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MEH > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

What is the typical range of glucose plasma conc?

A 
5 millimolar
(This is elevated in diabetes- random glycosylation of proteins)
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2
Q

What cells can only use glucose as their fuel?

A
  • RBC’s (no mitochondria- rely on glycolysis)
  • neutrophils (mitochondria used to create reactive oxidative species rather than in metabolism) (respiratory burst)
  • innermost cells of the kidney medulla (blood supply is low, not enough oxygen for oxidative phosphorylation)
  • lens of eye (not good blood supply)
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3
Q

Are maintained levels of plasma glucose important?

A

Yes, stable glucose level is essential for normal brain function.
If plasma glucose concentration falls you can get

HYPOGLYCAEMIA (diabetic patient who has taken injection of insulin but not eaten, acute alcohol poisoning, athlete pushing themselves beyond normal limit)

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4
Q

At what glucose concentration do you see the effects of hypoglycaemia?

A 
3 millimolar
-confusion
-weakness
-nausea
-muscle cramps
-brain damage 
-death
(As the concentration gets lower)
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5
Q

Why does hypoglycaemia effect the blood brain barrier?

A

Once the plasma glucose concentration drops below 0.6 millimolar the Glut1 transporter can no longer work due to it’s Km, no longer transport glucose into the brain.

Ketone bodies can be used as an energy source in the brain-but takes time, and only generates 50% of energy

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6
Q

Why do we need to store glucose?

A

We don’t eat all the time. In-between meals we need a store of glucose we can draw upon to maintain the plasma concentration.

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7
Q

How is glucose stored?

A

As glycogen stored as granules. (Appear dark on microscope)
Main stores: muscle (300g) & liver (100g)

In muscles there is intermyofibrillar glycogen (inbetween fibres) and intramyofibrilar glycogen (within fibre itself)

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8
Q

What is the structure of glycogen?

A

GLYCOGENIN (protein) acts as a primer: branches originate from here

  • branch like structure
  • chains of glucose joined by 1-4 glycosidic bonds
  • every 8-10 residues you have a branch by 1-6 glycosidic bonds
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9
Q

Why is glycogen branched?

A
  • Enzymes can react at multiple sites to release glucose.
  • tightly packed
  • glucose as monomers would have a large osmotic effect on the cell drawing lots of water, now in one molecule it doesn’t have the same osmotic effect
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10
Q

What is glycogenesis?

A

Synthesis of glycogen.

  1. Glucose to glucose-6-P, using ATP->ADP and hexokinase (glucokinase in liver)
  2. G-6-P converted to Glucose-1-P by phosphoglucomutase
  3. G-1-P converted to UDP-glucose and Pi: using UTP, G1P uridylyltransferase and water (energy requiring)
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11
Q

What is the importance of UDP-glucose?

A

It is added to glycogen polymer.
The UDP is released after binding

Glycogen(n residues) + UDP glucose > glycogen(n+1 residues) + UDP
Catalysed by:
-glycogen synthase (1/4 glycosidic bonds)
-branching enzyme (1/6 glycosidic bonds)

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12
Q

What is glycogenolysis?

A

Glycogen degradation.

  • glycogen phosphorylase
  • de-branching enzyme

Glycogen(n residues) + Pi > G-1-P + glycogen(n-1 residues)

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13
Q

How is G-1-P converted back to G-6-P?

A

Phosphoglucomutase.

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14
Q

What glycogen store is used to maintain plasma glucose levels?

A

Liver glycogen store. Glucose released into blood for use by other tissues.

In muscle, the glycogen is used for muscle contraction.

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15
Q

Why can’t glycogen in the muscle regulate plasma glucose concentrations?

A

It lacks the enzyme that converts G-6-P to glucose. (Glucose-6-phosphatase, which is present in liver)

G-6-P enters glycolysis for energy production.

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16
Q

What is the rate limiting enzyme in glycogen synthesis (glycogenesis), and how are they controlled?

A

Glycogen synthase.

Glucagon/adrenaline:
-phosphorylation (decrease in enzyme activity)
Insulin:
-de-phosphorylation (increase in enzyme activity)

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17
Q

What is the rate limiting enzyme in glycogen degradation? (Glycogenolysis)

A

Glycogen phosphorylase.

Glucagon/adrenaline:
-phosphorylation (increase enzyme activity)
Insulin:
-de-phosphorylation (decrease enzyme activity)

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18
Q

What does insulin promote/inhibit?

A

Promotes glycogen synthesis

Inhibits glycogen degredation

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19
Q

What does glucagon/adrenaline inhibit/promote?

A

Inhibits glycogen synthesis

Promotes glycogen degradation

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20
Q

What does glucagon have similar effects as?

A

Adrenaline.

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21
Q

Why does glucagon have no effect on muscles?

A

They don’t have glucagon receptors on their surface.

-therefore glucagon doesn’t effect the glycogen stores in the muscle

22
Q

What does AMP do in regulation of glycogen?

A

It is an allosteric activator of MUSCLE glycogen phosphorylase.
(Low energy in muscle, means low AMP, so AMP is a signal to enable muscle to release more glucose from glycogen stores)

23
Q

Name some glycogen storage diseases:

A

Von-Gierke’s disease: deficiency in G-6-Phosphatase (can’t release stores into plasma from liver)

McArdle Disease: muscle glycogen phosphorylase deficiency.

24
Q

What is gluconeogenesis and where does it occur?

A

The production of new glucose.

It occurs in the liver mainly, and less in the kidney cortex

25
Q

Why do we need to use gluconeogenesis when we have glycogenolysis?

A

Glycogen stores in liver last around 8 hours only.

-an alternative source of glucose is required and is made vis gluconeogenesis

26
Q

What are the three precursors from which we make glucose in gluconeogenesis?

A 
Lactate (produced from anaerobic glycolysis in exercising muscles and RBC’s)
Glycerol (from breakdown on triglycerides)
Amino acids (ALANINE)

(All have 2+ carbons)

27
Q

What cycle is lactate part of?

A

The Cori Cycle.

  • glucose converted to lactate in muscle
  • lactate enters blood and travels to the liver
  • liver, via gluconeogenesis, can convert lactate back to glucose
  • glucose travels in blood back to the muscle
28
Q

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

A

-also the pyruvate dehydrogenase reaction (pyruvate to acetyl-CoA) is irreversible so acetyl-CoA can’t be converted back to pyruvate, and therefore can’t be converted to glucose.

29
Q

What are the key enzymes in gluconeogenesis?

A

It is basically the reverse of glycolysis, however some steps are irreversible, so it is slightly different.

  1. PEPCK (phosphoenolpyruvate carboxykinase)
  2. Fructose 1,6-bisphosphate
  3. Glucose-6-phosphatase
30
Q

How does gluconeogenesis work? Only need to know key enzyme steps

A
  1. Glucogenic AA’s converted to pyruvate
  2. Pyruvate is converted to oxaloacetate
  3. Oxaloacetate converted to phosphoenolpyruvate
    PEPCK regulates oxaloacetate to phosphoenolpyruvate
  4. Fructose 1,6-bisphosphatase converts Fructose 1,6-bisphosphate to fructose 6-phosphate. (Usually phosphfructokinase in glycolysis but it is irreversible so requires a different enzyme)
  5. Glucose-6-phosphatase converts Glucose-6-phosphate to Glucose (opposite of hexokinase irreversible step of glycolysis)
31
Q

What are the 2 key regulator enzymes in gluconeogenesis?

A

PEPCK
Fructose 1,6-bisphosphatase

Regulated in response to stress, starvation, prolonged exercise

32
Q

What hormones regulate gluconeogenesis?

A

Glucagon/cortisol: stimulates
-increased amounts of PEPCK & Fructose 1,6-bisphosphatase

Insulin: inhibits
-decreases amounts of PEPCK & Fructose 1,6-bisphosphatase

33
Q

What is the time course for glucose utilisation?

A

Glucose from food: ~2hours
Glycogenolysis: ~8-10hours (glycogen stores)
Gluconeogenesis: ~8-10+ hours (lactate/glycerol/AA’s)

34
Q

How is triacylglycerol made/degraded?

A

Esterification (making)

Lipolysis (degrade)

35
Q

What is a triacylglyeride?

A

A glycerol molecule attached to 3 fatty acid chains

36
Q

Where are TAG’s stored?

A

In adipose tissue (they are hydrophobic so stored in anhydrous form), in ADIPOCYTES.

37
Q

Do TAG’s contain energy and when are the used/made?

A

Yes, they are the most energy dense molecule.
Energy content is twice that of carbohydrate/protein

  • Made when energy intake is in excess so it is converted to TAG for storage
  • used in prolonged exercise, stress, starvation, pregnancy
38
Q

What are adipocytes?

A
  • most of cytoplasm is TAG’s (cytoplasm and organelles pushed to the edge)
  • can expand 4x its size, and then it splits into 2 adipocytes
  • large lipid droplet
39
Q

What weight of adipocytes do we have in our body?

A

15kg
(Adipocyte regeneration is limitless. If obese person loses weight they still contain empty adipocytes, so it is easier for them to put the weight back on again)

40
Q

How is TAG metabolised?

A
  • TAG in small intestine
  • TAG > fatty acids + glycerol (via pancreatic lipase)
  • absorbed into epithelial cells
  • epithelial cells turn it back into TAG, and incorporate it into a lipoprotein particle: chylomicron
  • chylomicrons drain into lacteals and lymphatic system
  • they enter the blood once lymph system drains into circulatory system (at thoracic duct-into left subclavian vein)
  • travel to adipose tissue for storage/utilised by tissues for energy
41
Q

Where does TAG first enter our blood?

A

Left subclavian vein

42
Q

How does adipose convert back to TAG’s?

A

Hormone sensitive lipase
+ increased by glucagon/adrenaline
- decreased by insulin

43
Q

How are fatty acids synthesised and where? (lipogenesis)

A

In LIVER in the cytoplasm

  • glucose is prime substrate
  • glucose enters glycolysis in liver and is converted to pyruvate
  • want to get carbons out of pyruvate to add to the fatty acid tail
  • pyruvate enters mitochondria and TCA, and is converted to acetyl-CoA by pyruvate dehydrogenase. (Lose carbon via CO2)
  • acetyl-CoA combines with oxaloacetate to form citrate (c6)
  • citrate exported out to cytoplasm and converted back to oxaloacetate and acetyl-CoA
  • oxaloacetate is converted back to pyruvate and this generates production of NADPH
  • acetyl-CoA is converted to MALONYL CoA by acetyl-CoA carboxylase, using ATP
  • malonyl-CoA added to fatty acid tail, lose CO2 to make it 2 carbon
  • fatty acid synthase complex adds on the 2 carbons to the chain
  • fatty acids combine with glycerol 3-P made in glycolysis in liver cell to form TAG
44
Q

What are the key enzyme regulators of lipogenesis?

A

Acetyl-coA carboxylase

Fatty acid synthase complex (many enzymes in this)

45
Q

How do the fatty acid tails grow?

A

By adding 2 carbon units at a time, derived from acetyl-coA

46
Q

Why can’t the acetyl-CoA produced by pyruvate dehydrogenase be used for fatty acid synthesis?

A

Because the mitochondria don’t contain transporters for acetyl-CoA in their membrane.

47
Q

Why is the production of NADPH in lipogenesis important?

A

Because the fatty acid synthase complex in the cytoplasm requires NADPH
-the NADPH also comes from the pentose phosphate pathway

48
Q

How do TAG’s get transported out of the liver?

A

Via VLDL’s (very low density lipoprotein)

49
Q

What hormones regulate lipogenesis? Via Acetyl-CoA carboxylase

A

Insulin/citrate: increase activity

Glucagon/adrenaline/AMP: decrease activity

50
Q

What is lipolysis?

A

Fat mobilisation.
-hormone sensitive lipase
From adipose tissue (triacylglycerol) into blood (glycerol+fatty acids)

51
Q

Where do the glycerol/fatty acids go after lipolysis?

A

Glycerol: goes to liver as a source of gluconeogenesis

Fatty acids: used for energy production by beta oxidation. Travels bound to albumin to muscles and tissues

52
Q

How much adipose tissue can you have in an obese man?

A

80kg.

Difference in weight of people is due to the amounts of triacylglycerol ONLY. Not due to muscle or protein etc.

MEH (22 decks)

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