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Sem 2 - MEH > Energy Storage > Flashcards

Energy Storage Flashcards

1
Q

For what types of cells is glucose an absolute requirement?

A
  • Red Blood Cells - as no mitochondria
  • Neutrophils - mitochondria adapted for respiratory burst and not energy production.
  • Inner most cells of kidney medulla - Not same oxygen supply as deep into kidney. So, more anaerobic respiration.
  • Lens of the eye - limited blood supply as lense needs to be kept clear.

This is because they are not able to undergo the citric acid cycle.

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2
Q

What is the normal plasma glucose concentration?

A

5 mmol is normal plasma glucose concentration.

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3
Q

What hormone keeps blood glucose conc low?

A

Insulin - it turns glucose into Glycogen.

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4
Q

What happens if glucose stays above the normal limits for a long period of time?

A

Diabetes. Type 1 - can’t bring glucose down. Glucose reacts with proteins in glycation.

This is a non-enzymatic reaction when a high conc. of glucose reacts with proteins. Glycated haemoglobin in a good marker of this.

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5
Q

What happens if plasma glucose is above 8 mmol?

A

This is above the real threshold so you get glucose in the urine

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6
Q

What happens as glucose concentration in the blood drops?

A
  1. 8 - confusion
  2. 7 - Weakness and nausea
  3. 1 - Muscle Cramps as not enough glucose
  4. 6 - Brain damage and death
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7
Q

How and where is glycogen stored?

A

Glycogen is stored as granules

Muscles - 300mg - local store of glucose for the use of that muscle. It cant be converted into plasma glucose.

Liver - 100mg - Can be used as store of glucose to replenish plasma conc.

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8
Q

What is the structure of glycogen?

A

Glycogen is a polymer consisting of glucose residues.

Chains are organised like the branches of a tree originating from a dimmer of the protein GLYCOGENIN (acts as a primer at the core of glycogen structure)

Glucose residues are linked by a1,4 glycosidic bonds with a1,6 glycosidic bonds forming branch points every 8-10 residues.

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9
Q

Why can’t we use cellulose for energy?

A

Because they contain B1,4 glycosidic bonds and we dont have enzymes to break this bond. (We can only break a1,4 glycosidic bonds).

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10
Q

Why is this Glycogen structure good?

A

Lots of ends so, lots of points of contact for the enzyme which allows rapid release of energy.

No osmotic potential so stops the flow of water.

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11
Q

What enzyme is needed to convert glucose to glucose-6-phosphate?

A

Hexokinase (Glucokinase in liver)

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12
Q

What is the enzyme phosphoglucomutase use for?

A

It turns glucose-6-phosphate into glucose-1-phosphate.

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13
Q

What is G1P uridyltransferase?

A

It is an enzyme thay converts Glucose-1-phosphate + UTP + water into UDP-glucose + PPi

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14
Q

What are the enzymes glycogen synthase and branching enzyme used for?

A
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15
Q

What is glycogenolysis?

A

Glycogen degradation

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16
Q

What are the key enzymes in glycogenolysis?

A

Glycogen phosphorylase or De-branching enzyme - These convert glycogen + Pi into glucose-1-phosphate and glycogen.

Phosphoglucomutase - This converts glucose-1-phosphate into glucose-6-phosphate which is then used by the muscles or liver.

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17
Q

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

A

Glucose-6-phosphate is converted to glucose by glucose-6-phosphatase and exported to the blood for use by other tissues. T

his can occur because it contains the enzyme glucose-6-phosphatase.

Liver glycogen is a buffer of blood glucose levels.

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18
Q

What happens to glucose-6-phosphate in the muscles?

A

Used by muscles (enters glycolysis) for energy production.

Muscle G6P cannot be exported into the blood because it lacks the enzyme glucose-6-phosphatase.

19
Q

Why can’t muscles change the blood glucose concentration?

A

They dont have glucose-6-phosphatase so, they cannot convert glucose-6-phosphate into glucose. This means G6P has to enter glycolysis.

20
Q

What is an overview of glycogen metabolism?

A
21
Q

How is liver glycogen metabolism regulated?

A

Insulin is the hormone of plenty - gets released after a meal.

Insulin - Increase glycogen synthase and decrease activity of glycogen phosphorylase

Glucagon / Adrenaline - Decrease glycogen synthase and increase glycogen phosphorylase

22
Q

What are the rate limiting enzymes for glycogen synthesis and for glycogen degridation?

A

Glycogen synthesis = Glycogen synthase

Glycogen degridation = Glycogen phosphorylase

23
Q

What is the difference between liver and muscles glycogen stores?

A

Muscles glycogen stores differ in that glucagon has no effect.

Also, AMP is an allosteric regulator of muscle glucogen phosphorylase but not of the liver form of the enzyme.

24
Q

What are glycogen storage disease? What can increase and decrease glycogen stores lead tp?

A
  • These are inborn errors of metabolism (inherited diseases).
  • They arise form deficiencies or dysfunction of enzymes of glycogen metabolism.
  • There are 12 distict types.
  • The incidence varies.
  • The severity depedns on the enzyme / tissue affected.

Liver and or muscles can be affected.

Excess glycogen storage can lead to tissue damage.

Diminished glycogen stores can lead to hypoglycaemia and poor exercise tolerance.

25
Q

What are some examples of glycogen storage diseases?

A

Von Gierke disease - glucose-6-phosphotase deficiency. This means that the liver cant convert glucose-6-phosphate into glucose. It results in heptomegaly because you can’t remove the glycogen stores.

McArdle disease - This is muscle glycogen phosphorylase deficiency. This results in intolerance to exercise as they can no loner metabolise glucose.

26
Q

When and where does gluconeogenesis occur?

A

After 8 hours of fasting because the liver glycogen sotres start to deplete.

It occurs in the Liver and Kidney cortex.

27
Q

What are the three major precursors of gluconeogenesis?

A

Lactate - From anaerobic glycolysis in exercising muscles and red blood cells. (Cori cycle)

Glycerol - Released from adipose tissue breakdown of triglycerides.

Amino acids - mainly alanine.

28
Q

What is the cori cycle?

A
29
Q

Why is there no new synthesis of glucose from acetyl-CoA?

A

Because pyruvate dehydrogenase is irreversible.

Also only 2 C in A-CoA

30
Q

What are the 3 key enzymes in gluconeogenesis?

A

Glucose-6-phosphatase

Fructose 1,6 bisphosphatase

Phosphoenolpyruvate carboxykinase (PEPCK)

PEPCK and F1,6BP are main regulatory enzymes

31
Q

What do the enzyme in gluconeogenesis respond to?

A

Starvation / Fasting

Prolonged exercise

Stress

32
Q

How is gluconeogenesis regulated?

A
33
Q

What is the time course for glucose utilisation?

A
34
Q

What are lipids stored as?

A

Triacylglycerols (TAG)

35
Q

Why is the fact that lipids are stored at TAGs good?

A

TAGs are hydrophobic and therefore is stored in an anhydrous form is specialised adipose tissue.

They are a highly efficient energy store and are under hormonal control.

36
Q

When are TAGs used?

A
  • Prolonged Exercise
  • Stress
  • Starvation
  • Pregnancy
37
Q

What are adipocytes

A
  • Adipocytes are large lipid droplets mainily composed of TAG and cholestrol ester. The cytoplasm adn organelles are pushed to the edge.
  • A typical adipocyte is about 0.1mm in diameter. The cells expand as more fat is added. The avg adult has 30billion fat cells weighing about 15kg.
  • They can increase in size about fourfold on weight gain before dividing and increasing in total number of fat cells.
  • They secrete Lactin (apatite suppressant) and store fat.
38
Q

How are triacylglycerols metabolised?

A
39
Q

What is lipogenesis and how where does it occur?

A

Lipogenesis is fatty acid synthesis.

It occurs in the liver and uses dietary glucose as a major source of carbon.

40
Q

How does lipogenesis occur (summary)?

A

Pyruvate enters mitochondria and forms acetyl-CoA and Oxaloacetate which then condense to form citrate.

Citrate goes into the cytoplasma and is cleaved back to acetyl-CoA and Oxaloacetate.

Acetyl-CoA carboxylase (a key regulator enzyme) then produces malonyl-CoA from Acetyl-CoA.

Fatty acid synthase complex builds fatty acids by sequential addition of 2 C units provided by malonyl-CoA.

41
Q

That is the key enzyme in regulating lipogenesis?

A

Acetyl-CoA carboxylate.

Insulin (covalent de-phosphorylation) and citrate (allosteric) will increase activity.

Glucagon / Adrenaline (covalent phosphorylation) and AMP (allosteric) decrease activity.

42
Q

What is the difference between fatty acid oxidation and fatty acid synthesis?

A
43
Q

How is fat mobilised?

A

Using Hormone sensitive lipase (HSL).

Glucagon and Adrenaline leads to phosphorylation and ACTIVATION is HSL

Insulin leads to de-phosphorylation and INHIBITS HSL.

HSL turns triacylglycerols into glycerols and free fatty acids.

Sem 2 - MEH (22 decks)

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