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Yr 2 - GI & Metabolism > Carbohydrate Metabolism > Flashcards

Carbohydrate Metabolism Flashcards

1
Q

What are examples of simple sugars/monosaccharides?

A

Glucose, fructose

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2
Q

What are examples of complex sugars/polysaccharides?

A

Starch, glycogen, cellulose

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3
Q

Where does carbohydrate metabolism begin?

A

Salivary amylase in the mouth

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4
Q

After monosaccharides are transported across the wall of the SI and into the circulatory system, where do they pass?

A

To the liver

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5
Q

What occurs in the liver to monosaccharides?

A

Hepatocytes either pass the glucose on through the circulatory system or store excess glucose as glycogen

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6
Q

What polysaccharide does glucose come from?

A

Starch, glycogen

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7
Q

What polysaccharide does fructose come from?

A

Sucrose

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8
Q

What polysaccharide does galactose come from?

A

Lactose

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9
Q

What are the possible fates of glucose?

A
  • Metabolism to produce energy (ATP) - Conversion to glycogen for storage - Synthesis of other cellular components - Conversion to fat for storage
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10
Q

Where can glucose be stored as glycogen?

A

Liver or muscle

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11
Q

What happens if glucose level is too low/high?

A
  • Below 3mM = confusion, coma - Above 8mM = long term vascular damage occurs through protein glycation
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12
Q

In the presence of oxygen, what happens to pyruvate made during glycolysis?

A

The pyruvate molecules are transported across the mitochondrial membrane into the inner mitochondrial matrix Pyruvate –> acetyl CoA

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13
Q

In the Krebs cycle, what is pyruvate converted into?

A

Acetyl CoA (coenzyme)

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14
Q

What is produced at the end of glycolysis from one glucose molecule?

A

2 pyruvate molecules, 4 ATP molecules and 2 electron-carrying NADH molecules

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15
Q

What is the fate of pyruvate molecules produced?

A
  • Processed further through aerobic Krebs cycle - Converted into lactic acid or alcohol (yeast) - Used later for synthesis of glucose through gluconeogenesis
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16
Q

What is produced as a waste product of the Krebs cycle?

A

CO2

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17
Q

What does the Krebs cycle produce?

A

Reduced co-enzymes (NADH) which donate electrons to electron transport chain (ETC)

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18
Q

Where does NADH carry electrons to?

A

Inner mitochondrial membrane and transfer them ETC

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19
Q

As the electrons move down the ETC, what happens to the energy they contain?

A

Transferred into the proteins of the ETC and used to pump H+ ions across the membrane (to outside)

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20
Q

What does this H+ pump create?

A

An H+ gradient that is used for ATP synthesis

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21
Q

Where does glycolysis take place?

A

In cytosol of all cells (can generate ATP in presence or absence of O2)

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22
Q

What are the 2 phases of glycolysis?

A
  1. Preparative phase 2. Generating phase
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23
Q

Describe the preparative phase of glycolysis

A

Glucose to fructose 1,6 bisphosphate (requires ATP0

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24
Q

Describe the generating phase of glycolysis

A

Fructose 1,6 bisphosphate to (2) pyruvate – generates ATP and NADH (later converted into ATP under aerobic conditions)

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25
Q

Overall reaction equation for glycolysis?

A

Glucose + 2 ADP + 2 Pi + 2ATP + 2NAD+ –> 2 pyruvate + 2NADH + 4ATP + 2H+ + 2H2O

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26
Q

Under aerobic conditions, what is NADH used to generate?

A

Further 3-5 ATP molecules via oxidative phosphorylation

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27
Q

How many molecules of ATP/glucose does aerobic glycolysis generate?

A

5-7

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28
Q

How many molecules of ATP does complete oxidation of glucose via Krebs cycle yield?

A

30-32

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29
Q

Why is the first reaction of glucose –> glucose-6-phosphate in glycolysis irreversible?

A

Prevents glucose leaving cell (control of pathway)

30
Q

What enzyme controls glucose –> glucose-6-phosphate in glycolysis?

A

Hexokinase / glucokinase

31
Q

What are the 3 key enzymes that control glycolysis?

A
  1. Hexokinase / glucokinase 2. Phosphofructokinase 3. Pyruvate kinase
32
Q

What is pyruvate converted into in the absence of oxygen (anaerobic glycolysis)?

A

Lactate NAD+ is regenerated

33
Q

How many ATPs are generated per molecule of glucose in anaerobic glycolysis?

A

2

34
Q

When is anaerobic respiration vital?

A

Vital for muscles during severe exercise but also a short term survival mechanism for tissues that become anoxic – e.g cardiac muscle during angina or MI.

35
Q

Why is anaerobic respiration vital?

A

If no oxygen, need to get rid of pyruvate, which cannot be utilised by mitochondria, and regenerate NAD to allow glycolysis to continue. Anaerobic glycolysis accomplishes both by synthesis of lactate by LDH

36
Q

Describe glycolysis in tumour cells

A
  • High lactate production (use anaerobic glycolysis in preference to oxidative phosphorylation) even under aerobic conditions –> ‘Warburg effect’
  • Tumour cells absorb glucose more rapidly than normal cells
37
Q

What does the ‘Warburg effect’ allow?

A

Reasons unclear but allows tumours to grow in absence of good blood supply

38
Q

How do PET scans identify tumours?

A

Positron emission tomography (PET) using 2-18F- deoxyglucose identifies tumours by their increased glucose uptake & glycolysis

39
Q

What is glycogen and where is it mainly found?

A

Storage form of glucose, mainly found in liver and skeletal muscle

40
Q

Why is glycogen’s branched structure important?

A
  • Glucose can be rapdily added to glycogen (lots of points at which enzyme can act)
  • Glucose can be rapidly released from glycogen when needed
41
Q

What is function of liver glycogen?

A

Helps us to maintain blood glucose (if blood glucose drops, glycogen in liver is broken down and gucose released into bloodstream)

Liver glycogen levels fluctuate throughout day (low before you eat)

42
Q

What is glycogen synthesised from?

A
  • Conversion of glucose-6-phosphate to glucose-1-phosphate
  • Transferred onto UDP-glucose (carrier)
  • Then transferred onto the primer glycogenin or onto a growing chain attached to glycogenin
43
Q

What is the amount of glucose that you can store as glycogen limited by?

A

The amount of glycogenin and overall size the glycogen molecules can take

44
Q

What is the key control enzyme of glycogen synthesis?

A

Glycogen synthase

45
Q

What is glycogenolysis?

A

Breakdown of glycogen by glycogen phosphorylase (Glucose-1-phosphate converted to glucose-6-phosphate – enters glycolysis)

No ATP required

46
Q

Describe glycogenolysis in muscle cells compared to liver and kidneys

A
  • Glucose-6-phosphate goes straight into glycolysis
  • Enzyme that converts glucose-6-phosphate back to glucose found only in liver (and kidneys) (glucose-6-phosphatase)
47
Q

What is effect of athletic training on muscle?

A
  • increased numbers of mitochondria allow more aerobic respiration
  • increased muscle glycogen content
48
Q

What do long distance runners rely on? What does ‘final push’ at the end require?

A

Long distance runners rely on fat metabolism, but ‘final push’ at the end requires glycogen

49
Q

What is exhaustion and collapse at end of race caused by?

A

Depletion of glycogen

50
Q

Why do runners use high carbohydrate diet in preparation for racing?

A

Increases glycogen stores “glycogen loading”

51
Q

What can excess sugars be converted into?

A

Fatty acids

Glucose –> Acetyl CoA –> fatty acids

52
Q

What are the uses of fatty acids?

A
  • converted to triacylglycerols (triglycerides) for storage
  • used to synthesise other lipids for membranes etc.
53
Q

Where does fatty acid synthesis occur?

A
  • Mainly in liver
  • Adipose tissue
  • In breast tissue during lactation

In the cell cytosol

54
Q

What is the key control point for fat synthesis?

A

Acetyl CoA carboxylase turns Acetyl CoA into Malonyl CoA

55
Q

What is the source of cystolic acetyl CoA?

A

Citrate –> this can cross the mitochondrial membrane, but acetyl CoA can’t

56
Q

How are triacylglycerols synthesised?

A

Addition of 3 fatty acids to a molecule of glycerol-3-phosphate

57
Q

Where does triacylglycerol synthesis occur?

A

In endoplasmic reticulum

58
Q

What happens to fat that is produced in:

  • Adipose tissue
  • Liver
A
  • Adipose tissue –> stored in cytosol
  • Liver –> packaged to form VLDL
59
Q

What happens to VDL formed from triacyglycerols (TAGs) in liver?

A

Either:

  • adipose tissue for storage
  • other peripheral tissues for use as energy source
60
Q

What do levels of AMP act as?

A

Sensitive monitor of energy status

61
Q

What happens to levels of AMP if cell is running short of energy? What is overall effect of this?

A

AMP levels build up

  • Activates AMP-activated protein kinase that phosphorylates key enzymes involved in metabolism in heart, adipose tissue, liver, muscle

Overall effects:

  • to increase energy-providing pathways
  • to inhibit anabolic/synthetic pathways
62
Q

What is effect of insulin on blood glucose?

A

Allows muscle and adipose tissue to gain access to blood glucose (causes blood glucose to drop)

63
Q

What happens if G-6-P levels build up?

A

Hexokinase is inhibited by lots of G-6-P

64
Q

What are the enzymes that control:

  • Glycogen synthesis
  • Glycogen breakdown
A
  • Glycogen synthase
  • Glycogen phosphorylase
65
Q

What is effect of phosphorylation on glycogen phosphorylase and glycogen synthase?

A

Phosphorylation activates glycogen phosphorylase, but inactivates glycogen synthase.

66
Q

What is effect of glucagon on phosphorylation?

A

Hormone that promotes phosphorylation (and glycagon breakdown)

67
Q

What does glucagon inhibit?

A

Phosphofructokinase (main control of glycolysis)

N.B Phosphofructokinase also inhibited by ATP

68
Q

What does ATP inhibit in the glycolytic pathway?

A
  • Phosphofructokinase
  • Pyruvate kinase
69
Q

How does insulin influence glycolysis in muscle and adipose tissue?

A
  • Increases expression of genes which code for enzymes of glycolysis
  • Decreases expression of genes which code for enzymes of gluconeogenesis (making new glucose)

High insulin = glycolysis stimulated

70
Q

How does glucagon influence glycolysis in muscle and adipose tissue?

A

Regulates the level of fructose 2,6 bisphosphate (F2,6-BP) – which activates glycolysis and inhibits gluconeogenesis

This occurs via phosphorylation of a protein which catalyses synthesis AND degradation of F2,6-BP

when phosphorylated (glucagon high) the enzyme degrades F2,6-BP (glycolysis dec)

when dephosphorylated (glucagon low) the enzyme synthesises F2,6-BP (glycolysis inc)

High glucagon = glycolysis inhibited

Yr 2 - GI & Metabolism (51 decks)

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