Metabolism 5, 6 & 7 Flashcards

1
Q

How many molecules of acetyl-CoA are produced by catabolism of Palmitic acid, CH3(CH2)14CO2H, and how many cycles of the b-oxidation pathway are needed? (3)

A
  1. Palamic acid has 16 carbons
  2. Each round of beta-oxidation removes 2 carbons from the fatty acid chain as one acetyl-CoA molecule
  3. The 16-chain carbon chain will go through 7 rounds (as the final cycle splits the remaining 4 carbons into two acetyl-CoA) of beta-oxidation, producing 8 molecules of acetyl-CoA
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2
Q

How many molecules of acetyl-CoA are produced by catabolism of Arachidic acid, CH3(CH2)18CO2H, and how many cycles of the beta-oxidation pathway are needed? (3)

A
  1. Arachidic is has 20 carbons
  2. Each round of beta-oxidation removes 2 carbons from the fatty acid chain as one acetyl-CoA molecule
  3. The 20 chain carbon chain will go through 9 rounds (as the final cycle splits the remaining 4 carbons into two acetyl-CoA) of beta -oxidation, producing 10 molecules of acetyl-CoA
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3
Q

What conditions are there for the Krebs cycle to take place (2)

A
  1. Acetyl-CoA enters Krebs cycle if there is a balance between fats and carbohydrates
  2. Must be sufficient oxaloacetate from carbohydrate catabolism to combine with the acetyl-CoA
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4
Q

How does fasting conditions or diseases such as diabetes affect the krebs cycle (4)

A
  1. Oxaloacetate used to produce glucose via gluconeogenesis
  2. Acetyl-CoA cannot enter Krebs cycle as there is no oxaloacetate to combine with
  3. Instead forms acetoacetate and 3-hydroxybutyrate – collectively known as ketone bodies
  4. Acetoacetate is slowly decarboxylated to acetone which can be detected in the breath and urine
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5
Q

What is diabetes and what are the different types of diabetes? (3)

A
  1. Diabetes occurs when the body doesn’t produce enough insulin or the body’s cells don’t respond to insulin properly causing high levels of blood sugar or blood glucose.
  2. Type 1 - autoimmune - pancreatic cells are attacked by the immune system, so the pancreas produces little or no insulin
  3. Type 2 - the body becomes resistant to insulin or does not make enough insulin
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6
Q

Why do ketone bodies form in diabetic patients? (4)

A
  1. Insulin deficiency or ineffectiveness - prevents glucose from entering cells, leading to alternative fuel use
  2. Shift to fat as an alternate energy source
  3. Ketogenesis in the liver - produces ketone bodies as a byproduct of fat metabolism
  4. Accumulation of ketones in the blood (ketosis) - without adequate insulin regulation high ketone levels result in ketosis and potentially ketoacidosis
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7
Q

Where does metabolism of proteins take place and what is produced (3)

A
  1. Amino acid catabolism usually takes place in the liver; some can occur in the muscle
  2. Amino acids from proteins can be converted into glucose
  3. Excess amino acids are converted to triacylglycerols and stored in the adipose tissue
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8
Q

What are the steps of amino acid metabolism (4)

A
  1. Amino group is removed using transaminase enzymes and transferred to an acceptor (e.g. alpha-ketoglutarate) to form glutamate
  2. The acceptor is then oxidatively deaminated to form the ammonium cation (NH4+)
  3. NH4+ is converted to urea for excretion
  4. The remaining carbon skeleton metabolised by the formation of glucose, a Krebs cycle intermediate, or acetyl-CoA
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9
Q

What are the fates of amino acid catabolism (3)

A
  1. The 20 common amino acids are degraded by different pathways to produce seven products
  2. The seven products are metabolic intermediates of either glycolysis or the Krebs cycle.
  3. All amino acids are broken down to either glucogenic amino acids or ketogenic amino acids)
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10
Q

What is the electron transport chain (7)

A
  1. uses free oxygen as the final electron acceptor of the electrons removed from glycolysis
  2. Electrons are passed through a series of redox reactions, with a small amount of free energy to transport hydrogen ions across a membrane.
  3. This process contributes to the gradient used in chemiosmosis
  4. The electrons passing through the electron transport chain gradually lose energy
  5. High-energy electrons donated to the chain by either NADH or FADH2 complete the chain
  6. Low-energy electrons reduce oxygen molecules and form water.
  7. The end products of the electron transport chain are water and ATP.
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11
Q

What is oxidative phosphorylation (2)

A
  1. The production of ATP using the process of chemiosmosis in mitochondria
  2. The addition of a phosphate to ADP, forming ATP, using the potential energy of the hydrogen ion gradient.
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