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Semester 2 MEH > L3: Energy Storage Glycogen and Fat > Flashcards

L3: Energy Storage Glycogen and Fat Flashcards

1
Q

What is the normal plasma level of glucose?

A

5mM elevates after meal

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2
Q

What tissues have an absolute requirement for glucose?

A

RBC (few mitochondrial ↑SA for heamoglobin and O2)
Neutrophils (mitochondrial burst> metabolism)
Lens of the eye (poor blood supply- no OP)
Innermost cells of the kidney medulla

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3
Q

What is special about the brain and glucose?

A

Can use ketone bodies–> time to adapt + only 50% energy requirement
GLUT1 transport Km=0.6mM, plasma < doesn’t use glucose

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4
Q

What happens to excess glucose?

A

Stored as glycogen

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5
Q

Where does glycogen get stored?

A

Stored as granules in:
Skeletal muscle–> inter- between cells, intra- within cells
Liver–> hepatocytes

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6
Q

What is the structure of glycogen?

A

Polymer
Branched every 8-10 residues–> originates from dimer glycogenin
alpha 1-4 glycosidic bonds in chain
alpha 1-6 glycosidic bond to branches

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7
Q

Why is it stored as a branched molecule?

A

Branches–> more sites for synthesis or degradation
Easier to release glucose
Reduced osmotic effect –> less water

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8
Q

Name the process of glycogen synthesis?

A

Glycogenesis

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9
Q

Name the main enzymes involved in glycogenesis?

A
  1. Hexokinase (glucokinase in liver)
  2. Phosphoglucomutase
  3. G1P uridyltransferase
  4. Glycogen synthase or branching enzyme
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10
Q

What is each step of glycogenesis?

A

Step 1. Glucose + ATP –> Glucose-6-phosphate and ADP (requires hexokinase)
Step 2. Glucose-6-phosphate < –>Glucose-1-phosphate (phosphoglucomutase)
Step 3. Glucose-1-phosphate + UTP + H20 –> UDP-glucose + PPi (G1P Uridyltransferase) UTP=ATP
Step 4. Glycogen(n) + UDP-glucose –> Glycogen (n+1) + UDP (glycogen synthase alpha1-4 glycosidic bond or branching enzyme alpha1-6 glycosidic bond)

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11
Q

How many ATPs are required for glycogenesis?

A

2 ATP (1ATP and 1UTP)

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12
Q

What is glycogen breakdown called?

A

Glycogenolysis

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13
Q

What are the enzymes involved in glycogenolysis?

A

Glycogen phosphorylase or de-branching enzyme

Phosphoglutamutase

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14
Q

What is the common process of glycogenolysis in muscle and liver?

A

Glycogen(n) + Pi–> Glucose-1-phosphate + Glycogen(n-1) (glycogen phosphorylase or de-branching enzyme)
Glucose-1-phosphate –> glucose-6-phosphate (phosphoglucomutase)

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15
Q

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

A

Muslce –> lacks glucose-6-phosphatase–> GP6 enter glycolysis
Liver–> converted to glucose by glucose-6-phosphatase–> released into blood –> buffer of blood glucose

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16
Q

How is glycogen metabolism regulated in liver?

A

Hormonal control
Rate limiting enzymes= glycogen synthase and glycogen phosphorylase
Insulin and glucagon/adrenaline

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17
Q

How is glycogen metabolism regulated in the muscles? What is another allosteric activator?

A

Hormonal control
Rate limiting enzymes- glycogen synthase and glycogen phosphorylase
Insulin and adrenline –> no glucagon receptor
AMP allosteric activator of Glycogen phosphorylase

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18
Q

How does insulin and glucagon/adrenaline affect the rate limiting enzymes?

A

↑ Insulin and ↓ glucagon/adrenaline = ↑ glycogen synthase

↓ Insulin and ↑ glucagon/adrenaline = ↓glycogen phosphorylase

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19
Q

What are glycogen storage diseases?

A

Inherited
Dysfunctional or deficiency of enzymes of metabolism
12 distinct types
Severity–> varies–> depends on enzyme/tissue affected

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20
Q

What are the results of glycogen storage disease?

A

Liver +/or muscle affected
Excess –> tissue damage
Diminished –> hypoglycemia + poor exercise tolerance

21
Q

Give two examples of disease caused by excess storage and name the dysfunctional enzyme involved?

A

Von Gierke’s disease –> glucose-6-phosphase deficiency

McArdles disease –> glycogen phosphorylase deficiency (muscle)

22
Q

What is the production of new glucose called?

A

Gluconeogenesis

23
Q

Why do we need gluconeogenesis?

A

> 8hrs fasting –> ↓ glycogen stores –> alternative source

24
Q

Where does gluconeogenesis occur?

A

Majority –> liver

Minor –> kidney cortext

25
Q

What are the precursors for gluconeogenesis?

A

Lactate–> anaerobic glycolysis (muscle and RBC)- Cori cycle
Glycerol –> released from adipose tissue from TAG
Amino acids –> mainly alanine

26
Q

What is the Cori cycle?

A

Muscle –> glucose converted to 2x lactate –> blood–> liver (gluconeogenesis) –> glucose –> muscle
cyclic process

27
Q

Why can acetyl CoA not be used as a substrate for glucose synthesis?

A 
Acetyl CoA (2C) --> not converted to pyruvate--> pyruvate dehydrogenase reaction irreversible 
No net synthesis of glucose from Acetyl CoA as 2 xCO2 lost
28
Q

What are the key enzymes involved in gluconeogenesis?

A
  1. Phosphoenolpyruvate carboxykinase (PEPCK): pyruvate–> oxaloacetate –> phosphoenolpyruvate (PEPCK converts occeloacetate)
  2. Fructose 1,6- bisphosphatase: fructose 1,6-bisphophate –> fructose 6-phosphate
  3. Glucose 6-phosphatase: glucose 6-phosphate –> glucose

not simply the reversal of glycolysis as irreversible steps in glycolysis

29
Q

How is gluconeogenesis regulated?

A

Hormonal control; Insulin and glucagon/cortisol

key enzymes: PEPCK (phosphoryenolpyruvate carboxykinase) + Fructose 1,6-bisphosphate

30
Q

What affect does insulin and glucagon/cortisol have on gluconeogenesis?

A

Insulin –> inhibits–> ↓ PEPCK + fructose 1,6-bisphosphate

Glucagon/cortisol–> stimulates–> ↑ PEPCK + fructose 1,6-bisphosphate

31
Q

How long after eating does glycogenolysis and gluconeogenesis occur?

A

Glucose- 2 hours
Glycogenolysis >2 hours <8 hours
Gluconeogenesis >8 hours

32
Q

How is excess energy stored?

A

Converted to triacylglycerol for storage

33
Q

Where are triacylglycerides stored and how?

A

Adipose tissue
Hydrophobic –> stored anhydrous form
Highly efficient energy store
Energy content x2 of carbs/protein

34
Q

When are TAG utilised?

A

Prolonged exercise, stress, starvation and during pregnancy

35
Q

What controls the storage and utilisation of TAG?

A

Hormones

36
Q

What are the adipocytes? What are some of the characterisitcs?

A 
Fat storage cells
Large lipid droplet
Organelle at edge 
0.1mm diameter
30 billion--> 15kg
37
Q

How do adipocytes increase in number?

A

Expand –> Fourfold –>Divide

38
Q

How do fats get from your food into the adipocytes?

A

SI–> pancreatic lipase –> fatty acids and glycerol
Intestinal epithelial cell–> TAG reformed –>chylomicrons
Lymphatic system –> thoracic duct–> left subclavian vein –> blood
Stroage –> Adipose tissue

39
Q

How do we mobilise TAG for use?

A

Hormone sensitive lipase –> mobilise TAG
Regulated by insulin and glucagon/adrenaline
Broken down into FA and glycerol
Transported FA-albumin to tissue
Tissue –> fatty acid oxidation
Glycerol –> gluconeogenesis

40
Q

Which cells cannot use FA for energy?

A

Cells without mitochondria

Brain –> cannot pass BBB

41
Q

Where does fatty acid synthesis occur?

A

Liver

42
Q

What is lipogenesis?

A

Synthesis of fatty acids from acteyl CoA

43
Q

What is the process of lipogeneis?

A

Pyruvate (glycolysis of glucose)–> Acetyl CoA by pyruvate dehydrogenase (in mitochondria)
Combines with oxaloacetate –> citrate (in mitochondria)
In cytoplasm cleaved release Acetyl CoA and oxaloacetate
Acetyl CoA –> malonyl CoA by acetyl CoA carboxylase
Oxaloacetate –> malate –> pyruvate + NADPH (malic enzyme)
Malonyl CoA and NADPH –> fatty acid synthesis complex–> FA

44
Q

Why does pyruvate get converted to Acetyl Co-A to citrate and then broken back down again?

A

Pyruvate conversion to Acetyl CoA can only occur in the mitochondria
No transporters for Acetyl CoA–> converted to Citrate–> into cytoplasm–> broken down

45
Q

What are the key regulators of lipogenesis?

A

Acetyl CoA carboxylase (produces malonyl CoA from Acetyl CoA which is need for the fatty acid synthase complex)
Hormonal control
Insulin (dephosphorylates) and citrate (allosteric) –> ↑activity
Glucagon/ adrenaline (phosphorylation) and AMP (allosteric) –> ↓activity

46
Q

How does the fatty acid synthase complex work?

A

Addition of 2C provided by malonyl-CoA (produce CO2)

NADPH is required

47
Q

What happens to fatty acids once they have been synthesised?

A

Esterification to TAG with glycerol 3-phosphate

Transported by VLDL to tissue

48
Q

Compare and contrast fatty acid synthesis and oxidation (beta oxidation)?

A

Synthesis followed by oxidation

  • -> add 2C from malonyl CoA / removes 2C as acetyl CoA
  • -> Consumes acetyl CoA/ produces acetyl CoA
  • -> cytoplasm / mitochondria
  • -> multienzyme complex / separate enzymes
  • -> reductive (NADPH required) / oxidative (NADH and FADH2 produced)
  • -> Require ATP / Small amount ATP required
  • -> intermediate linked to FA synthase by carrier protein / intermediates linked to CoA
  • -> Regulated directly –> acetyl CoA carboxylase / Indirectly via avaliability of FA
  • -> Glucagon and adrenaline inhibit/ Stimulate
  • -> insulin stimulates / Inhibits
49
Q

What is the benefit of synthesis and oxidation occurring by different pathways?

A

Greater flexibility –> substrates and intermediates different
Better control –> independently or coordinately
Themodynamically irreversible steps bypassed

Semester 2 MEH (23 decks)

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