids?

A

isopentylpyrophosphate
geranylpyrophosphate
farnesylpyrophosphate

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55
Q

what is prenylation?

A

adding a farnesyl or geranyl lipid chain that anchors the small G protein to the intracellular face of the lipid membrane

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56
Q

which isoprenoid produces Ras small GTPase?

A

FPP - farnesylpyrophosphate

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57
Q

which isoprenoid produces Rho small GTPase?

A

GGPP - geranylgeranylpyrophosphate

58
Q

what do Ras and Rho affect?

A

cell signalling functions

gene expression

59
Q

what are the pleiotropic effects of statins?

A

antioxidant properties
inhibit inflammatory responses
stabilise atherosclerotic plaques
improve endothelial dysfunction

60
Q

how is the rate of cholesterol synthesis controlled?

A

controlling ACTIVITY or AMOUNT of HMG-coA reductase

61
Q

what happens to the activity of HMG-CoA reductase when energy levels are low?

A

glucagon inhibits phosphorylation of the enzyme so inhibits synthesis

62
Q

which 2 factors control the activity or amount of HMG-coA reductase?

A

energy levels and cholesterol levels

63
Q

how do energy levels effect cholesterol synthesis?

A

alter the activity of HMG-coA reductase

64
Q

how do high cholesterol levels inhibit the synthesis of cholesterol?

A

alter the amount of HMG-coA reductase present
inhibit trasncription
stimulate degredation

65
Q

why do high energy levels increase cholesterol synthesis?

A

insulin stimulates phosphoylation of HMG-CoA reductase

66
Q

how does insulin affect the amount of HMG-coA reductase present?

A

stimulates transcription of the enzyme

67
Q

how does cholesterol effect SREBP?

A

high levels of cholesterol inhibit the release of SREBP from the ER, which binds to sterol response unit of gene coding for HMG-coA reductase and is therefore required for its synthesis

68
Q

how is cholesterol removed from the body?

A

cannot be broken down so can only be excreted

secreted in bile –> excreted in faeces

69
Q

which 3 common diseases are linked with excess cholesterol?

A

coronary heart disease
steatohepatitis
alzheimers disease

70
Q

how are mono- and poly-unsaturated fats beneficial?

A

reduce CHD risk and may have other benefits

71
Q

why are saturated fats bad?

A

they increase the levels of LDL cholesterol in the blood

72
Q

How do trans fats affects lipoprotein levels?

A

increase the levels of LDLs and reduce the levels of HDLs

73
Q

what effect does dietary cholesterol have on lipoproteins?

A

can raise LDL levels but has less effect than others

74
Q

how is cholesterol transported in the blood?

A

insoluble therefore transported by lipoproteins

75
Q

what are the 4 types of lipoprotein and what are their roles?

A

Chylomicrons: dietary fats (cholesterol and triglycerides) transported from intestines to liver
VLDLs: lipids made in liver transported from liver to peripheral tissues
LDLs: main cholesterol carrier in blood for peripheral tissues
HDLS: cholesterol from peripheral tissues to liver (reverse cholesterol transport)

76
Q

what is the significance of apolipoproteins?

A

specific protein embedded in surface of lipoproteins determine start and end points for cholesterol transport

77
Q

which apolipoproteins do HDLs have?

A

Apo A-I and Apo A-II

78
Q

which apolipoproteins do LDLs have?

A

Apo B and Apo E

79
Q

how are LDLs taken up into cells?

A

LDL receptor binds Apo B-100 or Apo E
endocytosis of LDL and receptor
LDL released and LDL receptor recycled

80
Q

how is LDL receptor activity controlled?

A

high levels of cholesterol inhibit synthesis of LDL receptor so reduced expression of LDL receptors on cell surface so more LDLs circulating in blood

81
Q

how can HDLs protect against atherosclerosis?

A

scavenges cholesterol from cells and LDLs and transports it to the liver

82
Q

why do HDLs not cause atherosclerosis?

A

APo A apolipoproteins are resistant to oxidation

83
Q

how do LDLs contribute to atheroclerosis?

A

oxidised LDLs = very inflammatory and atherogenic

xs cholesterol deposited in arteries

84
Q

which phospholipid does cholesterol form a raft with in membranes?

A

sphingolipids –> reduce membrane fluidity

85
Q

what is Tangier disease?

A

lack of HDL –> at risk of CHD

86
Q

What is familial hypercholesteraemia?

A

lack of LDL receptors

mutations affecting LDL receptor or defective apo B100 so impaired binding of LDL

87
Q

how is high cholesterol linked to alzheimers disease?

A

APOE4 allele –> increased risk
increased plasma cholesterol correlates with increased risk
accumulation of AB peptide in animal models
statin therapy and decreased alzheimers?

88
Q

what is non-alcoholic steatohepatitis?

A

form of chronic liver disease
accumulation of triglycerides
associated with obesity and metabolic syndrome, use of some drugs, inherited metabolic disorders
insulin resistance –> increased insulin secretion –> stimulates fatty acid synthesis

89
Q

how does fat accumulation in the liver affect the tissue?

A

leads to inflammation and fibrosis

90
Q

what occurs in alcoholic steatohepatitis?

A

metabolism of high amounts of alcohol –> large amounts of NADH
fatty acid oxidation inhibited and excess triglyeride synthesis activated

91
Q

why might non-alcoholic steatohepatitis occur?

A

insulin resistance, obesity, metabolic disorders

92
Q

how do LDLs enter the subintimal space beneath the endothelium of blood vessels?

A

damage to endothelial cells from smoking or high blood pressure enables them to enter

93
Q

how do LDLs become foam cells?

A

oxidised LDLs engulfed by macrophages –> foam cells

94
Q

what is found within an atherosclerotic necrotic core?

A

cholesterol and necrotic cells damage

95
Q

in which layer do athersclerotic plaques form?

A

tunica intima

96
Q

what components form the fibrous cap of a plaque?

A

collagen and smooth muscle fibres

97
Q

which components make the necrotic core prothrombotic?

A

collagen (I, III) –> GPVI on platelets
LPA –> P2Y on platelets
TF –> FVIII –> activates coagulation

98
Q

how do macrophages assist in the degredation of the fibrous plaque cap?

A

secrete proteinase enzymes that degrade the cap

99
Q

why does steatohepatitis occur?

A

impaired energy metabolism

triglyercide export from liver is impaired –> accumulation of lipid droplets in hepatocytes

100
Q

what does the surface layer of lipoproteins consist of?

A

phospholipids and free cholesterol

101
Q

what does the hydrophobic core of lipoproteins consist of?

A

triglyceride and cholesterol esters

102
Q

what carrier is required to convert glucose-1-phosphate into glycogen?

A

UDP –> UDP-glucose

103
Q

what is the primer called that is required to build glycogen?

A

glycogenin

104
Q

where are the 1-6 bonds in the glycogen molecule?

A

at the branch sites

105
Q

where are the 1-4 glycosidic bonds in the molecule?

A

within the straight chains

106
Q

what are the advantages of glycogen as a storage molecule?

A

can be broken down quickly and can be built quickly

107
Q

which tissues store glycogen?

A

all to limited extent mainly the liver and skeletal muscle

108
Q

why is glycogen stored in the liver?

A

stored until early fasting when it is broken down to release glucose for the body

109
Q

why is glycogen stored in muscles?

A

to be broken down for muscle energy use

110
Q

what is the control point of glycogen synthesis?

A

glycogen synthase
prevents synthesis/ use occurring simultaneously
glycogen synthase and glycogen phosphorylase are reciprocally controlled

111
Q

what is the term for glycogen breakdown?

A

glycogenolysis

112
Q

what does glycogen phosphorylase do?

A

removes glucose units from glycogen

113
Q

what do additional enzymes do to break up glycogen?

A

remove branches

114
Q

is ATP required to breakdown glycogen?

A

no, nor UDP

115
Q

in which tissues can glucose-6-phosphate be broken down into glucose?

A

liver (and kidneys to some extent)

not muscle as don’t have the enzyme to convert glucose-6-phosphate into glucose

116
Q

in which tissues in glycogen broken down?

A

liver, kidneys to some extent

117
Q

what is ‘hitting the wall’?

A

depletion of glycogen supplies

slow adaptation to using fatty acids as oxygen supply

118
Q

what is the energy supply for the final sprint in a marathon race?

A

glycogen

119
Q

what happens when glycogen is depleted?

A

exhausation and collapse

120
Q

what adaptation do muscles need for marathon running?

A

increase number of mitochondria

increase storage of glycogen

121
Q

why is a defect in glycogen synthesis fatal?

A

muscle cramps and weakness

122
Q

what are the 2 phases of glycolysis?

A

preparative

generative

123
Q

which is produced by the preparative phase of glycolysis?

A

fructose 1,6 bisphosphate

124
Q

what are the products of glycolysis?

A

ATP, NADH, pyruvate, water

125
Q

what is the importance of phosphorylating glucose?

A

glucose is then unable to exit the cell and more glucose can enter along the concentration gradient

126
Q

at which 2 points in glycolysis is ATP required?

A

glucose –> glucose-6-phosphate

fructose-6-phosphate to fructose 1-6-bisphosphate

127
Q

why is anaerobic glycolysis important?

A

enables cardiac myocytes to generate ATP in the absence of oxygen (short term survival of anoxic muscle)

128
Q

which organ metabolises lactate?

A

liver

129
Q

how many ATP molecules are produced per glucose in anaerobic glycolysis?

A

2

130
Q

how does the liver use lactate?

A

lactate –> pyruvate –> gluconeogenesis

131
Q

at which 2 points in glycolysis is ATP produced?

A

1,3-bisphosphoglycerate –> 3-phosphoglycerate

phosphoenolpyruvate –> pyruvate

132
Q

which step in glycolysis requires NAD?

A

glyceraldehyde 3-phosphate –> 1,3-bisphosphoglyerate

133
Q

how are fructose and galactose metabolised?

A

broken down into compounds that enter glycolysis

134
Q

is fructose and galactose metabolism under hormonal control?

A

no only glucosse

135
Q

name 2 rare but life threatening inherited disorders with absence of enzymes from the pathways that metabolise sugars

A

hereditary fructose intolerance (1: 20,000 births)

galactosaemia (1: 23000 births)

136
Q

what are the 4 possible fates of glucose?

A

used to produce ATP for energy
conversion to glycogen for storage
synthesis of other cellular components
xs –> fatty acid synthesis –> storage

137
Q

which organ relies on glucose for energy?

A

brain

138
Q

what level should blood glucose be maintained at?

A

around 5mM

139
Q

at what level can hypoglycaemia cause confusion and coma?

A
140
Q

what happens if blood glucose increases above 8mM?

A

protein glycation –> long term vascular damage

141
Q

what is excess anaerobic glycolysis indicative of and why?

A

tumours because they absorb glucose more rapidly and use anaerobic respiration

142
Q

which scan shows up rapid glucose uptake and glycolysis?

A

PET scans

GI (10 decks)

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