5 Energy Storage (glycogen and fat) Flashcards

1
Q

Tissues with absolute requirement for glucose

A

-RBCs - no mitochondria
-lens of eye
-neutrophils - located in areas of low O2
-innermost cells of kidney medulla - low O2 environment

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2
Q

Outline glycogen storage

A

Stored as granules
- muscles - 300mg only be used by muscles, no glucose 6 phosphate
-liver 100mg used to buffer plasma glucose

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3
Q

Glycogenesis definition

A

Synthesis of glycogen
Anabolic-reducing

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4
Q

Is glycogenesis reducing or oxidative?

A

Anabolic so reducing

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5
Q

Glycogenolysis definition

A

Breaking down glycogen to glucose

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6
Q

Two examples of glycogen storage disease

A

1- Von Gierke’s disease: glucose 6 phosphate deficiency
2- McArdle disease: muscle glycogen phosphorylase deficiency

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7
Q

Consequence of increased glycogen storage

A

Tissue damage

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8
Q

Consequence of decreased glycogen storage

A

Hypoglycaemia
Poor exercise tolerance

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9
Q

Gluconeogenesis definition

A

Production of new glucose from an originally non glucose source
After 8 hours of fasting

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10
Q

Where and when does gluconeogensis occur?

A

Mainly liver
Partially in kidney cortex

~ 8 hours of fasting

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11
Q

What are the non glucose sources in gluconeogensis?

A
  • amino acids: mainly alanine
  • glycerol: release from adipose tissue-breakdown of triglycerides
  • lactate: from anaerobic respiration
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12
Q

What is the cori cycle?

A

Lactate being used as a non glucose source in gluconeogensis

1- muscles used up glucose
2- lactate is produced in anaerobic respiration
3- lactate transported to liver in blood
4- glucose made in liver via gluconeogensis

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13
Q

3 key enzymes involved in gluconeogenesis

A

PEPCK
Fructose 1,6 phosphatase
Glucose 6 phosphatase

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14
Q

Which enzymes are regulated in gluconeogensis and how?

A

PEPCK and fructose 1,6 phosphatase

Stimulated by glucagon and adrenaline - glucose needed in times of starvation and stress

Inhibited by insulin - glucose not needed

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15
Q

When are lipids used as an energy source?

A

-prolonged exercise
-stress
-starvation
-during pregnancy

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16
Q

How are TAGs stored?

A

-hydrophobic
-stored in anhydrous form - no osmotic effect
-in adipose tissue

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17
Q

How can you identify adipose in a H&E stain?

A

-white fat broken down during fixation
-nucleus and cytoplasm pushed to side

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18
Q

Lipogenesis definition

A

Fatty acid synthesis

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19
Q

Where are fatty acids synthesised?

A

Liver

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20
Q

What is the regulator enzyme in lipogenesis?
Describe the regulation

A

-acetyl CoA carboxylase

  • inhibited by glucagon,adrenaline and AMP: acetyl CoA needed for respiration
  • stimulated by insulin+citrate
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21
Q

What does the fatty acid synthase complex do?

A

Additions of 2C units from malonyl CoA (from beta oxidation) to make fatty acids

22
Q

Lipolysis definition

A

Fat mobilisation

23
Q

How are fatty aids transported to muscle?

A

In the blood
Albumin complex

24
Q

Weight and energy content of TAG in healthy 70kg man

A

15kg
600,000kJ

25
Q

Weight and energy content of TAG in obses 135kg man

A

80kg
3,000,000kJ

26
Q

Glucose synthase function

A

Adds glucose molecules onto existing branches on glycogen making a1-4 glycosidic bonds

27
Q

Branching enzyme function

A

Creates new branches off of glycogen from the formation of a1-6 glycosidic bonds

28
Q

Hexokinase/glucokinase function

A

-kinase: adds a phosphate group
Glucose > glucose 6 phosphate
Glucokinase in liver

29
Q

Phosphoglucomutase function

A

Reversible reaction of G6P to G1P

30
Q

G1P uridyl transferase function

A

Transfers phosphate group on G1P to UDP
G1P > UDP glucose

31
Q

Glycogen phosphorylase function

A

Breaks a1-4 glycosidic bonds in the chains of glycogen

32
Q

De-branching enzyme

A

Breaks a1-6 glycosidic bonds on glycogen branches

33
Q

Why does insulin stimulate fatty acid production?

A

Lots of glucose > lots of glycolysis > lots of acetyl CoA > acetyl CoA made into malonyl CoA to make fatty acids

34
Q

Why can’t glycogen stored in muscles be used to raise blood sugar?

A

They don’t have glucose 6 phosphatase

35
Q

Signs and symptoms of baby with Von Gierke’s Disease

A
  • protuberant abdomen (looks like a potato) from heptaomegaly as glycogen is deposited in liver and not broken down fully
  • sweating and pallor from hypoglycaemia
  • high blood fatty acids from gluconeogensis to compensate for low blood glucose
36
Q

Normal blood glucose range

A

4-6 mmol/L

37
Q

What is the role of insulin on lipogenesis?

A

Stimulates fatty acids synthesis via dephosphylation of acetyl CoA carboxylase

38
Q

What is the renal threshold for glucose?

A

10mmol/L

39
Q

Describe the molecular structure of glycogen

A

a 1-4 glycosidic chain bonds
a 1-6 glycosidic branch bonds

40
Q

Outline the steps in glycogenesis

A

Glucose + ATP > glucose 6 phosphate + ATP
hexokinase/glucokinase

Glucose 6 phosphate > glucose 1 phosphate
phosphoglucomutase

Glucose 1 P + UTP + H2O > UDP-glucose + Pi
uridyl transferase

Glycogen (n residues) + UDP-glucose > glycogen (n+1 residues) + UDP
glycogen synthase / branching enzyme

41
Q

Outline glycogenolysis

A

Glycogen (n residues) + Pi > glycogen (n-1 residues) + glucose 1 P
*glycogen phosphorylase / debranching enzyme)

Glucose 1 P > glucose 6 P
phosphoglucomutase

Glucose 6 P > released into blood as glucose (liver)
> used for glycolysis (muscle)

42
Q

What is the rate limiting enzyme for glycogenolysis?

A

Glycogen phosphorylase

43
Q

What is the rate limiting enzyme in glycogenesis?

A

Glycogen synthase

44
Q

What effect does glucagon + adrenaline have on the rate limiting enzymes in glycogen metabolism?

A

Mechanism: phosphorylation

Decreases glycogen synthase
Increases glycogen phosphorylase

45
Q

What effect does insulin have on the rate limiting enzymes in glycogen metabolism?

A

Mechanism - dephosphorylation

Increases glycogen synthase
Decreases glycogen phosphorylase

46
Q

How do glycogen storage diseases occur?

A

Arise from deficiency or dysfunction of enzymes or glycogen metabolism

47
Q

Why can glucose not be made from acetyl CoA?

A

Acetyl CoA can’t be converted to pyruvate
PDH reaction is irreversible

48
Q

Outline lipogenesis

A

In liver
+oxaloacetate
Glucose > pyruvate > acetyl coA > citrate

Citrate > acetyl coA + oxaloacetate in cytoplasm

Acetyl coA > malonyl coA
acetyl coA carboxylase

Malonyl coA + 2C units > fatty acids
fatty acid synthase complex

49
Q

Outline lipolysis

A

Triacylglycerol > glycerol + fatty acids
hormone sensitive lipase

50
Q

What is the regulation of lipolysis

A

inhibited by insulin > phosphorylation
stimulated by glucagon + adrenaline > dephosphorylation