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MEH > Session 2: Energy Storage - Glycogen and Fat > Flashcards

Session 2: Energy Storage - Glycogen and Fat Flashcards

1
Q

What cells require glucose? Why?

A

Red blood cells - no mitochondria
Neutrophils - mitochondria used for oxidative burst instead of energy production
Innermost cells of kidney medulla - Their deep in the tissue and not a lot of blood vessels have access to them so oxygen is not rich here.
Lens of the eye - because a lot of light has to shine through in order for us to see it wouldn’t make sense to have a lot of blood vessels here, this means less oxygen.

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2
Q

What is hypoglycaemia?

A

A low level of glucose in the blood.

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3
Q

What are consequences of hypoglycaemia?

A
  1. 8 mmol/L - confusion
  2. 7 mmol/L - weakens and nausea
  3. 1 mmol/L - muscle cramps
  4. 6 mmol/L - brain damage and death
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4
Q

What is the usual level of glucose in the blood?

A

Around 5 mmol/L

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5
Q

What is glucose stored as?

A

Glycogen.

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6
Q

Where is glycogen stored?

A

Muscles and liver.

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7
Q

What is the ratio of muscle storage to liver storage?

A

3:1. 300 gram in muscles, 100 gram in liver.

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8
Q

Where in the muscles is glycogen stored?

A

Both intracellular in myofibrils and intercellular as granules.

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9
Q

Where in the liver is glycogen stored?

A

Stored as granules in hepatocytes.

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10
Q

Outline the structure of glycogen.

A

A polymer of glucose residues joined by glycosidic bonds.
There are two glycosidic bonds:
alpha - 1 - 4
alpha - 1 - 6
The structure is a protein in the middle called glycogenin. On the periphery there are branches of glycogen.

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11
Q

What is the difference between the two glycosidic bonds?

A

1 - 4 joins the chains

1 - 6 forms branch points

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12
Q

What is glycogenesis?

A

The synthesis of glycogen.

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13
Q

There are 4 steps of glycogenesis. Outline step 1, what enzyme is involved.

A

Glucose and ATP forms glucose 6-phosphate and ADP. This is done by hexokinase in muscles and glucokinase in liver.
This is also the first step of glycolysis.

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14
Q

Outline step 2.

A

Glucose-6-phosphate forms glucose-1-phosphate by the help of the enzyme phosphoglucomutase.

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15
Q

Outline step 3.

A

Glucose-1-phosphate and UTP and H2O forms UDP-glucose and PPi (pyrophosphate). This is done by the enzyme G1P uridylyltransferase.

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16
Q

Outline step 4.

A

Glycogen and its residues is already formed. The UDP-glucose that is formed by glycogenesis in step 3 is added onto the existing Glycogen molecule. This gives glycogen with an extra residue and UDP.

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17
Q

What enzymes are used in step 4? How do they differ?

A

Glycogen synthase and branching enzyme.

Glycogen synthase adds on to the existing chain, branching enzyme adds a branching point.

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18
Q

What is glycogenolysis?

A

Breaking down glycogen into smaller constituents.

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19
Q

Outline step 1 of glycogenolysis. What enzyme(s) is used?

A

Glycogen(n residues) and inorganic phosphate turn into glucose-1-phophate and glycogen with one less residue.
Glycogen phosphorylase or de-branching enzyme.

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20
Q

Outline step 2 of glycogenesis. What enzyme is used?

A

Glucose-1-phosphate turns into glucose-6-phosphatase. This is done by the enzyme phosphoglucomutase.

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21
Q

What is important to remember about glycogenolysis and glycogenesis?

A

Glycogenolysis is not just the reverse reaction of glycogenesis. The two reactions have different enzymes.

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22
Q

Why is it important that the two reactions have different enzymes?

A

That allows simultaneous inhibition of one of the pathways and stimulation of the other.

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23
Q

What happens to the glucose-6-phosphate in the liver contra the muscle?

A

In the liver glucose-6-phosphate will turn into glucose and then go into blood glucose. However in the muscle it can’t, it will undergo glycolysis immediately and be used in the muscle. Usually producing lactate.

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24
Q

What enzyme do the muscles lack in order to be used as a buffer of blood glucose levels as the liver is?

A

Muscles lack the enzyme glucose-6-phosphatase. This enzymes turns G-6-P into glucose. Instead G-6-P directly enters glycolysis.

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25
Q

What is the rate limiting enzyme of glycogen synthesis?

A

Glycogen synthase

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26
Q

What is the rate limiting enzyme of glycogen degradation?

A

Glycogen phosphorylase

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27
Q

What does glucagon do to the rate limiting enzymes of glycogen metabolism?

A

Glycogen synthase activity is decreased

Glycogen phosphorylase activity is increased

28
Q

What does insulin do to the rate limiting enzymes of glycogen metabolism?

A

Glycogen synthase activity is increased

Glycogen phosphorylase activity is decreased.

29
Q

Another hormone have the same general function as glucagon. Which?

A

Adrenaline.

30
Q

What types of receptors do glucagon bind to?

A

GPCRs

31
Q

What types of receptors do adrenaline bind to?

A

GPCRs

32
Q

What types of receptors do insulin bind to?

A

Tyrosine Kinase receptors

33
Q

Glucagon has no effect on muscle glycogen storage. It doesn’t increase the degradation. Why?

A

Because muscles do not have any receptors for glucagon.

34
Q

How is the rate of glycogen phosphorylase then regulated in muscle?

A

It is regulated by the allosteric activator AMP which is a low energy molecule. The liver form of the enzyme is however not stimulated by AMP.

35
Q

What is the general problem in glycogen storage diseases?

A

There is a deficiency or dysfunction in one or more of the enzymes in glycogen metabolism.

36
Q

What are consequences of glycogen storage diseases?

A

Liver and/or muscle can be affected.
Excess glycogen storage can lead to tissue damage.
Diminished glycogen stores can lead to hypoglycaemia and poor exercise tolerance.

37
Q

Give two examples of glycogen storage disease.

A

von Gierke’s disease - glucose-6-phosphatase deficiency (enlarged liver)
McArdle disease - muscle glycogen phosphorylase deficiency (quickly fatigued from exercise)

38
Q

What is gluconeogenesis?

A

When you haven’t been eating for around 8 hours the storage of glycogen in the liver will start to deplete and glucose needs to be found from another source.

39
Q

Where does gluconeogenesis occur?

A

Mostly in the liver but some can occur in the kidney cortex.

40
Q

What are the three major precursors of glucose used in gluconeogenesis.

A

Lactate from exercising muscles and red blood cells.
Glycerol from adipose tissue
Amino acids (mainly alanine)

41
Q

What is the cori cycle?

A

Muscles use glucose and turns it into lactate. Lactate is transported to the liver and turned into glucose again. Then glucose is transported into the muscle again.

42
Q

Is acetyl CoA a precursor used in gluconeogenesis?

A

No, acetyl CoA can’t be converted into pyruvate due to its irreversible step. There is therefore no net synthesis of glucose from acetyl CoA as it is only 2 carbons.

43
Q

Is gluconeogenesis glycolysis in reverse? Why?

A

No, it’s not completely in reverse. It has some steps that require different enzymes than glycolysis. These are the irreversible steps.

44
Q

Which are the key enzymes in gluconeogenesis?

A

Phosphoenolpyruvate carboxykinase (PEPCK) which turns oxaloactetate into phosphoenolpyruvate.
Fuctose 1,6-biphosphate which is used instead of PFK (phosphofructokinase)
Glucose-6-phosphatase which is used instead of glucokinase.

45
Q

Outline where the precursors of glucose enter gluconeogenesis.

A

Lactate and glucogenic amino acids are generally turned into pyruvate. Glucogenic amino acids can also turn directly into oxaloacetate. Pyruvate is then turned into oxaloacetate and by PEPCK turned into phosphoenolpyruvate.
Glycerol is fed into gluconeogenesis at step 4 into fructose 1,6-bis phosphate.

46
Q

What are the main regulating enzymes in gluconeogenesis?

A

Fructose 1,6-biphosphatase

PEPCK

47
Q

What are they regulated in response to?

A

Starvation/fasting
Prolonged exercise
Stress

48
Q

What hormones regulate the rate-limiting enzymes?

A

Glucagon, Cortisol

Insulin

49
Q

What do glucagon and cortisol do?

A

It stimulates PEPCK and F 1,6-BP to increase the amount of glucose produced.

50
Q

What does insulin do?

A

It decreases the activity of PEPCK and F 1,6-BP to decrease the amount of glucose produced. This is when you’ve had a meal, then you don’t have to have more glucose produced.

51
Q

How are fats stored?

A

As TAG (triacylglycerol)

52
Q

Give some important features of TAGs.

A

They are hydrophobic and stored in an anhydrous form.

53
Q

Where are TAGs stored?

A

In adipose tissue.

54
Q

What regulates the storage and mobilisation of TAGs?

A

Hormones

55
Q

What happens to adipocytes when you gain weight?

A

They will take up more storage of TAGs and get bigger. They can increase fourfold in size. However after this they will divide.

56
Q

What is the consequence of the division of adipocytes?

A

They will want more TAGs. The adipocytes are more prone to take up more TAGs so this means if you have been obese once it is easier to put on weight again.

57
Q

Briefly outline the storage of TAGs.

A

In the small intestines fat is lipolysed into fatty acids and glycerol. This is by pancreatic lipase. In the intestinal epithelial cells the fatty acids and glycerol are transported via chylomicrons (lipoprotein) into the lymph. At the thoracic duct the carried fats TAGs first enter the blood. Here they can go to adipose tissue for storage or to other demanding tissues to be used as energy in beta-oxidation of fatty acids. Glycerol is directly fed into glycolysis.

58
Q

What is hormone sensitive lipase?

A

A hormone which controls the release of TAGs into the blood stream by cleaving it to fatty acids and glycerol.

59
Q

What is lipogenesis?

A

The synthesis of fatty acids by adding carbons.

60
Q

Where does lipogenesis generally take place?

A

In the liver.

61
Q

Briefly outline lipogenesis.

A

Glucose enters the hepatocyte, turns into pyruvate in cytoplasm.
Pyruvate enters mitochondria to turn into acetyl CoA and enter TCA cycle.
Citrate is formed, transported out of the mitochondria.
Citrate is turned into oxaloacetate and acetyl-CoA again.
Acetyl CoA is turned into malonyl CoA by Acetyl-CoA carboxylase and ATP turning into ADP.
Malonyl CoA is fed into the fatty acid synthase complex. Malonyl CoA loses a carbon.
With the use of NADPH malonyl CoA is synthesised into Fatty acids by the fatty acid synthase complex.
Glycerol-3-P and Fatty acids -> TAGs.
TAGs are then carried out of the hepatocyte by VLDL (very low density lipoprotein)

62
Q

What is they key regulatory enzyme of lipogenesis?

A

Acetyl-CoA carboxylase.

63
Q

What stimulates Acetyl-CoA carboxylase?

A

Insulin and citrate increase the activity.

64
Q

What decreases the activity of Acetyl-CoA carboxylase?

A

Glucagon/adrenalie and AMP decrease the activity.

65
Q

NADPH is needed for lipogenesis. Where is the NADPH formed that is needed?

A

When malate from oxaloacetate is turned into pyruvate it uses magic enzyme and NADP+ goes to NADPH.
Also from the pentose phosphate pathway.

MEH (22 decks)

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