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BM 210: Introduction to Biochemistry > Block B Part 2: Carbohydrates, Lipids and Cholesterol > Flashcards

Block B Part 2: Carbohydrates, Lipids and Cholesterol Flashcards

1
Q

What are 3 uses of carbohydrates?

A

Answers include:
Coating of cell surfaces
Modification of secreted proteins
Part of receptors for a variety of pathogens
Form basis of human blood groups
Allow tremendous structural diversity
(Lecture 3, Slide 4)

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2
Q

What are the names of 3,4,5,6 and 7 carbon monosaccharides?

A

Trioses
Tetroses
Pentoses
Hexoses
Heptoses
(Lecture 3, Slide 5)

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3
Q

What is the general formula that most sugars conform to?

A

(CH2O)n where n is between 3 and 7
(Lecture 3, Slide 6)

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4
Q

What are the 2 groups that sugars contain 1of?

A

An aldehyde or a ketone group
(Lecture 3, Slide 6)

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5
Q

What makes sugars reactive?

A

Carbon-oxygen double bonds
(Lecture 3, Slide 6)

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6
Q

What are monosaccharides?

A

The smallest type of sugars (trioses)
(Lecture 3, Slide 7)

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7
Q

What are the 2 forms of glucose?

A

Ring-form and open chain form
(Lecture 3, Slide 9)

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8
Q

What form of glucose is favoured at equilibrium?

A

The ring form, with less than 0.1% of molecules in open chain form
(Lecture 3, Slide 9)

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9
Q

Why is glucose primarily found in the ring form at equilibrium?

A

As it’s energetically more stable
(Lecture 3, Slide 10)

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10
Q

How are sugar alcohols formed?

A

The reduction of the aldehyde group (R−CH=O) to a hydroxyl group (-OH)
(Lecture 3, Slide 12)

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11
Q

What 2 things are monosaccharides joined to alcohols, amines and phosphates useful for?

A

Signal molecules
Facilitate metabolism
(Lecture 3, Slide 13)

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12
Q

What is an O-glycosidic bond?

A

A chemical bond between an oxygen atom and a carbon atom that connects a monosaccharide to another monosaccharide, an alcohol or a protein
(Lecture 3, Slide 13)

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13
Q

What is an N-glycosidic bond?

A

A chemical bond between a nitrogen atom and a carbon atom that connects a monosaccharide to a nitrogenous base or the amino acid lysine in a protein
(Lecture 3, Slide 13)

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14
Q

What occurs in a phosphorylation reaction to a monosaccharide?

A

A phosphoryl group (a phosphorus atom bonded to 3 oxygen atoms) is added to the monosaccharide
(Lecture 3, Slide 14)

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15
Q

What 3 things does phosphorylation of a monosaccharide do?

A

Makes thesugar anionic (a substance that possess a negative charge)
Traps the sugar within a cell
Creates a reactive intermediate of sugar metabolism
(Lecture 3, Slide 14)

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16
Q

What 3 things are classified as sugars?

A

Monosaccharides
Disaccharides
Oligosaccharides
(Lecture 3, Slide 17)

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17
Q

What 2 things are classified as polysaccharides?

A

Starches
Non-starch polysaccharides
(Lecture 3, Slide 17)

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18
Q

How are disaccharides formed?

A

By condensation between 2 monosaccharides, forming an O-glycosidic bond
(Lecture 3, Slide 18)

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19
Q

How many monosaccharides are in an oligosaccharide?

A

3 - 10
(Lecture 3, Slide 18)

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20
Q

Are oligosaccharides digested by the body?

A

Generally not
(Lecture 3, Slide 18)

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21
Q

What are intrinsic sugars?

A

Sugars contained within plant cell walls
(Lecture 3, Slide 18)

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22
Q

What are extrinsic sugars?

A

Sugars that are free in solution (such as dental plaque, caries)
(Lecture 3, Slide 18)

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23
Q

Are intrinsic and extrinsic sugars good or bad for the body?

A

Intrinsic sugars are good for the body whereas extrinsic sugars are bad for the body
(Lecture 3, Slide 18)

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24
Q

What sugar is an exception to extrinsic sugars being bad?

A

Lactose being a desirable extrinsic sugar from milk
(Lecture 3, Slide 18)

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25
Q

What are 3 simple sugars?

A

Answers Include:
Sucrose
Fructose
Glucose
Galactose
Maltose
Lactose
Mannose
(Lecture 3, Slide 19)

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26
Q

What are the 3 most common disaccharides?

A

Sucrose
Lactose
Maltose
(Lecture 3, Slide 19)

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27
Q

What monosaccharides are in sucrose?

A

1 glucose and 1 fructose
(Lecture 3, Slide 19)

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28
Q

What monosaccharides are in lactose?

A

1 glucose and 1 galactose
(Lecture 3, Slide 19)

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29
Q

What monosaccharides are in maltose?

A

2 glucose monosaccharides
(Lecture 3, Slide 19)

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30
Q

What is the formula of sucrose, lactose and maltose?

A

C12H22O11
(Lecture 3, Slide 19)

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31
Q

What 2 places can we get sucrose from naturally?

A

Sugar cane or sugar beet
(Lecture 3, Slide 21)

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32
Q

Where is maltose originally isolated from?

A

Malt
(Lecture 3, Slide 22)

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33
Q

How is maltose produced?

A

In germinating cereals in the brewing process
(Lecture 3, Slide 23)

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34
Q

How is “malting” barley done?

A

Through maltose-producing amylases
(Lecture 3, Slide 23)

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35
Q

What does mashing permit in barley?

A

The amylases to convert the cereal’s starches into maltose
(Lecture 3, Slide 23)

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36
Q

What 2 things are produced when yeast ferments maltose?

A

Ethanol and carbon dioxide
(Lecture 3, Slide 23)

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37
Q

How are the carbons in ring forms of sugars numbered?

A

Moving clockwise from the top right oxygen atom
(Lecture 3, Slide 25)

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38
Q

What is starch?

A

A large molecule with a variable amount of glucose units, a storage carbohydrate of plants
(Lecture 3, Slide 27)

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39
Q

Is starch osmotically active?

A

No
(Lecture 3, Slide 27)

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40
Q

What 2 polysaccharides are components of starch?

A

Amylose and amylopectin
(Lecture 3, Slide 27)

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41
Q

What type of glycosidic bonds do starch and glycogen have?

A

α-1,4 glycosidic linkages
(Lecture 3, Slide 27)

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42
Q

How often does glucose branch to other glucose residues in amylopectin?

A

Every 30th glucose molecule
(Lecture 3, Slide 27)

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43
Q

How is glycogen different from amylopectin?

A

Glucose branches to other glucose residues every 10th glucose molecule in glycogen, as opposed to every 30th in amylopectin
(Lecture 3, Slide 27)

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44
Q

Can our bodies digest non-starch polysaccharides?

A

No
(Lecture 3, Slide 27)

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45
Q

State 1 example of a non-starch polysaccharide.

A

Cellulose , chitin or pectin
(Lecture 3, Slide 27)

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46
Q

What type of glycosidic bond does cellulose have?

A

ß-1,4 glycosidic linkages
(Lecture 3, Slide 27)

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47
Q

Why is uncooked starch resistant to digestion?

A

As it’s present as small insoluble molecules
(Lecture 3, Slide 28)

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48
Q

Why does cooking starch remove it’s resistance to digestion?

A

As cooking swells the granules
(Lecture 3, Slide 28)

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49
Q

What level does lactose activity drop to compared to the level it is at birth (%age)?

A

5 - 10% of level at birth
(Lecture 3, Slide 30)

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50
Q

Why is the decrease in lactose activity compared to birth level not as pronounced in northern Europeans?

A

As they are adapted to milk-producing domesticated animals
(Lecture 3, Slide 30)

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51
Q

What is lactose used as an energy source for?

A

Microorganisms in the colon
(Lecture 3, Slide 30)

52
Q

What does lactose ferment to and what 2 things are also produced?

A

Ferments to lactate with methane and hydrogen gas also being produced
(Lecture 3, Slide 30)

53
Q

Why does flatulence and diarrhea draw water into the intetine?

A

As lactate is osmotically active
(Lecture 3, Slide 30)

54
Q

What is glycogen?

A

A readily mobilised storage form of glucose
(Lecture 3, Slide 34)

55
Q

Why is glycogen not as energy-rich as fatty acids?

A

It is less reduced
(Lecture 3, Slide 34)

56
Q

What does the controlled release of glucose from glycogen maintain?

A

Blood glucose level
(Lecture 3, Slide 34)

57
Q

What 2 places are glycogen mainly stored?

A

The liver and skeletal muscle
(Lecture 3, Slide 34)

58
Q

In liver hepatocytes (cells) what percentage of the fresh weight can glycogen make up?

A

8-10%
(Lecture 3, Slide 34)

59
Q

How much percent of muscle mass can be glycogen?

A

1-2%
(Lecture 3, Slide 34)

60
Q

Why does the uterus store glycogen during pregnancy?

A

To nourish the embryo
(Lecture 3, Slide 34)

61
Q

How do polysaccharides have directionality?

A

As they have a reducing and a non-reducing end
(Lecture 3, Slide 36)

62
Q

What is an acetal?

A

A molecule with 2 single bonded oxygens attached to the same carbon atom
(Lecture 3, Slide 28)

63
Q

Why does glycogen not have a reducing end?

A

As it is not free but is covalently bonded to a protein named glycogenin as a beta-linkage to a surface tyrosine molecule
(Lecture 3, Slide 39)

64
Q

What is glycogenin?

A

It’s a glycosyltransferase
(Lecture 3, Slide 39)

65
Q

Is glycogenin a monomer, dimer or polymer?

A

Dimer
(Lecture 3, Slide 39)

66
Q

Where does glycogenin sit in glycogen?

A

In the core
(Lecture 3, Slide 39)

67
Q

What 2 things do glycogen granules contain?

A

Glycogen and the enzymes of glycogen synthesis and degradation
(Lecture 3, Slide 39)

68
Q

What facilitates glycogen’s rapid synthesis and catabolism?

A

It’s many non-reducing ends
(Lecture 3, Slide 40)

69
Q

What is the core structure of a phospholipid?

A

2 fatty acids connected to a glycerol molecule, with the glycerol also being connected to a phosphate, which is attached to an alcohol
(Lecture 4, Slide 4)

70
Q

What are 3 major functions of cellular lipids?

A

P1 is a precursor of signalling molecules
P2 is a key signal in apoptosis
PC is a structural component of membranes
PE donates functional groups to membrane anchored proteins and has some structural roles and regulates curvature
(Lecture 4, Slide 6)

71
Q

What is the difference between saturated and unsaturated fatty acids?

A

Saturated fatty acids have no double bonds whereas unsaturated fatty acids do
(Lecture 4, Slide 8)

72
Q

What are 3 variations in fatty acyl (fatty acid) side chains in glycerophospholipids?

A

Carbon length (usually between 11 and 22 C)
Some GPLs exhibit enrichment of fatty acid content
Saturated vs unsaturated fatty acids
(Lecture 4, Slide 8)

73
Q

What does enrichment of fatty acid content mean in the context of glycerophospholipids?

A

Deliberate modification of fatty acids in order to achieve a specific fatty acid profile
(Lecture 4, Slide 8)

74
Q

What are 2 non-glycerol-lipids?

A

Sphingolipids and cholesterol
(Lecture 4, Slide 9)

75
Q

What is an amphipathic molecule?

A

A molecule containing both hydrophilic and hydrophobic parts
(Lecture 4, Slide 10)

76
Q

Which part of lipids are hydrophilic and hydrophobic?

A

Lipids have a hydrophobic tail and hydrophilic head
(Lecture 4, Slide 10)

77
Q

Membranes are said to be “fluid” - what does this mean?

A

They accommodate protein conformational changes without loss of integrity
(Lecture 4, Slide 11)

78
Q

What signalling molecule can lipids produce?

A

P1
(Lecture 4, Slide 12)

79
Q

What can phosphorylate the inositol ring of a lipid?

A

Kinases
(Lecture 4, Slide 12)

80
Q

What are the 2 products resulting from certain signals catalysing the breakdown of PtdIns(4,5)P2 (lipid with phosphorylated inositol ring)?

A

Inositol triphosphate and Diacylglycerol (DAG)
(Lecture 4, Slide 13)

81
Q

What enzyme does glycerophospholipid (GPL) biosynthesis occur through?

A

Phosphatidate
(Lecture 4, Slide 15)

82
Q

Where does glycerophospholipid GPL biosynthesis occur?

A

The endoplasmic reticulum
(Lecture 4, Slide 15)

83
Q

How are phospholipids made from Phosphatidate?

A

An alcohol polar head group is added to the phosphate
(Lecture 4, Slide 15)

84
Q

Why is phosphatidic acid phosphatase a key regulatory enzyme in lipid synthesis?

A

As when active, it can generate diacylglycerol (DAG)
(Lecture 4, Slide 16)

85
Q

Why is generating diacylglycerol from phosphatidate important?

A

As it can activate with activated alcohols to form phospholipids it with fatty acyl CoA to form triacylglycerols
(Lecture 4, Slide 16)

86
Q

What is phosphatidate converted into when phosphatidic acid phosphatase (PAP) is inactive and why?

A

CMP-DAG (Cytidine Monophosphate Diacylglycerol) for the synthesis of different phospholipids
(Lecture 4, Slide 16)

87
Q

What is phosphatidylcholine (PC)?

A

A major component of lung surfactant, with it’s function being to maintain “surface tension” of fluid to keep alveoli “open”
(Lecture 4, Slide 18)

88
Q

What happens when there are low levels of phosphatidylcholine (PC)?

A

Alveoli collapse
(Lecture 4, Slide 18)

89
Q

What is respiratory distress syndrome?

A

It often affects premature babies and results in laboured breathing and blue fingers or toes
(Lecture 4, Slide 18)

90
Q

How is respiratory distress syndrome treated?

A

With O2 ventilation and artificial surfactant
(Lecture 4, Slide 18)

91
Q

What is the precursor for sphingomyelin?

A

Ceramide
(Lecture 4, Slide 19)

92
Q

What are 2 functions of sphingomyelin?

A

It’s a major structural component of membranes and the source of messenger molecules
(Lecture 4, Slide 19)

93
Q

How are sphingolipids further modified?

A

The addition of sugars
(Lecture 4, Slide 20)

94
Q

What are gangliosides and what do they do?

A

They are a type of glycosphingolipid and are important cell surface molecules which are highly prevalent in nervous tissue
(Lecture 4, Slide 20)

95
Q

What is Tay Sachs disease?

A

An inherited disorder where the body cannot degrade gangliosides, resulting in lysosomes becoming filled with them
(Lecture 4, Slide 21)

96
Q

What is the treatment for Tay Sachs disease?

A

No treatment exists
(Lecture 4, Slide 21)

97
Q

Is sphingosine present in all sphingolipids?

A

Yes, it is a key component of all sphingolipids
(Lecture 4, Slide 22)

98
Q

Sphingosine is phosphorylated by ______ to generate _________, which is a key signalling molecule?

A

Sphingosine kinase, sphingosine 1-phosphate
(Lecture 4, Slide 22)

99
Q

What is cholesterol?

A

Cholesterol is an essential component of membranes which helps maintain membrane bilayer integrity and regulate permeability
(Lecture 4, Slide 24)

100
Q

What 3 things is cholesterol the precursor of?

A

Steroids, vitamins and bile salts
(Lecture 4, Slide 24)

101
Q

What is excess cholesterol associated with?

A

Cardiovascular disease
(Lecture 4, Slide 24)

102
Q

What happens in the first step of cholesterol biosynthesis?

A

Synthesis of isopentyl pyrophosphate via mevalonate
(Lecture 4, Slide 25)

103
Q

What happens in the second step of cholesterol biosynthesis?

A

Condensation of 6 molecules isopentyl pyrophosphate to form squalene
(Lecture 4, Slide 25)

104
Q

What happens in the third step of cholesterol biosynthesis?

A

Cyclisation of squalene and further processing to form cholesterol
(Lecture 4, Slide 25)

105
Q

What does the rate of cholesterol depend on and how much does this vary?

A

Rate of cholesterol varies several hundred fold and depends on diet
(Lecture 4, Slide 31)

106
Q

What type of synthesis does cholesterol experience?

A

Feedback regulation (rate of synthesis is dependant on how much cellular cholesterol is present)
(Lecture 4, Slide 31)

107
Q

Where are 2 major sites of synthesis for cholesterol?

A

The liver and intestines
(Lecture 4, Slide 31)

108
Q

What step does HMG-CoA reductase catalyse of cholesterol biosynthesis and how does this help regulate the biosynthesis?

A

It catalyses the committed step of cholesterol synthesis, therefore regulating cholesterol synthesis by its amount and activity
(Lecture 4, Slide 31)

109
Q

What is the committed step of a metabolic pathway?

A

The slowest step
(Lecture 4, Slide 31)

110
Q

What are the 4 ways in which HMG-CoA reductase regulates cholesterol biosynthesis?

A
  1. Rate of synthesis of HMG-CoA reductase mRNA
  2. Rate of translation of HMG-CoA reductase to protein
  3. Rate of degradation of HMG-CoA reductase protein
  4. Phosphorylation state of HMG-CoA reductase protein
    (Lecture 4, Slide 32)
111
Q

Why is the rate of HMG-CoA reductase mRNA controlled?

A

As HMG-CoA helps catalyse cholesterol biosynthesis
(Lecture 4, Slide 33)

112
Q

How is HMG-CoA reductase mRNA controlled?

A

When cholesterol levels are low, sterol regulatory element binding protein transcription factor (SREBP)is activated and binds to the promoter region of the HMG-CoA reductase gene

When cholesterol levels are high, serine protease cleaves off SREBP in a 2 step process, decreasing production of HMG-CoA reductase
(Lecture 4, Slide 33)

113
Q

How is the rate of translation of HMG-CoA reductase mRNA to a protein controlled?

A

Translation is inhibited by nonsterol metabolites derived from mevalonate
(Lecture 4, Slide 34)

114
Q

What is the first step of HMG-CoA reductase protein being degraded?

A

HMG-CoA reductase membrane domain senses increasing levels of sterols then interacts with ubiquitinating enzymes.
(Lecture 4, Slide 34)

115
Q

What is the second step of HMG-CoA reductase protein being degraded?

A

HMG-COA reductase becomes polyubiquitinated and is extracted from the membrane and then is degraded by the proteasome
(Lecture 4, Slide 34)

116
Q

How does phosphorylation of HMG-CoA reductase stop cholesterol synthesis?

A

It decreases its catalytic activity
(Lecture 4, Slide 35)

117
Q

What phosphorylates HMG-CoA reductase?

A

AMP-activated protein kinase
(Lecture 4, Slide 35)

118
Q

What is cholesterol transported in the body by?

A

By body fluid in lipoprotein particles
(Lecture 4, Slide 36)

119
Q

What is the structure of lipoprotein particles?

A

They consist of a hydrophobic lipid core, surrounded by polar lipids and proteins
(Lecture 4, Slide 36)

120
Q

What is “good” and “bad” cholesterol?

A

HDL (High density lipoprotein) is the good cholesterol
LDL (Low density lipoprotein) is the bad cholesterol
(Lecture 4, Slide 36)

121
Q

What are bile salts?0

A

Detergents
(Lecture 4, Slide 37)

122
Q

Where are bile salts synthesised?

A

In the liver
(Lecture 4, Slide 37)

123
Q

Where are bile salts stored and released?

A

They are stored in the gall bladder and released into the small intestine
(Lecture 4, Slide 37)

124
Q

What are the 5 classes of steroid hormones?

A

Progestagens
Glucocorticoids
Mineralocorticoids
Androgens
Oestrogens
(Lecture 4, Slide 38)

125
Q

What are the 2 steroid hormones in women?

A

Progesterone and estrogen
(Lecture 4, Slide 39)

126
Q
A

BM 210: Introduction to Biochemistry (12 decks)

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