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MCBG > Topic 6 - Energy Production Carbohydrates (glycolysis/krebs cycle/oxidative phosphorylation) > Flashcards

Topic 6 - Energy Production Carbohydrates (glycolysis/krebs cycle/oxidative phosphorylation) Flashcards

1
Q

What are the 4 stages of catabolism?

A

Stage 1 - Complex molecules are converted to building block molecules that can be taken up by cells, absorbed into circulation by G tract, no energy released, Extracellular (GI tract)
Stage 2 - Building block molecules converted into even simpler molecules, oxidative, coenzymes are reduced, some energy produced in ATP form, intracellular (cytosolic and mitochondrial) e.g glycolysis
Stage 3 - Krebs cycle, oxidative, requires FAD and NAD+, mitochondrial
Stage 4 - electron transport, oxidative phosphorylation, ATP synthesis, O2 required (reduced to H20), NADH and FAD2H oxidised, large amounts of ATP produced, mitochondrial

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2
Q

What are the classes of carbohydrate?

A 
Monosaccharide = one monomer,single sugar unit
Disaccharide = 2 units
Oligosaccharide = 3-12 units (dextrins)
Polysaccharides = 10 -1000s units (glycogen, starch, cellulose)
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3
Q

What are the three main dietary monosaccharides?

A

Glucose, fructose and galactose

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4
Q

Which cells have an absolute requirement of blood glucose?

A
  • red blood cells
  • neutrophils
  • innermost cells of kidney medulla
  • lens of the eye
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5
Q

What constitutes stage 1 metabolism of dietary carbs?

A
  • salivary amylase in mouth (breaks em into dextrins), pancreatic amylase in duodenum (breaks em into monosaccharides), disaccharidases (lactase/sucrase/isomaltase) in small intestine brush border lining of epithelium (monosaccharides as well)
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6
Q

Why can humans not hydrolyse the polysaccharide cellulose?

A
  • no present enzyme to break the beta 1-4 glycosidic bonds in cellulose
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7
Q

Explain briefly in very broad terms lactose intolerance.

A
  • a deficiency of lactase enzyme
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8
Q

Describe the types of lactose intolerance.

A

Primary lactase deficiency - absence of lactase persistence allele so cannot produce enzyme after infancy (grow out of production)
Secondary lactase deficiency - caused by injury to small intestine (Gastroenteritis, coeliac, crohns, ulcerative colitis)
Congenital lactase deficiency - autosomal recessive defect in lactase gene, very rare, means production is hindered from birth

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9
Q

Why does lactose intolerance cause vomiting, flatulence and bloating/cramps?

A

Lactose cannot be digested so remains in GI system, it is an osmalite which means it will attract water

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10
Q

Explain the absorption of monosaccharides by intestinal epithelia.

A
  1. Active transport into epithelium cell via Sodium dependant glucose transporter
  2. Then passive transport into blood supply via glucose transporter
  3. Blood carries to target tissues
  4. Target cells take it in via facilitated diffusion using transport proteins (GLUT 1-5)
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11
Q

What is the basic overall goal of glycolysis?

A

Glucose (6C) ——> 2x pyruvates (2x 3C)

Cleavage

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12
Q

Why does phosphorylation of glucose occur in early stage of glycolysis?

A

Makes glucose negatively charged so it cannot be passed back across the membrane

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13
Q

Why so many steps in glycolysis?

A
  1. Chemistry is easier in small stages
  2. Efficient energy conservation
  3. Allows interconnections with other pathways
  4. Can be controlled
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14
Q

How could glycolysis be used for the imaging of tumours?

A
  • glycolysis rate elevated in cancerous cells (200x)

- can measure uptake of modified, radioactive enzyme used in first stage of glycolysis using PET scanning

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15
Q

Why is the glycolytic intermediate DHAP (dihydroxyacetone-p) important?

A
  • goes on to form glycerol phosphate under enzyme action

- Glycerol phosphate is important to synthesis of triglycerides and phospholipids

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16
Q

Why is the glycolytic intermediate BPG (bisphosphoglycerate) important?

A
  • goes onto form an isomer under enzyme action

- This isomer is produced in erythrocytes and regulates haemoglobin O2 affinity (promotes release)

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17
Q

Why is it important to have an alternate pathway after stage 2?

A
  • if there are low O2 conditions, this is bad because stage 4 requires oxygen
  • some cells like RBCs don’t have stage 3 or 4 so need another way of producing NAD+
  • need NAD+ to be regenerated
18
Q

What is the name of the enzyme used in lactate production?

A
  • lactate dehydrogenase
19
Q

What is lactate production?

A

NADH + H+ + pyruvate = NAD+ + lactate

- NAD IS REGENERATED YAY!

20
Q

What happens to lactate once its been produced?

A

Travels in blood:
The heart - LDH catalyses reformation of pyruvate and its entered back into stage 3 and oxidation
Liver and kidney - LDH catalyses reformation of pyruvate and its used for gluconeogenesis

21
Q

What are the boundaries of lactate plasma for hyperlactaemia and lactic acidosis?

A

Hyperlactaemia = 2-5mM, below renal threshold, no change in blood pH
Lactic acidosis = above 5mM, above renal threshold, lowers blood pH (buffering capacity exceeded)

22
Q

What is Essential fructosuria?

A
  • fructokinase enzyme missing, fructose passes into urine and excreted no clinical signs
23
Q

What is Fructose intolerance?

A
  • adolase B enzyme missing, fructose-1-p accumulates in liver, leads to liver damage
24
Q

What is galactosaemia?

A
  • Accumulation of galactose and/or galactose-1-p
  • problem is galactose enters other pathways like becoming galactitol which oxidises NADPH to NADP+
  • This causes improper formation of disulphide bridges
  • structural damage to the lens of the eye, cataracts
25
Q

What is the resting range of glucose in the blood?

A

4.5-5mmol

26
Q

What is allosteric regulation of enzymes?

A
  • inhibition or activation of an enzyme via binding of a substrate to an alternate site (not the active site)
27
Q

Which types of steps in a pathway are potential sites of regulation?

A
  • ONLY irreversible are regulated NOT reversible
28
Q

Catabolic pathways are inhibited by _________ and activated by _________.

A
  1. High energy signals (ATP, NADH, FAD2H)

2. Low energy signals (ADP, AMP, NAD+, FAD)

29
Q

What is phosphoregulation?

A

Where phosphorylation/dephosphorylation will either be activatory or inhibitory depending on the specific enzyme

30
Q

What is the committing step?

A
  • the step beyond which the reaction becomes irreversible
31
Q

Which enzyme is a key regulator of glycolysis?

A

phosphofructokinase-1 (PFK), its the third enzyme in glycolysis

32
Q

How does allosteric and hormonal regulation of PFK in glycolysis work?

A
  1. High ATP = inhibits PFK
    High AMP = stimulates
  2. Glucagon = inhibits
    Insulin = stimulates
33
Q

Where is the committing step in glycolysis?

A
  • the third step catalysed by PFK enzyme
34
Q

What happens between the end of glycolysis and the beginning of the Krebs cycle?

A

Pyruvate —————> Acetyl coA (pyruvate dehydrogenase catalyses)

35
Q

Why could enzymic activity be sensitive to vitamin B1 deficiency?

A
  • B vitamins provide co factors that are required by various enzymes (FAD, lipoic acid)
36
Q

Where is the Krebs cycle regulated?

A

At irreversible steps! 4 o’clock and 6 o’clock where a carbon is lost at each
- activation by low energy compounds, inhibition by high ones

37
Q

What is ATP synthesis at the final stage of metabolism?

A 
Electron transport (electrons on FAD2H and NADH transferred through carriers to oxygen)
\+
Oxidative phosphorylation (Free energy released and used to drive ATP synthesis)
38
Q

Explain mitochondrial electron transport?

A
  1. Electrons are transferred through carrier proteins to O2 with release of energy
  2. Energy used to drive H+ movement across membrane into inter membrane space
  3. H+ gradient causes a proton motive force
  4. Protons return via ATP synthase and this drives ATP synthesis
39
Q

How is oxidative phosphorylation regulated?

A
  • if ADP is low there’s no substrate for ATP synthase to use
  • so inward flow of H+ stops (inhibition)
  • reverses with high ADP
    OR
    Other inhibitors can block electron transport like cyanide
40
Q

What do uncouplers do in oxidative phosphorylation?

A
  • increase the permeability of the mitochondrial inner membrane to protons
  • dissipates the proton gradient, reducing proton motive force
  • no drive for ATP synthesis

MCBG (6 decks)

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