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Metabolism, Endocrinology, Haematology > Metabolism Session 1 > Flashcards

Metabolism Session 1 Flashcards

1
Q

Which tissues have an absolute requirement for glucose?

A
  • Red blood cells (no mitochondria
  • Neutrophils (respiratory burst)
  • Cells of kidney medulla (low blood supply)
  • Lens of eye (low blood supply)
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2
Q

What happens when glucose levels drop below 0.6 mmol/L?

A
  • GLUT1 can no longer transport glucose into brain

= Brain damage and death occur

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3
Q

When can hypoglycaemia occur?

A
  • Diabetes

- Acute alcohol poisoning

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4
Q

How is glycogen stored in muscles?*

A
  • Granules
  • 300g
  • Between intra and intermyofibrils (in myofibrils/between myofibrils)
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5
Q

How is glycogen stored in the liver?*

A
  • 100g

- Stored as granules in hepatocyte

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6
Q

What is the structure of glycogen?*

A
  • Polymer of chains of glucose residues
  • Organised like branches
  • Originate from a dimer of glycogenin protein
  • Tightly packed
  • Not osmotically active
  • Branches allow quick release of glucose
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7
Q

What is the difference between alpha-1-6 and alpha-1-4 glycosidic bonds?*

A
  • Alpha-1-4 glycosidic bonds join the glucose residues to form chains
  • Alpha-1-6 glycosidic bonds form branch points between 8-10 residues
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8
Q

What are the steps of glycogenesis?*

A
  • Glucose + ATP = glucose-6-phosphate + ADP
    (catalysed by hexokinase)
  • Glucose-6-phosphate = glucose-1-phosphate
    (catalysed by phosphoglucomutase)
  • Glucose-1-phosphate + UTP + H2O = UDP-glucose + PPi
    (catalysed by G1P uridylyltransferase)
  • Glycogen residues (n) + UDP-glucose = Glycogen (n+1) = UDP
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9
Q

What enzymes catalyse the last step of glycogenesis?

A
  • Glycogen synthase (alpha-1-4, elongation)

- Branching enzyme (alpha-1-6, branching)

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10
Q

What is glycogenolysis?

A

Glycogen degeneraton

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11
Q

What are the steps of glycogenolysis?

A

Glycogen residues (n) + Pi = Glucose-1-phosphate + glycogen (n-1)

Glucose-1-phosphate = glucose-6-phosphate
(catalysed by phosphoglucomutase)

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12
Q

What enzymes are involved in the first step of glycogenolysis?

A
  • Glycogen phosphorylase (1-4)

- Debranching enzyme (1-6)

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13
Q

What is the function of glycogen stores in the liver?*

A
  • Glucose released into blood for use by other tissues

- Buffers plasma glucose levels

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14
Q

What is the function of glycogen stores in the muscle?*

A
  • Lacks enzyme to buffer plasma glucose (GLUCOSE-6-PHOSPHATASE)
  • Used by muscle for energy production
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15
Q

Describe glycogen metabolism.*

A

Slide 9.

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16
Q

What enzymes regulate glycogen synthesis and degradation?

A
  • Glycogen synthase

- Glycogen phosphorylase

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17
Q

How do glucagon and adrenaline act on the 2 enzymes?

A
  • Phosphorylate them
  • Decrease activity of synthase
  • Increase activity of phosphorylase
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18
Q

How does insulin act on the 2 enzymes?

A
  • Dephosphorylation
  • Increase activity of synthase
  • Decrease activity of phosphorylase
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19
Q

How does AMP act on muscle?

A

It’s an allosteric activator of muscle glycogen phosphorylase (not of liver form)

Low energy states mobilise glycogen release.

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20
Q

What are glycogen storage diseases?

A
  • Inborn metabolism errors
  • Deficiency/dysfunction of enzymes of metabolism
  • Can affect liver and/or muscle
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21
Q

What can excess glycogen stores cause?

A

Tissue damage

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22
Q

What can diminished glycogen stores cause?

A
  • Hypoglycaemia

- Poor exercise tolerance

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23
Q

What is von Gierke’s disease?

A

Glucose-6-phosphatase deficiency that can cause hypoglycaemia.

24
Q

What is McArdle disease?

A

Muscle glycogen phosphorylase deficiency.

25
Q

What is gluconeogenesis?

A

Production of new glucose

26
Q

When and where does gluconeogenesis occur?

A
  • Beyond 8 hours of fasting as liver glycogen stores deplete
  • Mostly liver, slightly in kidney
27
Q

What are the 3 major precursors to gluconeogenesis?

A

LACTATE: from anaerobic glycolysis

GLYCEROL: from adipose tissue and triglyceride breakdown

AMINO ACIDS: alanine

28
Q

What is the Cori cycle?*

A
  • Glucose is metabolized to pyruvate and then to lactate in muscle
  • Lactate is released into the blood and carried to the liver
  • Reconverted to pyruvate and used for gluconeogenesis,
  • Glucose is released into blood and travels back to muscle.
29
Q

Why can’t acetyl-CoA or ethanol be converted into pyruvate?

A

There are 2 carbon atoms (CO2) lost per TCA cycle, and both compounds only have 2 carbons which would result in no net synthesis of glucose.

30
Q

What are the three key enzymes in gluconeogenesis?*

A
  • Glucose-6-phosphatase
  • Fructose-1,6-bisphosphatase
  • Phosphoenolpyruvate carboxykinase (PEPCK)
31
Q

What reaction does glucose-6-phosphatase catalyse?

A

Glucose to glucose 6-phosphate

32
Q

What reaction does fructose 1,6-bisphosphatase catalyse?

A

Fructose 6-phosphate to fructose 1,6-bisphosphate

33
Q

What reaction does PEPCK catalyse?

A

Oxaloacetate to phosphoenolpyruvate.

34
Q

Why are the three enzymes not simple reversals of corresponding glycolysis steps?

A

The three steps in glycolysis are IRREVERSIBLE and therefore need different enzymes.

35
Q

Which 2 enzymes are regulated by starvation, prolonged exercise and stress?

A
  • Fructose 1,6-bisphosphatase

- Phosphoenolpyruvate carboxykinase

36
Q

What effects do glucagon and cortisol have on PEPCK and fructose 1,6-bisphosphatase?

A
  • Increased amounts

- Stimulation of gluconeogenesis

37
Q

What effects does insulin have on PEPCK and fructose 1,6-bisphosphatase?

A
  • Decreased amounts

- Inhibition of gluconeogenesis as glucose is getting stored

38
Q

What is the time course of glucose utilisation?

A
  • Feeding: glucose from food used for 2 hours
  • Glycogenolysis for up to 8-10 hours
  • Gluconeogenesis happens from 10 hours onwards
39
Q

How does lipid storage occur?*

A

Glycerol + 3 fatty acids = triacylglycerol + H2O

esterification to make, lipolysis to break

40
Q

How are TAGs stored and why?

A

TAGs are hydrophobic.

  • Stored in an anhydrous form
  • In ADIPOSE TISSUE
41
Q

How is storage and mobilisation of TAGs controlled?

A

Hormones

42
Q

When are TAG stores used?

A
  • Prolonged exercise
  • Stress
  • Starvation
  • Pregnancy
43
Q

What are adipocytes?*

A
  • ‘White adipose tissue’
  • Mainly TAGs and cholesterols esters in one large lipid droplet
  • Cytoplasm and organelles pushed to edges
  • Increase fourfold in size on weight gain before dividing.
44
Q

How are dietary triacylglycerols mobilised?*

A
  • Broken down in small intestine into fatty acids and glycerol by pancreatic lipase
  • Reform in intestinal epithelial cells into TAGs and are packaged into chylomicrons
  • Chylomicrons drain into lymph from thoracic duct to the left subclavian vein into blood
  • Stored in adipose
  • Controlled by hormone sensitive lipase
  • Mobilised as a FA-albumin complex
  • Into tissues for energy
45
Q

How does hormone sensitive lipase work?

A
  • Releases TAGs with high glucagon and adrenaline

- Inhibits TAG release with insulin

46
Q

Why can’t the brain use fatty acids for energy?

A

They do not cross the blood brain barrier easily.

47
Q

Where does lipogenesis occur?

A

Liver

48
Q

Describe the process of fatty acid synthesis **

DIAGRAM PAGE 20 PLEASE!!

A
  • Glycolysis in cytoplasm
  • Pyruvate combines with Acetyl CoA + OAA = citrate (mitochondria)
  • Citrate cleaved back into Acetyl-CoA + OAA in cytoplasm
  • Acetyl-CoA carboxylase produces malonyl-CoA from Acetyl-CoA
  • Fatty acid synthase complex builds fatty acids by sequential addition of 2 carbon units provided by malonyl-CoA
49
Q

What does lipogenesis require?

A
  • ATP

- NADPH

50
Q

What activates Acetyl-CoA carboxylase?

A

Insulin and citrate

51
Q

What inhibits Acetyl-CoA carboxylase?

A

Glucagon, adrenaline and AMP

52
Q

What are the features of fatty acid oxidation?

A
  • Remove C2
  • Removed as Acetyl-CoA
  • Mitochondria
  • Oxidative (NADH + FAD2H made)
  • Inhibited by insulin
  • Stimulated by glucagon and adrenaline
53
Q

What are the features of fatty acid synthesis?

A
  • Adding C2
  • Added as malonyl-CoA
  • Cytoplasm
  • Reductive (uses ATP and NADPH)
  • Inhibited by glucagon/adrenaline
  • Stimulated by insulin
54
Q

How does fat mobilisation occur?*

A
  • Hormone sensitive lipase is activated and phosphorylated by glucagon and adrenaline
  • Released into the blood where it splits into glycerol and FA
55
Q

Where does glycerol travel?

A

To the liver to be used as a carbon source for gluconeogenesis

56
Q

Where do fatty acids travel?

A

FA-Albumin complex in blood to muscles and other tissues, where beta oxidation will occur.

57
Q

How much fat is in an average 70kg man?

A

15kg of triacylglycerol which is 600,000kJ

Metabolism, Endocrinology, Haematology (16 decks)

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