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MEH > Session 4 > Flashcards

Session 4 Flashcards

1
Q

Name some cells/tissues that have an absolute requirement for glucose (4)

A

Red blood cells
Neutrophils
Innermost cells of kidney medulla
Lens of the eye

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2
Q

What are some symptoms of hypoglycaemia?

A

Confusion, weakness, nausea, muscle cramps, brain damage, coma, death

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3
Q

Hypoglycaemia is generally considered as a blood sugar level below…

A

4 mM/L

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4
Q

Glycogen is a polymer of _________

In what form is glycogen stored?

A

Glucose

As granules

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5
Q

What are two types of glycogen found in the body?

A

Muscle glycogen

Liver glycogen

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6
Q

How is muscle glycogen and liver glycogen distinguished from each other?

A

Muscle glycogen - found as either intra- or intermyofibrillar granules

Liver glycogen - found as granules within hepatocytes

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7
Q

Which parts of the body use liver glycogen stores?

A

The whole body calls upon the liver glycogen stores affecting whole body glucose levels

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8
Q

How are the chains of glycogen arranged?

A

Like the branches of a tree

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9
Q

Glycogen consist of chains of glucose originating from…

A

A dimer of the protein glycogenin

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10
Q

Which bonds between glucose residues does glycogen contain?

A

a-1-4 glycosidic bonds

With a-1-6 glycosidic bonds forming branch points ever 8-10 residues

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11
Q

How often are a-1-6 glycosidic bonds found between glucose residues in glycogen?

A

Every 8-10 residues

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12
Q

Why can cellulose not be digested in humans?

A

There are no enzymes present to break down the B-1-4 glycosidic bonds

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13
Q

Does synthesis of glycogen require energy? If so, in which form?

A

Yes

ATP, UTP

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14
Q

Glucose has to be converted into which form to be added onto an existing glycogen chain?

A

UDP-glucose

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15
Q

Which enzyme phosphorylates glucose to glucose-6-phosphate?

A

Hexokinase

In liver - glucokinase

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16
Q

Which enzyme converts glucose-6-phosphate to glucose-1-phosphate?

A

Phosphoglucomutase

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17
Q

Which enzyme forms UDP glucose from G1P?

A

G1P uridylyltransferase

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18
Q

Which enzyme forms the a-1-4 glycosidic bonds seen in glycogen?

A

Glycogen synthase

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19
Q

Which enzyme forms the a-1-6 glycosidic bonds seen in glycogen?

A

Branching enzyme

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20
Q

What is glycogenolysis?

A

Glycogen degradation

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21
Q

During glycogenolysis, glycogen is first broken down to which molecule?

A

Glucose-1-phosphate

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22
Q

Which enzyme breaks the a-1-4 glycosidic bonds in glycogen?

A

Glycogen phosphorylase

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23
Q

Which enzyme breaks the a-1-6 branches in glycogen?

A

De-branching enzyme

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24
Q

Which enzyme converts glucose-1-phosphate into glucose-6-phosphate during glycogenolysis?

A

Phosphoglucomutase

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25
Q

Glucose-6-phosphate is produced as the end-product of glycogenolysis. What happens to this glucose-6-phosphate in the…

I) muscle
II) liver

A

I) glycolysis for energy production

II) converted to glucose released into the blood, travels to other tissues

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26
Q

What are the functions of glycogen in the liver?

A

Gluconeogenesis

G6P produced from glycogen degradation converted to glucose and released into the blood

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27
Q

Liver glycogen acts as a __________ of blood glucose levels

A

Buffer

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28
Q

Which enzyme converts glucose-6-phosphate to glucose in the liver? Why does this not take place in the muscle?

A

Glucose-6-phosphatase

Muscle does not have this enzyme

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29
Q

What is the function of glycogen in muscle?

A

To be broken down into glucose-6-phosphate which can enter glycolysis

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30
Q

Which enzyme regulates glycogen synthesis in liver? (Rate-limiting enzyme)

A

Glycogen synthase

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31
Q

Which enzyme regulate glycogen degradation in the liver?

Rate-limiting enzyme

A

Glycogen phosphorylase

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32
Q

What effect does glucagon/adrenaline have on the activity of glycogen synthase and glycogen phosphorylase?

By which mechanism does it affect these enzymes?

A

Glycogen synthase - decreased
Glycogen phosphorylase - increased

Phosphorylation

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33
Q

What effect does insulin have on the activity of glycogen synthase and glycogen phosphorylase?

By which mechanism does it affect these enzymes?

A

Glycogen synthase - increased activity
Glycogen phosphorylase - decreased activity

De-phosphorylation

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34
Q

What effect does glucagon have on muscle glycogen stores?

A

No effect - no receptors for glucagon in muscle

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35
Q

What effect does AMP have on glycogen stores?

A

Only has an effect in the MUSCLE

Increases activity of glycogen phosphorylase

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36
Q

What type of disease are glycogen storage diseases? What do they involve?

A

Inherited diseases?

Deficiency or dysfunction of enzymes of glycogen metabolism

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37
Q

Excess glycogen storage can lead to…

A

Tissue damage

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38
Q

Dimished glycogen stores can lead to…

A

Hypoglycaemia/poor exercise tolerance

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39
Q

Give an example of a glycogen storage disease and its cause?

A

Von Gierke’s disease

Glucose-6-phosphatase deficiency

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40
Q

What is gluconeogenesis?

A

Production of new glucose

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41
Q

When does gluconeogenesis occur?

A

Beyond ~8 hours of fasting when liver glycogen stores begin to deplete

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42
Q

Where does gluconeogenesis take place? (2)

A

In the liver

And to a lesser extent in the kidney cortex

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43
Q

What are three major precursors for gluconeogenesis?

A

Lactate

Glycerol

Amino acids

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44
Q

Where does the lactate come from that can be used as a precursor for gluconeogenesis?

A

From anaerobic glycolysis in exercising muscle and red blood cells

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45
Q

Where does the glycerol that can be used as a precursor for gluconeogenesis come from?

A

From the breakdown of TAGs in adipose tissue

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46
Q

Which amino acid is typically used as a precursor for gluconeogenesis?

A

Alanine

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47
Q

Why can there be no net synthesis of glucose from acetyl-CoA?

A

It is too small

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48
Q

What are three key enzymes in gluconeogenesis?

How do they play an important role in gluconeogenesis?

A

Glucose-6-phosphatase
Fructose-1,6-bisphosphatase
PEPCK

Bypass the irreversible reactions of glycolysis so the precursors can be used to synthesise new glucose

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49
Q

Which two key enzymes are involved in the regulation of gluconeogenesis?

A

PEPCK

Fructose-1,6-bisphosphatase

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50
Q

PEPCK and fructose-1,6-bisphosphatase are regulated by hormones which respond to… (3)

A

Starvation/fasting
Prolonged exercise
Stress

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51
Q

Which hormone has an overall effect of stimulating gluconeogenesis?

A

Glucagon

Cortisol

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52
Q

Which hormone has the overall effect of inhibiting gluconeogenesis?

A

Insulin

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53
Q

What effect does glucagon (and cortisol) have on PEPCK and fructose-1,6-bisphosphatase?

A

Increased amount of PEPCK

Increased amount AND activity of fructose-1,6-bisphosphatase

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54
Q

What effect does insulin have on PEPCK and fructose-1,6-bisphosphatase?

A

Decreased amount of PEPCK

Decreased amount AND activity of fructose-1,6-bisphosphatase

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55
Q

Which type of receptors does glucagon act on?

A

GPCR type receptors

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56
Q

What type of receptors does insulin work on?

A

Tyrosine kinase type receptors

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57
Q

What type of receptors does cortisol work on?

A

Intracellular steroid receptors

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58
Q

In what form are lipids stored?

A

As TAGs

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59
Q

What is a TAG composed of?

A

Glycerol and 3 fatty acids

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60
Q

Are lipids stored in hydrous or anhydrous form? In which tissue?

A

Anhydrous form - lipids are hydrophobic

Adipose tissue

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61
Q

How many kg of TAG will be found in a typical 70kg man?

A

~15kg

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62
Q

How does the energy content of TAGs compare to carbohydrates/protein?

A

Energy content per gram twice that of carbohydrate/protein

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63
Q

In what circumstances are TAGs used for energy production?

A

Prolonged exercise
Stress
Starvation
Pregnancy

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64
Q

Storage/mobilisation of fatty acid stores is under _____________ control

A

Hormonal

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65
Q

What happens to adipocytes as a result of weight gain?

A

Can increase in size around fourfold

Then divide and increase total number of fat cells

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66
Q

How does an adipocyte appear under the microscope?

A

With a large lipid droplet and the cytoplasm/organelles pushed to the edge of the cell

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67
Q

Which enzyme in the small intestine breaks down fat into fatty acids and glycerol?

A

Pancreatic lipase

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68
Q

What happens to the fatty acids and glycerol formed from the breakdown of TAGs in the small intestine?

A

Reformed into TAGs in intestinal epithelial cells

69
Q

What happens to the TAG molecules that are reformed in intestinal epithelial cells?

A

They are transported as chylomicrons in the lymphatic system

70
Q

Where doe TAGs in the lymphatic system enter the blood?

A

Drains at the thoracic duct and enters the bloodstream via the left subclavian vein

71
Q

Once TAGs enter the bloodstream what two purposes can they be used for?

A

Mobilisation - fatty acid oxidation to produce energy

Storage - adipose tissue

72
Q

Fatty acids are transported in the blood bound to…

A

Albumin

73
Q

Fatty acid oxidation doesn’t take place in which cells?

A

Cells without a mitochondria (e.g. RBCs)

Brain - can’t pass blood-brain barrier

74
Q

Which enzyme is involved in the mobilisation of TAG from adipose tissue?

A

Hormone sensitive lipase

75
Q

What effect do glucagon, adrenaline and insulin have on hormone sensitive lipase?

A

Glucagon/Adrenaline - Increase activity

Insulin - Decrease activity

76
Q

What is lipogenesis?

A

Fatty acid synthesis

77
Q

Where does lipogenesis mainly take place? What acts as the major source of the carbons required for lipogenesis?

A

Liver

Excess dietary glucose

78
Q

Lipogenesis requires _______ and _______

A

ATP

NADPH

79
Q

Describe the process of lipogenesis

A

1) Glucose —> Pyruvate (Glycolysis - Cytoplasm)
2) Pyruvate —> Acetyl CoA + Oxaloacetate —> Citrate (Mitochondria)
3) Citrate —-> Acetyl CoA + Oxaloacetate (Cytoplasm)
4) Acetyl CoA —> Malonyl CoA (acetyl CoA carboxylase)
5) Building of fatty acids by the sequential addition of 2 carbons provided by malonyl CoA (Fatty acid synthase complex)

80
Q

What reaction is catalysed by…

I) Acetyl CoA carboxylase
II) Fatty acid synthase complex

A

I) Acetyl CoA —-> Maonlyl CoA (requires NADPH)

II) Fatty acids from sequential addition of 2 carbon units from malonyl CoA (requires ATP)

81
Q

What is a key regulatory enzyme for lipogenesis?

A

Acetyl-CoA Carboxylase

82
Q

Name two substances that increase the activity of acetyl CoA carboxylase

A

Insulin

Citrate

83
Q

Name two substances that decrease the activity of acetyl CoA carboxylase

A

Glucagon/adrenaline

AMP

84
Q

Is lipogenesis a reductive or oxidative process?

A

Reductive - requires NADPH

85
Q

By which mechanism does insulin lead to decreased activity of hormone sensitive lipase?

By which mechanism does glucagon/adrenaline lead to increased activity of hormone sensitive lipase?

A

De-phosphorylation

Phosphorylation

86
Q

Hormone sensitive lipase breaks down TAGs in adipose tissue to glycerol and fatty acids that travel in the blood. What happens to the glycerol produced?

A

Travels to the liver and used as a source of carbon or gluconeogenesis

87
Q

Name 5 different classes of lipids

A 
TAGs
Fatty acids
Cholesterol 
Phospholipids 
Vitamins A, D, E & K
88
Q

In what two ways are lipids transported in the blood? Why can’t lipids travel freely in the blood?

A

Bound to albumin (usually fatty acids) - only ~2%
As lipoprotein particles - ~98%

They are hydrophobic and insoluble so transported bound to carriers

89
Q

What is the typical plasma lipid concentration range for TAGs?

A

0-2.0 mmol/L

90
Q

What is the typical plasma lipid concentration range for total lipids?

A

4000 - 8500 mg/L

91
Q

What is the structure of a phospholipid?

A

Choline, phosphate and glycerol (hydrophilic polar head)

Fatty acid tail (hydrophobic non-polar tail)

92
Q

What are three structures that phospholipids can form?

A

Liposome
Micelle
Bilayer sheet

93
Q

What is the structure of liposomes and micelles?

A

Liposome - bilayer of phospholipids in a sphere, with a central cavity

Micelle - single layer of phospholipids arranged in a sphere, with a cavity able to transport hydrophobic cargo

94
Q

Where do we get most of our cholesterol from?

A

Most is synthesised in the liver

Some cholesterol is obtained in the diet

95
Q

Where is most of the cholesterol in the body synthesised?

A

Liver

96
Q

What are three functions of cholesterol?

A

Essential component of membranes (regulates fluidity)
Precursor for bile acids
Precursor for steroid hormones

97
Q

What is an example of a steroid hormone?

A

Testosterone

98
Q

In which form is cholesterol transported?

A

As cholesterol esters

99
Q

What is the structure of a cholesterol ester?

Which enzyme catalyses the esterification of cholesterol —> cholesterol ester?

A

Cholesterol with an added fatty acid

LCAT

100
Q

What is the function of lipoproteins?

A

Transport lipids around the body

101
Q

What is the general structure of a lipoprotein?

A

Consists of a phospholipid monolayer with a small amount of cholesterol

Has peripheral and integral apolipoproteins in its monlayer and a cargo within

102
Q

What are two examples of peripheral apolipoproteins?

What are two examples of integral apolipoproteins?

A

apoC
apoE

apoA
apoB

103
Q

Give three examples of cargo that can be transported in lipoproteins

A

Fat soluble vitamins
TAGs
Cholesterol ester

104
Q

What are the 5 different types of lipoproteins (ordered by density)

A 
Chylomicrons 
VLDL
IDL
LDL
HDL
105
Q

Chylomicrons are the main carrier of…

A

Dietary TAG

106
Q

VLDLs are the main carrier of…

A

Liver synthesised TAGs

107
Q

IDLs mainly carry…

A

Cholesterol

108
Q

LDLs mainly carry…

A

‘Bad’ cholesterol

109
Q

HDLs mainly carry…

A

‘Good’ cholesterol

110
Q

Each type of lipoprotein contains variable amounts of ___________________

A

Apolipoproteins

111
Q

How is the density of lipoproteins obtained?

A

By flotation ultracentrifugation

112
Q

How is the density of lipoproteins related to their diameter?

A

Diameter inversely proportional to density

113
Q

Chylomicrons are only normally present in the blood…

A

4-6 hours after a meal

114
Q

What sort of appearance will chylomicrons take in a fluid, e.g. The blood?

A

Creamy appearance

115
Q

Apolipoproteins can be either…

A

Integral or peripheral

116
Q

State a structural and functional function of apolipoproteins?

A

Structural - package hydrophobic lipids

Functional - acts as a cofactor for enzymes/ligands for cell surface receptors

117
Q

Chylomicrons are loaded in the _________ _____________ and ____________ added before entering the ______________ __________

A

Small intestine
ApoB-48
Lymphatic system

118
Q

Which apolipoprotein is added to chylomicrons in the small intestine before they enter the lymphatic system?

A

ApoB-48

119
Q

Where do chylomicrons in the lymphatic system drain into the bloodstream?

A

At the thoracic duct which drains into the left subclavian vein

120
Q

What happens to the chylomicrons once they enter the blood at the left subclavian vein?

A

They acquire 2 new apoproteins - apoC and apoE

121
Q

What is the function of apoC on chylomicrons?

A

It binds lipoprotein lipase on adipocytes and muscle, releasing the fatty acids into the cells

122
Q

When does apoC dissociate from the chylomicrons? What happens to the chylomicron at this point?

A

When TAG content reduces to ~20%

Becomes a chylomicron remnant - returns to the liver

123
Q

What happens to the chylomicron remnant in the liver?

A

LDL receptor on the hepatocyte binds to apoE and the chylomicron is taken up by receptor mediated endocytosis

124
Q

By which process is the chylomicron remnant taken up by the hepatocyte?

A

Receptor mediated endocytosis

125
Q

What happens to the remaining contents of chylomicrons in the hepatocytes?

A

Released by lysosomes for use in metabolism

126
Q

What is the function of lipoprotein lipase?

What does it require as a cofactor?

Where is it found in the body?

A

Hydrolyses TAG in lipoproteins

ApoC-II

Attached to the surface of endothelial cells in capillaries of muscle/adipose

127
Q

Where are VLDLs made?

A

In the liver

128
Q

What is added to VLDLs during their formation?

A

ApoB100
ApoE
ApoC

129
Q

The apoC and apoE added to VLDLs during their formation comes from…

A

HDL particles in the blood

130
Q

How do VLDLs transport TAG to other tissues from the liver?

A

Bind to LPL on endothelial cells in muscles/adipose

Becomes depleted of TAG

131
Q

What are the fatty acids released from VLDLs used for in…

I) muscle
II) adipose

A

I) energy

II) storage

132
Q

What happens to the VLDL as the TAG content drops?

A

VLDL dissociates from LPL and returns to the liver

133
Q

When does a VLDL become an IDL?

A

When VLDL content drops to ~30%

134
Q

What happens to the IDL once it is produced?

A

Either taken up by liver or rebinds to LPL

135
Q

When does an IDL become an LDL? What changes does the lipoprotein undergo from IDL —> LDL?

A

When depletion reaches ~10%

Loses apoC and apoE

136
Q

What is the primary function of LDLs?

A

Provide cholesterol from the liver to peripheral tissues, peripheral cells express LDL receptor and take up LDL through receptor mediate endocytosis

137
Q

Why are LDLs not efficiently cleared by the liver?

A

They do not have apoC or apoE

138
Q

Why are LDLs associated with ‘bad’ cholesterol?

A

They have a long half life so are more susceptible to oxidative damage, oxidised LDLs are taken up by macrophages, forming foam cells which contribute to the formation of atherosclerotic plaques

139
Q

What happens to oxidised LDLs?

A

Taken up by macrophages

Macrophages —> Foam cells

140
Q

Foam cells contribute to the formation of…

A

Atherosclerotic plaques

141
Q

Cells requiring cholesterol express which receptors?

What acts as a ligand for these receptors?

A

LDL receptors

ApoB-100

142
Q

LDLs taken up by reactor mediated endocytosis fuse with…

A

Lysosomes to release cholesterol/fatty acids

143
Q

What controls LDL receptor expression on the surface of cells?

A

Intracellular cholesterol concentration

144
Q

Name three ways in which HDLs can be produced

A

Synthesised by the liver/intestine

Bud off from chylomicrons/VLDLs as they are digested

Free apoA-1 can acquire cholesterol and phospholipid to form HDLs

145
Q

What happens to the initially ‘empty’ HDLs that are produced?

A

They accumulate phospholipid and cholesterol from cells lining blood vessels

146
Q

Does the filling of HDLs with phospholipids/cholesterol from cells lining blood vessels require the activity of enzymes?

A

No

147
Q

What is the function of HDLs?

A

Transport excess cholesterol from cells to the liver for disposal and bile salts or to other cells requiring cholesterol

148
Q

Which protein within the cell allows the transfer of cholesterol to the HDL?

The cholesterol is converted into which form for transport in the HDL? Which enzyme catalyses this conversion?

A

ABCA1 protein

Cholesterol ester
LCAT

149
Q

What two things can happen to a mature HDL?

A

Can be taken up by the liver —-> Bile salts

Can be taken up by other cells via scavenger receptors

150
Q

How can HDLs interact with VLDLs?

A

They can exchange cholesterol ester for TAGs via cholesterol exchange transfer protein

151
Q

Hyperlipoproteinaemias are either as a result of ___________________ or _________________

A

Over-production

Under-removal

152
Q

What is the cause of type I hyperlipoproteinaemia? What will be seen in type I hyperlipoproteinaemia?

A

Defective lipoprotein lipase

Chylomicrons in fasting plasma

153
Q

What is the cause of type IIa hyperlipoproteinaemia?

A

Defective LDL receptor

154
Q

What is the cause of type III hyperlipoproteinaemia? What will be seen?

A

Defective apoE

Raised IDL and chylomicron remnants

155
Q

Hyperlipoproteinaemias (excluding type I) are associated with…

A

Coronary artery disease

156
Q

What is Hypercholesterolaemia?

A

High level of cholesterol in the blood

157
Q

Name 3 clinical signs of hypercholesterolaemia

A

Xanthelasma
Tendon Xanthoma
Corneal Arcus

All involve cholesterol deposition at different parts of the body

158
Q

What is a xanthelasma?

A

Yellow patches on eyelids

159
Q

What is tendon xanthoma?

A

Nodules on tendons

160
Q

What is corneal arcus?

A

Obvious white circles around the eye

161
Q

Raised serum LDL is associated with…

A

Formation of foam cells (lipid-laden macrophages)
Formation of fatty streaks
Formation of atherosclerotic plaques

162
Q

What changes to the diet would be recommended in the treatment of hyperlipoproteinaemias?

A

Reduce cholesterol/saturated lipids in diet

Increase fibre intake

163
Q

What lifestyle changes would be recommended in the treatment of hyperlipoproteinaemias?

A

Increase exercise

Stop smoking

164
Q

Name two drugs that may be prescribed in the treatment of hyperlipoproteinaemias

A

Statins

Bile salt sequestrants

165
Q

How do statins work in the treatment of hyperlipoproteinaemias?

A

Reduce cholesterol synthesis by inhibiting HMG-CoA reductase

166
Q

How do bile salt sequestrants help in the treatment of hyperlipoproteinaemias?

A

Bind bile salts in the GI tract, forcing the liver to use more cholesterol to produce more bile salts

167
Q

Total cholesterol:HDL ratio above __________ is considered high risk

A

6

168
Q

What should TAG levels be in a fasted sample?

A

Less than 2 mmol/L

MEH (9 decks)

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