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Metabolism > Energy Production - Carbohydrates > Flashcards

Energy Production - Carbohydrates Flashcards

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1
Q

What are the 3 types of carbohydrate? but what are the 2 main forms they take and from what?

A

monosaccharide, disaccharide, polysaccharide. either ‘aldoses’ (from glyceraldehyde) or ‘ketoses’ (from dihydroxyacetone)

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2
Q

What is the range of no. of C a monosaccharide can contain, but what forms are they most commonly in?

A

3 - 9 Carbons, normally triose, pentose or hexose

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3
Q

What structure do monosaccharides with 5 or more Cs exist as? and why?

A

ring structure because aldehyde/ketone group has reacted with an alcohol group in the same sugar to form a hemiacetal ring.

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4
Q

What are there physical characteristics of -CHO

A

Hydrophilic = attract water, water soluble and don’t pass across cell membranes without help
Partially oxidised = need less O2 than fatty acids for complete oxidation

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5
Q

Where is the chiral carbon on a ring structured in an aldose and ketose?. What is the name given to the C-atom and what are its 2 forms?

A

The ring structure has a new chiral carbon at C1 of an aldose (C2 for ketose). This is known as the anomeric C-atom and can have two forms: α or β.

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6
Q

How are disaccharides formed? What kind of bond is formed?

A

Formed by condensation of 2 monosaccharides with the elimination of water and formation of an O-glycosidic bond

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7
Q

What are the 3 main disaccharides and what are their subunits?

A

Maltose - glucose + glucose
Lactose - glucose + galactose
Sucrose - glucose + fructose

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8
Q

How can disaccharides be non-reducing?

A

If the aldehyde or ketone groups of the two sugars are both involved in the forming the glycosidic bond

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9
Q

How are alpha and beta glycosidic bonds different?

A

Different stereoisomerism. α-glycosidic bond is formed when both carbons have the same stereochemistry (Both have same D or L type), whereas a β-glycosidic bond occurs when the two carbons have different stereochemistry (have different D and L types)

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10
Q

3 main polysaccharides?

A

Glycogen, starch and cellulose

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11
Q

Glycogen - polymer of? type of bonds? properties relating to function?

A

a polymer of glucose found in animals. The glucose units joined together in α-1,4 and α-1,6 glycosidic linkages (10:1). Glycogen is highly branched = less osmotic so easier to store.

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12
Q

Starch - found where? polymer of? bonds? where is it hydrolysed and what is released?

A

Starch is found in plants. It contains amylose (α-1,4 linkages) and amylopectin (α-1,4 and α-1,6 linkages). Starch can be hydrolysed to release glucose and maltose in the human GI tract.

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13
Q

Cellulose - found where? role? monomer? bond? use in human body?

A

found in plants where it has a structural role. Glucose monomers are joined by β-1,4 linkages to form long linear polymers. A healthy human diet contains plenty of cellulose for fibre, but humans do not posses the required enzymes to digest β-1,4 linkages.

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14
Q

Name 2 dietary polysaccharides and what are they hydrolysed by and what do they release? Where does it occur with which enzymes?

A

Dietary polysaccharides (starch & glycogen) are hydrolysed by glycosidase enzymes. This releases glucose, maltose and leaves smaller polysaccharides (dextrins). This begins in the mouth with salivary amylase and continues in the duodenum with pancreatic amylase.

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15
Q

Where does digestion of the disaccharides take place?

A

Digestion of maltose, dextrins and dietary disaccharides lactose and sucrose occurs in the duodenum and jejunum.

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16
Q

Which enzymes are involved in the digestion of disaccharides, what types of enzymes are they and where are they located?

A

The major enzymes are lactase, glycoamylase and sucrase/isomaltase. The glycosidase enzymes involved are large glycoprotein complexes that are attached to the brush border membrane of the epithelial cells lining the duodenum and jejunum.

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17
Q

What is released from the digestion of disaccharides?

A

They release the monosaccharides glucose, fructose and galactose.

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18
Q

What does low activity of lactase show? (clinical condition?)

A

Low activity of lactase is associated with a reduced ability to digest the lactose present in milk products and may produce the clinical condition of lactose intolerance.

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19
Q

How are monosaccharides absorbed into blood?

A

Actively transported into intestinal epithelial cells and are absorbed into blood.

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20
Q

How are the monosaccharides transported into the epithelial cells? and how is it controlled?

A

facilitated diffusion using transport proteins (GLUT1 -GLUT5) which have different tissue distribution and affinities. controlled hormonally e.g. insult controls GLUT4

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21
Q

What is blood glucose conc in healthy people?

A

around 5mM

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22
Q

which tissues does glycolysis take place in?

A

all tissues (= cytosolic)

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23
Q

Functions of glycolysis

A

oxidise glucose, NADH production, synthesis of ATP from ADP, produces C6 and C3 intermediates

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24
Q

Characteristics of glycolysis

A

Exergonic, oxidative, is only pathway that can operate anaerobically

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25
Overall reaction of glycolysis
Glucose + 2Pi + 2ADP + 2NAD+ -> 2 Pyruvate, 2ATP, 2NADH, 2H+ + 2H2O
26
Why isn't cellulose digested in human GI tract?
In the glucose polymer cellulose, glucose monomers are joined together by β-1,4 glycosidic linkages. Humans do not posses the enzyme to digest these linkages.
27
Describe the glucose-dependency in some tissues
All tissues can remove glucose, fructose and galactose from the blood. However the liver is the major site of fructose and galactose metabolism. Glucose concentration in the blood is normally held relatively constant. This is because some tissues have an absolute requirement for glucose and the rate of glucose uptake is dependant on its concentration in the blood. The minimum glucose requirement for a healthy adult is ~180g/day: - ~ 40g/day is required for tissues that only use glucose Eg RBCs, WBCs, kidney medulla and lens of the eye - ~ 140g/day is required by the CNS as this prefers glucose - Variable amounts are required by tissues for specialised functions Eg synthesis of triacylglycerol in adipose tissue, glucose metabolism provides the glycerol phosphate.
28
What happens to ATP in glycolysis?
2 moles of ATP are required to activate the process. This is an energy investment to make glucose a little bit unstable in order to carry out reactions on it. 4 moles of ATP are produced to give a net gain of 2 moles of ATP
29
Which steps in glycolysis are irreversible and which enzymes do they use?
Steps 1, 3 and 10 Step 1 is catalysed by Hexokinase (in the liver glucokinase) Step 3 is catalysed by Phosphofructokinase-1 Step 10 is catalysed by Pyruvate kinase
30
Is CO2 lost in glycolysis?
No, C6 -> 2C3 = no loss of C therefore no loss of CO2
31
Which step is the committing step? and what happens in it?
Step 3: Fructose-6-phosphate + ATP (+ Phosphofructokinase-1) -> fructose-1,6-bisphosphate + ADP
32
What happens in anaerobic glycolysis? what enzyme is required and what is the reaction?
When the oxygen supply is inadequate or in cells without mitochondria, pyruvate is reduced to lactate by the enzyme lactate dehydrogenase (LDH). 2 Pyruvate + 2 NADH + 2 H+ → 2 Lactate + 2 NAD+
33
Why is anaerobic glycolysis required?
NAD+ is required to allow some ATP to be produced.
34
Where is lactate produced?
Red blood cells and skeletal muscle
35
What happens to the lactate produced?
metabolised by liver and heart via lactate dehydrogenase. In heart: converted back to Pyruvate and oxidised to CO2 In liver: converted to glucose (gluconeogenesis)
36
What features of the heart and liver make lactate breakdown possible?
They are usually well supplied with O2
37
What is normal plasma lactate conc?
Plasma lactate
38
Give e.g. of how plasma lactate conc. can increase and from what conc does it start causing problems and why?
e.g. strenuous exercise, pathological conditions e.g. shock and congestive heart disease. When conc reaches > 5mM causes a problem, as it exceeds the renal threshold and it begins to affect the buffering capacity of the plasma causing lactic acidosis.
39
Plasma lactate conc = 2-5mM?
Hyperlactaemia, below renal threshold, no change in blood pH (buffering capacity)
40
Plasma lactate conc > 5mM?
Lactic acidosis, above renal threshold, lowered blood ph
41
Why is normal plasma lactate conc constant at 1mM?
Normally the amount of lactate produced equals the amount of lactate utilised
42
How is plasma lactate conc determined?
Production of lactate, utilisation of lactate (liver, heart, muscle), and disposal of lactate (kidney)
43
Which enzyme is used to convert 1,3-Bisphosphoglycerate into 2,3-Bisphosphoglycerate
Bisphosphoglycerate mutase
44
Where is 2,3-BPG present in the body, what is it's conc, what is it's role?
Found in red blood cells, conc is approx 5mM, important regulator of O2 affinity of haemoglobin (tense form)
45
Where does fructose metabolism take place?
Liver
46
Fructose -> Fructose -1-Phosphate conditions? enzymes?
ATP -> ADP, fructokinase
47
Fructose-1-Phosphate -> 2-Glyceraldehyde-3-Phosphate enzymes? what does product do?
Aldolase, 2-GLyceraldehyde-3-Phosphate enters glycolysis
48
Clinical importances of fructose metabolism
Essential fructosuria - fructokinase missing, fructose in urine, no clinical signs Fructose intolerance - aldolase missing, fructose-1-phosphate accumulates in liver = liver damage, treatment = remove fructose from diet
49
Where does galactose metabolism take place?
Liver
50
galactose -> galactose-1-phosphate?
galactokinase enzyme, ATP -> ADP
51
galactose-1-phosphate -> glucose-1-phosphate?
UDP-glucose (catalyst) -> UDP-galactose (intermediate for catalyst) uses Galactose-1-phosphate uridyl transferase (UDP-galactose 4'-epimerase to reverse)
52
Clinical importance of galactose metabolism
``` Galactosaemia - 1 in 30000 births - unable to utilise galactose galactokinase deficiency (rare) - galactose accumulates Transferase deficiency (common) - galactose and galactose-1-phosphate accumulates problem caused = galactose enters other pathways e.g.. Galactose -> Galactitol (NADPH -> NADP+ using aldose reductase) Causes NADPH levels to be depleted, prevents maintenance of free sulphydryl groups on proteins, causing inappropriate disulphide bond formation, causing loss of structural and functional integrity of some proteins that depend on free -SH groups - causes cataracts in eyes The accumulation of Galactose and Galactitol in the eye may lead to raise intra-ocular pressure (glaucoma) which if untreated may cause blindness. Accumulation of Galactose 1-phosphate in tissues causes damage to the liver, kidney and brain and may be related to the sequestration of Pi making it unavailable for ATP synthesis. treatment = no lactose in diet (lactose = glucose + GALACTOSE) ```
53
How many stages in the pentose phosphate pathway? What happens in each stage?
2 stages oxidative decarboxylation: Glucose 6-phosphate + 2 NADP+ → C5 sugar phosphate + 2NADPH + 2H+ + 2CO2 (in presence of glucose-6-phosphate dehydrogenase Rearrangement of C5 to glycolytic intermediates: 3 pentose sugars -> 2 Frucose-6-phosphates + glyceraldehyde-3-phosphate
54
In pentose phosphate pathway any ATP produced? Reversible? Controlled reaction?
No ATP produced, irreversible due to loss of CO2, controlled by NADP+/NADPH ratio
55
Where does pentose phosphate pathway take place in the body? Where in the cells?
In the liver, RBCs and adipose tissue. All reactions ae cytoplasmic, take place in cytoplasm/cytosol
56
Functions of the pentose phosphate pathway?
Produce NADPH in the cytoplasm Reducing power for anabolic processes such as lipid synthesis therefore has high activity in liver + adipose tissue In RBCs maintains free –SH groups (cysteine) on certain proteins to prevent oxidation of disulphide bonds Used in various detoxification mechanisms Produce C5 ribose for the synthesis of nucleotides. The pathway therefore has a high activity in dividing tissues e.g. bone marrow
57
What is the role of glucose-6-phsphate dehydrogenase in the pentose phosphate pathway? how does it do it?
Glucose 6-phoshate dehydrogenase is the rate-limiting enzyme in the pentose phosphate pathway, used to increase NADPH concentration.
58
What causes a deficiency of glucose-6-phosphate dehydrogenase and how does this affect NADPH levels?
Deficiency in this enzyme is caused by a point mutation in the X-linked gene coding for the enzyme. The mutation results in reduced activity of the enzyme and therefore low levels of NADPH
59
What does NADPH do -SH groups? In a G6PD deficiency, what does a lack of NADPH cause?
The structural integrity and functional activity of proteins in RBCs depends on free –SH groups. –SH groups tend to form disulphide bridges unless prevented by NADPH. In G6PD deficiency the NADPH levels are sometimes too low to prevent the formation of these disulphide bridges.
60
How can a lack of NADPH in RBCs lead to anaemia?
Less NADPH = disulphide bonds form, causes protein to change shape - Hb denatured = homeless = anaemia
61
How can a lack of NADPH in the eye lead to cataracts?
Less NADPH = disulphide bond formation = protein changes shape -protein in lens denatures = causes cataracts
62
Equation showing conversion of pyruvate -> acetyl CoA?
CH3COCOOH + CoA + NAD+ -> CH3CO-CoA + CO2 + NADH + H+
63
How many enzymes are in the pyruvate dehydrogenase (PDH) complex?
5
64
What are the control mechanisms that regulate activity of pyruvate dehydrogenase?
AcetylCoA from the β-oxidation of fatty acids rather than from glucose is used in stage 3 catabolism (acetylCoA allosterically inhibits PDH) The reaction is energy sensitive. ATP/NADH inhibit and ADP promotes allosterically. The enzyme is activated when there is plenty of glucose to be catabolised (insulin activates the enzyme by promoting its Dephosphorylation). Sensitive to Vitamin B1 deficiency as the different enzyme activities in PDH require various cofactors provided by B1 vitamins
65
Is the reaction reversible? why?
Irreversible due to loss of CO2 = key regulatory step
66
Can AcetylCoA be converted back into glucose?
AcetylCoA cannot be converted back to Pyruvate, as reaction is irreversible, for use in gluconeogenesis to produce glucose
67
What does pyruvate dehydrogenase deficiency cause?
lactic acidosis
68
What is overall equation for 1 cycle of krebs (Tricarboxylic Acid/TCA cycle)?
CH3CoA + 3NAD+ + FAD + GDP + Pi + 2 H2O -> 2CO2 + CoA + 3NADH + 3H+ + FADH2 + GTP
69
What kind of pathway is the Krebs cycle and where does it take place?
Oxidative pathway that occurs in mitochondria
70
How many molecules of ATP are produced per molecule of glucose in the TCA cycle?
32 molecules of ATP per molecule of glucose
71
How many turns of the TCA cycle does 1 molecule of glucose cause?
2
72
In 1 turn of the TCA cycle, how many molecules of NADH, FADH2, CO2 and GTP are produced?
6NADH, 2FADH2, 4CO2, 2GTP
73
What are the anabolic functions of the TCA cycle?
``` C5 and C4 intermediates (e.g. α-ketoglutarate, succinate, malate and oxaloacetate) used for the synthesis of non-essential amino acids C4 intermediates (e.g. succinate and oxaloacetate) used for the synthesis of haem and glucose C6 intermediates (e.g. citrate) used for the synthesis of fatty acids ```
74
Can the TCA cycle occur in anaerobic conditions?
no
75
How is CO2 produced from the TCA cycle?
C-C bond in acetate broken and C oxidised to CO2
76
How is the TCA cycle regulated?
ATP:ADP ratio and NADH:NAD+ ratio One of the irreversible steps in the TCA (catalysed by isocitrate dehydrogenase) is allosterically inhibited by the high-energy signal NADH and activated by the low-energy signal ADP
77
Where does oxidative phosphorylation take place?
Inner mitochondrial membrane
78
What happens in oxidative phosphorylation?
Electron Transport, electrons in NADH and FADH2 are transferrerd through a series of carrier molecules to oxygen, releasing free energy. Reoxidation of NADH and FADH2 ATP synthesis, the free energy released in electron transport drives ATP synthesis from ADP + Pi
79
What is the proton motive force? And how is it created?
The H+ gradient (membrane potential) across the inner mitochondrial membrane. created by complexes in e- transport chain pumping protons across the inner mitochondrial membrane
80
How many complexes are there in the e- transport chain, and which ones can pump protons across the membrane and from which carrier?
4 complexes, complex I, III and IV can pump H+ across membrane, NADH donates to all carriers, FADH2 only donates to complex III and IV
81
What is final e- acceptor in the etc?
O2
82
What are 2 uses of reducing power in ATP synthesis?
Electron transport and oxidative phosphorylation
83
Why does NADH use more proton transport complexes than FADH2?
e- in NADH have more energy than in FADH2
84
Why does H+ conc grad across inner mitochondrial membrane increase?
H+ being pumped across by proton transport complexes and the membrane is impermeable to H+
85
Protein translocating complexes transform chemical bond energy of e- into what? what is this called?
Electro-chemical gradient known as Proton Motive Force
86
Can the electron transport chain and pmf formation take place in anaerobic conditions? why?
No, O2 is final e- acceptor so e- stuck at PTCs, so no H+ pumped across membrane because no flow of e-
87
How do H+ cross the inner mitochondrial membrane and what does this lead to?
Protons can normally only re-enter the mitochondrial matrix via the ATP synthase complex, driving the synthesis of ATP from ADP and Pi
88
How many moles of ATP are created from 2 moles of NADH and FADH2?
The oxidation of 2 moles of NADH gives 5 moles of ATP | The oxidation of 2 moles of FAD2h gives 3 moles of ATP
89
What happens to electron transport and oxidative phosphorylation when ATP levels are high?
When [ATP] is high, ADP is low = no substrate for ATP synthase = stops inward flow of H+ = accumulation of H+ in intermitochondrial space = prevents further H+ pumping = stops e- transport
90
How can cyanide inhibit oxidative phosphorylation?
cyanide binds to cytochrome c in complex IV, blocks flow of e- = no e- transport = no pmf = no oxidative phosphorylation
91
How can CO inhibit oxidative phosphorylation?
cyanide binds to cytochrome c in complex IV, blocks flow of e- = no e- transport = no pmf = no oxidative phosphorylation. Also, CO binds to Hb so less O2 to act as final e- carrier
92
What is uncoupling?
The dissipation of the proton gradient before use for energy in oxidative phosphorylation
93
How do uncouplers inhibit oxidative phosphorylation without inhibiting electron transport? give e.g. of uncouplers
increase permeability of membrane to H+, H+ enters mitochondria without driving ATP synthase = dissipates pmf, no oxidative phosphorylation of ADP, no inhibition of e- transport. e.g. dinitrophenol, dinitrocresol, fatty acids
94
What is the role of uncoupling proteins?
To uncouple electron transport from ATP production to produce heat
95
What are the 3 uncoupling proteins, where are they located and what do they do?
UCP1 - (previously known as thermogenin) is expressed in brown adipose tissue and involved in non-shivering thermogenesis enabling mammals to survive the cold. UCP2 – Quite widely distributed in the body. Research suggest it is linked to diabetes, obesity, metabolic syndrome and heart failure. UCP3 – Found in skeletal muscle, brown adipose tissue and the heart. It appears to be involved in modifying fatty acid metabolism and in protecting against ROS damage
96
How does noradrenaline increase heat production?
Stimulates lipolysis by activating lipase which releasing fatty acids from triaglycerol to provide fuel for oxidation in brown adipose tissue. NADH and FADH2 are formed as a result of β-oxidation of the fatty acids. NADH and FAD2H drive ET and increase p.m.f. However, noradrenaline also activates UCP1, allowing protons to cross the inner mitochondrial membrane without passing through the ATP synthase complex. The higher p.m.f. is dissipated as heat
97
Compare the processes of oxidative phosphorylation and substrate level phosphorylation
Oxidative phosphorylation: Requires membrane associated complexes (inner mitochondrial membrane) Energy coupling occurs indirectly through generation and subsequent utilisation of a proton gradient (p.m.f.) Cannot occur in the absence of oxygen Major process for ATP synthesis in cells that require large amounts of energy Substrate Level Phosphorylation Requires soluble enzymes. (Cytoplasmic and mitochondrial matrix) Energy coupling occurs directly through formation of a high energy of hydrolysis bond (phosphoryl-group transfer) Can occur to a limited extent in absence of oxygen Minor process for ATP synthesis in cells that require large amounts of energy

Metabolism (5 decks)

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