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Carbohydrates Flashcards

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1
Q

What are 4 properties of carbohydrates?

A

Highly oxidisable
Store potential energy
Have structural/protective functions
Contribute to cell-cell communication

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2
Q

What are monosaccharides?

A

Single sugar carbohydrates.

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3
Q

What are the 3 primary monosaccharides?

A

Glucose
Galactose
Fructose

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4
Q

What are disaccharides?

A

Double-unit polymers of sugar monomers linked by glycosidic bonds.

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5
Q

What bonds are disaccharides linked by?

A

Glycosidic bonds.

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6
Q

How are glycosidic bonds created?

A

A glycosidic bond is a covalent bond formed when the OH group of one sugar interacts with the anomeric carbon of another.

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7
Q

What is an anomeric carbon?

A

First carbon on the glucose residue- stabilises the sugar structure and is the only residue that can be oxidised.

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8
Q

What are the 3 primary disaccharides?

A

Maltose
Lactose
Sucrose

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9
Q

Describe maltose.

A

Maltose is the breakdown product of starch. There is nt much in the diet (found in malt wheat, beer etc).
Can be oxidised- REDUCING AGENT.

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10
Q

Is maltose a reducing agent?

A

Yes.

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11
Q

Describe lactose.

A

Main sugar in milk- glycosidic bond between glucose and galactose.

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12
Q

Is lactose a reducing agent?

A

Yes.

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13
Q

Describe sucrose.

A

Main dietary table sugar- only made by plants, accounts for 25% of dietary carbohydrates.

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14
Q

Is sucrose a reducing agent?

A

No- no free anomeric C1 carbon (no oxidation site).

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15
Q

What are polysaccharides?

A

Sugar polymers of a medium/high molecular weight.

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16
Q

How are polysaccharides distinguished from each other?

A

Identity of sugar chains, length, bonds and branching.

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17
Q

What are the 2 classifications of polysaccharide based on sub-units?

A

Homopolysaccharides

Heteropolysaccharides

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18
Q

What are homopolysaccharides?

A

Multiple sugar polymers of the same monomer.

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19
Q

What are heteropolysaccharides?

A

Multiple sugar polymers of different monomers.

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20
Q

What does starch contain?

A

Two sugar monomers- amylose and amylopectin.
Amylose- thousands of A1-4 residues
Amylopectin- similar structure but branched

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21
Q

What do amylose and amylopectin form?

A

Alpha helices- many reducing ends and few non-reducing ends.

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22
Q

Why do amylose and amylopectin have non-reducing ends?

A

Allows them to be readily synthesised/degraded to form monomers.

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23
Q

What is glycogen?

A

Storage carbohydrate in animals.

More branched than starch. (A1-4 with A1-6 branches every 8-12 residues).

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24
Q

Where is 90% glycogen stored in the body?

A

Liver- acts to replenish blood sugar when fasting.

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25
Q

Why is sugar stored in polymers?

A

Compactness
Allows degradation to monomers
Form hydrated gels- osmotically inactive which prevents a state of constant sugar movement

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26
Q

What are glycoproteins?

A

Proteins with carbohydrate molecules covalently attached. (Protein > carb)

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27
Q

What are glycosaminoglycans?

A

Unbranched polymers made from repeated units of hexuronic acid and amino sugars (used to be called mucopolysaccharides due to involvement in mucus and synovial fluid).

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28
Q

What are proteoglycans?

A

Carbohydrate molecules with proteins covalently attached. (Carb > protein), form much of connective tissue.

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29
Q

Describe the 4 areas of carbohydrate digestion.

A

Mouth- salivary enzymes break down A1-4 bonds.
Stomach- no carb digestion
Duodenum- pancreatic amylase works like in mouth
Jejunum- final digestion by mucosal cell-surface enzymes.

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30
Q

What mucosal cell surface enzymes are involved in carbohydrate digestion in the jejunum?

A

Isomaltase- hydrolyses A1-6 bonds
Glucoamylase- removes Glc sequentially from N-R ends
Sucrase- hydrolyses sucrose
Lactase- hydrolyses lactose

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31
Q

What are the main products of carbohydrate digestion?

A

Glucose, galactose and fructose (the monosaccharide constituents that provide the basis for which all other secondary carbohydrates are formed).

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32
Q

How is glucose absorbed?

A

Glucose symport (indirect ATP-powered process)

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33
Q

How does glucose symport work?

A

The ATP-driven NaKATPase pump maintains high extracellular Na+, so glucose can continually be moved into the epithelial cells.

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34
Q

How is galactose absorbed?

A

Similar method as glucose.

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35
Q

How is fructose absorbed?

A

Binds to the channel protein GLUT5 and simply moves down its concentration gradient (high in lumen, low in gut).

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36
Q

How are cellulose and hemicellulose digested?

A

Cannot be digested by the gut but needed in the diet to increase faecal bulk and decrease digestive transit time.
Their polymers are broken down by gut bacteria which produces methane as a byproduct.

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37
Q

What are disaccharide deficiencies?

A

Disorders relating to malabsorption of carbohydrates.

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38
Q

How may disaccharide deficiencies arise?

A

Severe intestinal infection
Inflammation of gut lining
Drug damage to gut wall
Surgical removal of intestine

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39
Q

What are disaccharide deficiencies characterised by?

A

Abdominal indigestion and cramps.

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40
Q

What does diagnosis of disaccharide deficiencies require?

A

Laboratory tests of intestinal secretions.

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41
Q

How does lactose intolerance work?

A

Most people lose their lactase activity after weaning- however, Western whites usually retain it.
If lactase activity is lacking, the ingestion of milk will result in disaccharide deficiency symptoms.

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42
Q

What happens to glucose following absorption?

A

Diffuses through intestinal epithelial cells into the hepatic portal tract (liver circulatory tract) and on into the liver.

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43
Q

What happens when glucose enters the liver?

A

Immediately phosphorylated into Glucose-6-phosphate by hepatocytes.

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44
Q

Why can’t G6P diffuse out of the cell?

A

GLUT4 transporters will not recognise it- effectively traps it in liver cells.

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45
Q

How do glucokinase and hexokinase act regarding sugar?

A

When BS is normal, the liver doesn’t grab all the glucose up and leaves it for the rest of the body.
When BS >, the glucokinase Vmax allows it to trap all of the glucose in the liver fast.
The low Km (high affinity) of hexokinase means it can effectively trap glucose better (can grab more even if there is less actually there)- the low Vmax means it can be easily satisfied too.

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46
Q

Where is glycogen stored?

A

Liver and skeletal muscle.

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47
Q

What happens to glycogen in the liver?

A

Phosphorylated into G6P- when blood sugar decreases, glucose-6-phosphatase converts it into glucose.

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48
Q

What enzyme converts G6P into normal glucose during times of low blood sugar?

A

Glucose-6-phosphatase.

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49
Q

What happens to glycogen in the skeletal muscle?

A

There is no glucose-6-phosphatease so the glycogen is converted into lactate as part of the lactic acid mechanism within glycolysis.

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50
Q

How is glycogen synthesised?

A

Glycogenin starts the process by covalently binding glucose from uracil diphosphate (UDP-glucose) to form chains of approximately 8 glucose residues. Following this, glycogen synthase takes over and extends the glucose chains. The chains formed by glycogen synthase are then broken by glycogen-branching enzyme and re-attached at A1-6 points to give branching points.

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51
Q

What enzymes are involved in glycogen synthesis?

A

Glycogenin- starts process by covalently binding glucose from UDP glucose
Glycogen synthase- takes over and extends chains
Glycogen-Branching enzyme- breaks chains and reattaches to give branching points

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52
Q

How is glycogen mobilised?

A

Glycogen phosphorylase removes the glucose monomers one at a time from the reducing ends as glucose-1-phosphate.
Following this, de-branching enzyme removes the branches and enables glycogen to be utilised.
Glucosidase activity releases free glucose.

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53
Q

What is glycolysis?

A

Glycolysis is a catabolic pathway in which glucose is turned into pyruvate. It saves potential energy from glucose through substrate-level phosphorylation.

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54
Q

Does glycolysis require oxygen?

A

No- it is essentially the only way for cells to make energy in the absence of oxygenation.

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55
Q

What are the 2 stages of glycolysis?

A

Preparatory phase

Pay-off phase

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56
Q

How is energy formed in the preparatory and pay-off phases?

A

2ATP are used up in the preparatory phase but 4ATP are gained during the pay-off phase so there is a net gain of 2ATP.

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57
Q

How much ATP is produced in glycolysis?

A

2ATP.

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58
Q

What happens in the preparatory phase?

A 
Glucose > G6P (hexokinase) 
G6P > F6P
F6P > F-1,6bisP (phosphofructokinase)
Cleavage of F-1,6bisP (6C-two 3C)
Interconversion of 2 triose sugars to form G3P.
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59
Q

What catalyses the conversion of glucose into G6P?

A

Hexokinase.

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60
Q

What does phosphofructokinase catalyse?

A

F6P > F-1,6bisP

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61
Q

What is the first committed step in glycolysis and why?

A

F6P > F-1,6bisP because F-1,6bisP is only used in glycolysis.

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62
Q

Why are the cleaved triose sugars interconverted in the preparatory phase?

A

Only one is useful in the pay-off phase.

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63
Q

What is the end product of the preparatory phase?

A

Glucose-3-phosphate.

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64
Q

What happens in the pay-off phase?

A

G3P is oxidised to 1,3-bisPG
Phosphate transferred from 1,3-bisPG to ADP
(produces 2ATP- substrate level phosphorylation)
3PG > 2PG
2PG > PEP
Transfer of PEP to ADP + pyruvate
(2ATP produced)

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65
Q

What step in the pay-off phase produces pyruvate?

A

Transfer of PEP to ADP + pyruvate (produces 2ATP).

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66
Q

What does NAD do?

A

Oxidising agent cofactor- accepts electrons from other molecules.

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67
Q

Can glycolysis function without NAD?

A

No- if there is no NAD there is no glycolysis.

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68
Q

Where does NAD come from?

A

Vitamin niacin- it is limited in the cell.

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69
Q

Is NAD limited in the cell?

A

Yes.

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70
Q

What is redox balance?

A

Redox balance describes the fact that NAD will always be regenerated regardless of the fate taken by pyruvate.

71
Q

What are the fates of pyruvate?

A

Pyruvate > Acetyl CoA
Pyruvate > Lactic acid
Pyruvate > Ethanol

72
Q

What does acetylaldehyde do?

A

Converts pyruvate into ethanol in plants and other microorganisms.

73
Q

When is pyruvate converted into lactic acid?

A

When cells are lacking oxygen.

74
Q

What converts pyruvate into lactic acid?

A

Lactate dehydrogenase.

75
Q

How does the conversion of pyruvate into lactic acid allow redox balance through NAD replenishment?

A

Oxidation of NADH into NAD.

76
Q

What does lactic acid cause in muscles?

A

Pain/discomfort/injury.

77
Q

What is the Cori Cycle?

A

A coupled muscle/liver action in which when the body doesn’t have enough energy, substrate-level phosphorylation occurs and produces lactic acid. The liver later replenishes glucose through gluconeogenesis, repaying the oxygen debt ran up by skeletal muscles.

78
Q

When is pyruvate converted into Acetyl CoA?

A

When there is sufficient oxygen supply present.

79
Q

Where is pyruvate converted into acetyl CoA?

A

Mitochondria.

80
Q

What enzyme converts pyruvate into acetyl CoA?

A

Pyruvate dehydrogenase.

81
Q

Why does NADH give up its hydrogen ion during conversion of pyruvate to acetyl CoA?

A

To allow replenishment of NAD for redox balance.

82
Q

What is gluconeogenesis?

A

Process used to create glucose from other molecules- essentially glycolysis in reverse.

83
Q

Why is gluconeogenesis required?

A

Some tissues rely solely on glucose as a source of energy (e.g. brain).

84
Q

Why is gluconeogenesis not a direct reversal of glycolysis?

A

It can only achieve 7/10 reactions.

85
Q

Why can gluconeogenesis only achieve 7 out of the 10 glycolytic reactions?

A

Large -ve △G prevents reversibility.

86
Q

How does gluconeogenesis overcome the energetically unfavourable stages?

A

Bypass reactions.

87
Q

What are bypass reactions?

A

Reactions which allow gluconeogenesis to skip around the impossible glycolytic reactions.

88
Q

How do bypass reactions work?

A

Cell uses bypass reactions with enzymes that catalyse a separate set of irreversible reactions.

89
Q

How many bypass reactions are there?

A

4

90
Q

What do bypass allow?

A

Independent control of glycolysis/gluconeogenesis pathways- prevents them from cancelling each other out.

91
Q

Where do the bypass reactions occur?

A

Cytosol (C+D) and mitochondria (A+B)

92
Q

What bypass reactions occur in the cytosol?

A

C + D

93
Q

What bypass reactions occur in the mitochondria?

A

A + B

94
Q

What reaction do bypass reactions A + B overcome?

A

Pyruvate to PEP (10th step of glycolysis)

95
Q

What is bypass reaction A?

A

Pyruvate > Oxaloacetate

96
Q

What catalyses bypass reaction A?

A

Pyruvate carboxylase.

97
Q

What is bypass reaction B?

A

Oxaloacetate > PEP

98
Q

What catalyses bypass reaction B?

A

PEPCK (PEP carboxylkinase)

99
Q

What is bypass reaction C?

A

F-1,6bisP > F6P

100
Q

What catalyses bypass reaction C?

A

Fructose-1,6-phosphatase.

101
Q

What is bypass reaction C?

A

G6P > Glucose

102
Q

What catalyses bypass reaction C?

A

Glucose-6-phosphatase.

103
Q

What catalyses the conversion of pyruvate into oxaloacetate?

A

Pyruvate carboxylase.

104
Q

What catalyses the conversion of oxaloacetate into PEP?

A

PEPCK (PEP-carboxylkinase).

105
Q

What catalyses the conversion of F-1,6bisP into F6P?

A

Fructose-1,6phosphatase.

106
Q

What catalyses the conversion of G6P into glucose?

A

Glucose-6-phosphatase.

107
Q

Where does the formation of free glucose actually occur?

A

Lumen of the endoplasmic reticulum.

108
Q

What is the end point of gluconeogenesis?

A

G6P formation- allows it to be trapped.

109
Q

What does the final step to make free glucose require?

A

Requires G6P to be shuttled into the lumen and glucose to be shuttled back out.

110
Q

Does the body have pathways for the catabolism of fructose and galactose?

A

No- despite both being primary dietary monosaccharides the body has no mechanisms to catabolise them.

111
Q

Where can fructose and galactose enter glycolysis?

A

Various different points.

112
Q

Where is most fructose metabolised?

A

Liver.

113
Q

How does fructose enter glycolysis?

A

Fructose-1-phosphate pathway.

114
Q

How does galactose enter glycolysis?

A

Converted to G1P by a sugar-nucleotide derivative called UDP-galactose.

115
Q

What is the function of the pentose-phosphate pathway?

A

To produce NADPH- needed for FA synthesis.
To produce pentoses (5C sugars)
To metabolise the small amounts of pentoses in the diet (usually come from nucleotide ingestion)

116
Q

What does the pentose-phosphate pathway produce?

A

Pentoses and NADPH.

117
Q

What are pentoses?

A

5C sugars.

118
Q

Where are pentoses ingested in the diet?

A

Usually ingested from nucleotides.

119
Q

What are the 2 parts of the pentose-phosphate pathway?

A

Oxidative, irreversible

Non-oxidative, reversible

120
Q

What does NADPH do?

A

Links anabolic and catabolic processes.

121
Q

What is the difference between NAD+ and NADP+

A

NAD has key role in catabolic process as seen in glycolysis whereas NADP+ has key role in anabolic processes as seen in fatty acid synthesis.

122
Q

What is NADP+ also used as?

A

Antioxidant.

123
Q

What is the citric acid cycle?

A

Gateway to aerobic metabolism; common metabolic pathway for all fuel molecules.

124
Q

Is the citric acid cycle still a catabolic process?

A

Yes.

125
Q

Does the citric acid cycle yield more ATP than glycolysis?

A

Yes- as it leads into the electron transport chain.

126
Q

Does the citric acid cycle include oxygen as a reactant or direct product?

A

No.

127
Q

What is the function of the citric acid cycle?

A

Removes electrons and passes them on to form NADH/FADH2 which enter the electron transport chain and complete oxidative phosphorylation.

128
Q

Why is the citric acid cycle very efficient?

A

Cyclical nature

Small amounts of acetyl CoA can make large amounts of NADH/FADH2.

129
Q

Why is the citric acid cycle referred to as a black box cycle?

A

2C molecule enters (acetyl CoA) and 2C molecules removed (2 CO2) therefore there is a constant state of intemediatory metabolites.

130
Q

Why is there a constant state of intemediatory metabolites in the citric acid cycle?

A

2C molecule (acetyl CoA) enters whilst 2C CO2 removed.

131
Q

How is entry into the citric acid cycle controlled?

A

Pyruvate dehydrogenase which converts pyruvate into acetyl CoA is controlled by its own immediate products and by ATP formation to allow correct balance.

132
Q

What is pyruvate dehydrogenase controlled by?

A

Immediate products

ATP formation

133
Q

What are the other control points in the citric acid cycle?

A

Isocitrate dehydrogenase

Alpha-ketoglutarate

134
Q

What are isocitrate dehydrogenase and alpha-ketoglutarate responsible for?

A

Acting as control points.

135
Q

What do control points allow?

A

Redirection of cellular resources.

136
Q

Why is the citric acid cycle an amphibolic pathway?

A

Serves both anabolic and catabolic processes.

137
Q

What does the citric acid cycle also provide?

A

Biosynthetic precursors.

138
Q

How does the citric acid cycle produce biosynthetic precursors?

A

When cellular energy needs are met throughout the cycle, it can produce the building blocks for other biosynthetic products. However, this can lead to a reduction in the intermediary metabolites available within the citric acid cycle.

139
Q

What are the mitochondria?

A

Site of aerobic respiration.

140
Q

What needs to be in the mitochondrial matrix in order for aerobic respiration to occur?

A

NADH/FADH2.

141
Q

What transports the NADH/FADH2 to the mitochondrial matrix?

A

Glycerol-phosphate shuttle.

142
Q

What does the glycerol phosphate shuttle do?

A

Transports excess NADH/FADH2 into the mitochondrial matrix.

143
Q

What is the mitochondrial membrane impermeable to?

A

NAD

144
Q

How is NAD transported into the mitochondrial membrane?

A

Glycerol-3-phosphate passes on NAD electrons to FADH2.

145
Q

How is an energetic price paid for the glycerol-phosphate shuttle?

A

Oxidation of FADH2 in the electron transport chain generates less ATP per mol than NADH2. Therefore, there is an energetic price paid for using cytosolic reduced co-substrates in terminal respiration.

146
Q

What does the electron transport chain consist of?

A

4 enzyme complexes.

147
Q

What are the 4 complexes of the electron transport chain?

A

NADH-Q Oxioreductase
Succinate Q-reductase
Q-Cytochrome C Oxioreductase
Cytochrome C Oxidase

148
Q

What are on either side of the electron transport chain?

A

Matrix and intermembrane space.

149
Q

What does Complex 1 do?

NADH-Q Oxioreductase

A

Oxidises NADH and passes the electrons to ubiquinone to form ubiquonol.

150
Q

What does Complex 2 do?

Succinate Q-reductase

A

Oxidises FADH2 and passes the electrons to ubiquinone to form ubiquinol.

151
Q

What do Complexes 1/2 do?

A

Oxidise NADH and FADH2 and pass electrons on to ubiquinone to form ubiquinol.

152
Q

What do complexes 1/2 pass electrons to?

A

Ubiquinone.

153
Q

What is ubiquinol?

A

Molecule formed when oxidised electrons are passed to ubiquinone from Complexes 1/2 following the oxidation of NADH and FADH2.

154
Q

What does Complex 3 do?

Q-Cytochrome C Oxioreductase

A

Takes electrons from ubiquinol and passes them to Cytochrome C.

155
Q

What does Complex 4 do?

Cytochrome C oxidase

A

Passes electrons to molecular O2.

156
Q

What happens to protons as electrons move along the electron transport chain?

A

Protons move from the matrix to the intermembrane space.

157
Q

Is the movement of protons from the matrix to the intermembrane space a vectoral movement?

A

Yes.

158
Q

Why is the movement of protons from the matrix to the intermembrane space a vectoral movement?

A

Vectoral movement because it has a direction and acts as an energy transformation.

159
Q

What do protons do when they move back down the gradient to the matrix?

A

Release energy.

160
Q

What is the proton-motive force?

A

Protons move from the matrix to the intermembrane space whilst electrons are travelling along the ETC. When they move back down, they release energy.

161
Q

What do protons outside of the membrane act as?

A

Store of potential energy.

162
Q

What do protons approach when they come back down their concentration gradients?

A

Approach ATP synthase.

163
Q

What is ATP synthase?

A

Large multi-unit complex which converts ADP+Pi to ATP for use.

164
Q

What happens to protons as they approach ATP synthase?

A

ATP synthase has a mechanism to allow proton entry.

165
Q

How does ATP synthase generate ATP?

A

Utilises the energy generated from the proton gradient and uses it to convert ADP and Pi into ATP.

166
Q

What does generated ATP do?

A

ATP takes this potential energy and uses it to carry out tasks in the body.

167
Q

What is the final step in metabolising food molecules into energy?

A

ATP production by ATP synthase.

168
Q

What is ATP synthase also commonly called?

A

ATPase.

169
Q

What is the binding-change mechanism?

A

The binding-change mechanism refers to the fact that not all binding sites are equivalent and protons will move from the positive to negative side of membrane as part of sequential binding.

170
Q

How many ATP are yield from one glucose molecule?

A

30/32 ATP.

171
Q

Why is the electron transport chain said to be coupled to ATP synthase?

A

ETC is coupled to ATP synthase because if there was no ETC there would be no generation of an electrochemical gradient which drives ATP synthase.

172
Q

How does uncoupling occur?

A

If the inner mitochondrial membrane becomes permeable to protons, the proton gradient cannot be generated. If this happens, electron transport can still occur but no ATP is generated.

173
Q

What is an example of pathological uncoupling?

A

Malignant hyperthermia.

174
Q

What is an example of physiological uncoupling?

A

Brown fat in infants.

Science for Medicine (19 decks)

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