Energy Storage Flashcards

1
Q

What are the three major energy stores? (70KG man)

A

Triacyclglycerols (15KG)- Stored in adipose tissue.
Glycogen (0.4KG) - Stored in the liver.
Muscle Proteins (6KG) - Only used during starvation.

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2
Q

Outline the reactions involved in glycogen synthesis:

A

Glucose is phosphorylated to form Glucose 6-phosphate by hexokinase.

Glucose 6P is converted to Glucose 1P

Glucose 1P reacts with UTP to form UDP-glucose - an inorganic phosphate molecule is released.

UDP-glucose then reacts with glycogen. The glucose monomer is added to the glycogen polymer. UDP is released and reforms UTP with a phosphate molecule.

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3
Q

Which enzymes are used to catalyse the addition of glucose from UDP-Glucose to glycogen?

A
Glycogen Synthase (a1-4 glycosidic bond)
Branching enzyme. (a1-6 glyosidic bond)

Remember that glycogen is a branched molecule (which means lots of glucose monomers can be broken off at once). Branching enzyme adds glucose via bonds which produce those branches.

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4
Q

Outline glycogen breakdown:

A

Either glycogen phosphorylase or de-branching enzyme cleave a molecule of glucose 1-P from glycogen. A molecule of phosphate is needed as a substrate.

Glucose 1-P is converted to glucose 6-P which can be used metabolically.

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5
Q

How does the functions of liver and muscle glycogen vary?

A

In both Glucose 6-P is produced from glycogenolysis.

In muscle Glucose 6-P is used for glycolysis to produce energy.

In the liver Glucose6-P is converted back to glucose by glucose-6-phosphatase and released into the blood for use in other tissues.

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6
Q

In the liver what are the rate-limiting enzymes for glycogen synthesis and glycogenolysis?

A

Glycogen synthesis - Glycogen synthase

Glycogenolysis - Glycogen Phosphorylase

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7
Q

How do glucagon and adrenaline regulate glycogen metabolism?

A

Remember glucagon and adrenaline are produced to trigger a ‘fight or flight’ response.

They stimulate glycogen phosphorylase so that more energy is released.

They inhibit glycogen synthase to limit the amount of energy put into storage.

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8
Q

How does insulin regulate glycogen metabolism?

A

Remember insulin is produced as a hormone to begin ‘rest and digest’ responses.

It stimulates glycogen synthase to put more energy into storage.

It inhibits glycogen phosphorylase to limit the blood glucose levels.

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9
Q

Name two glycogen storage diseases:

A

Von Gierke’s disease -
Glucose 6-phosphatase deficiecy.
(Inefficiency of the liver to convert G6P to glucose for transport around the body)

McArdle Disease -
Muscle glycogen phosphorylase deficiency.
(Inefficiency in glycogen mobilisation)

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10
Q

What are the clinical consequences of glycogen storage diseases?

A

Can affect either the liver or muscle.

Excess glycogen can lead to tissue damage.

Diminished glycogen stores can lead to hypoglycaemia.

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11
Q

When does gluconeogenesis occur?

A

Beyond 8 hours of fasting the liver’s glycogen storage is depleted.
It therefore starts to produce glucose from non-carbohydrate sources.

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12
Q

Where does gluconeogenesis occur?

A

Mainly in the liver but also in the kidney cortex.

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13
Q

What precursors can be used for gluconeogenesis?

A

Lactate (Produced from anaerobic glycolysis)
Glycerol (Released from adipose tissue)
Glucogenic Amino Acids (Mostly alanine)

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14
Q

Outline gluconeogenesis:

A

Lactate and glucogenic amino acids are converted into oxaloacetate.

Oxaloacetate is fed into a chain of reactions by the enzyme PEPCK.

Eventually Fructose 1,6-bis phosphate is produced as an intermediate.

This is converted to fructose 6P by fructose 1,6-bis phosphatase.

Fructose 6P is converted to Glucose 6P and then from that to glucose by Glucose-6-phosphatase.

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15
Q

What are the key regulatory enzymes in gluconeogenesis?

A

PEPCK (Converts oxaloacetate into an intermediate)

Fructose 1,6-bis phosphotase (Converts fructose 1,6-bids phosphotase into Fructose 6P)

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16
Q

How is gluconeogenesis regulated?

A

Glucagon and Cortisol:
Stimulate PEPCK and fructose 1,6-bisphosphatase

Insulin:
Inhibits PEPCK and fructose 1,6-bis phosohatase

17
Q

Why can triacyclglycerols be stored in adipose tissue?

A

Triacyclglycerols (TAGs) are hydrophobic and so can be stored in an anhydrous form in adipose tissue.

18
Q

Describe how dietary TAGs are processed for storage.

A

Broken down by pancreatic lipase to glycerol and fatty acids in the small intestine.

Absorbed across the wall of the small intestine . Repackaged into TAGs within chylomicrons.

Chylomicrons are sent in lymphatic system, enter the systemic circilation via the left subclavian vein and then to adipose tissue for storage.

19
Q

Outline B-oxidation (fatty acid oxidation):

A

Fatty acids are combined with CoA to form activated fatty acids. (They can’t traverse the membrane in their normal state)

The fatty acids are now transported across the mitochondrial membrane with the carnitine shuttle.

Oxidation of the fatty acid now occurs in the mitochondria -
Units of Acetyl CoA are cleaved off.
Which each unit removed a molecule of FAD and NAD+ are reduced.
The Acetyl CoA can also then be used in the Krebs cycle.

20
Q

Outline lipogenesis (fatty acid synthesis):

A

Mainly occurs in the liver when in high energy states.

Glucose is first converted to pyruvate via glycolysis. Pyruvate then enters the mitochondria.

Pyruvate is converted to Acetyl CoA which combines with oxaloacetate to form citrate.

Citrate is transported out of the mitochondria and is cleaved back to Acetyl CoA and Oxaloacetate.

Oxaloacetate is converted to malate and oxidised to pyruvate again. This produces NADPH which is used later on.

Acetyl CoA is converted to malonyl CoA by the enzyme Acetyl-CoA carboxylase.

A fatty acid is synthesised from malonyl CoA units by a fatty acid synthase complex. This process requires lots of reducing power (NADPH)

21
Q

Why is the pentose phosphate pathway so important to fatty acid synthesis?

A

It produces lots of NADPH which is needed for the fatty acid synthase complex to produce a fatty acid from malonyl CoA units.

22
Q

Name 5 differences between lipogenesis and B-oxidation:

A
  1. Lipogenesis adds C2 units and B-oxidation cleaves C2 units.
  2. Lipogenesis uses Malonyl CoA whereas B-Oxidation produces Acetyl CoA.
  3. Lipogenesis occurs in the cytoplasm whereas B-Oxidation occurs in the mitochondria.
  4. Lipogenesis is reductive (requires NADPH) but B-Oxidation is oxidative (produces NADPH and FAD2H).
  5. Lipogenesis is stimulated by insulin and B-oxidation is inhibited bu insulin.