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intro to biomedical sciences IBMS > Glycogen breakdown > Flashcards

Glycogen breakdown Flashcards

1
Q

what other types of fuels are present when we don’t have carbs

A

proteins form our muscles

triglycerol from our diet or from adipose tissue

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2
Q

what is PROTEIN broken down into

A

amino acids

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3
Q

what is triacylglycerol broken down into

A

fatty acids

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4
Q

what do we do if our body is in a starved state

A

want to breathe-by engaging muscles

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5
Q

how is protein used as a fuel

A

broken down into amino acids

then into ammonia and then incorporated into the urea cycle

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6
Q

how else can acetyl coa be made

A

from fatty acids and amino acids

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7
Q

what type of fuel does our brain and some cells with no mitochondria use

A

only glucose

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8
Q

how is protein converted into glucose

A

broken down into amino acids
converted into CoenzymeA
converted into pyruvate
converted into glucose

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9
Q

how is triacylglycerol converted to glucose

A

broken down into glycerol and then glucose

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10
Q

can fatty acids be converted into glucose

A

NO

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11
Q

what is stored in the muscles

A

glycogen

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12
Q

what is glycogen used for

A

used as fuel on demand

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13
Q

where is glycogen stored

A

in muscles or in the liver

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14
Q

what happens to the glycogen stored in the liver

A

it is used for glycogen derived glucose for the pentose phosphate pathway

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15
Q

what happens during fight or flight

A

the liver also mobilises its glycogen stores and releases glucose for use by muscles

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16
Q

what happens after prolonged fasting

A

glycogen reserves will be used up and the metabolism needs to start synthesising glucose from non carbohydrates to maintain levels

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17
Q

what is it called when glucose is made from non carbohydrates

A

gluconeognesis

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18
Q

how long is prolonged fasting

A

more than 24 hours

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19
Q

what is necessary for human life

A

a constant supply of blood glucose

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20
Q

what is the energy source for exercising muscles

A

glucose- it is the substrate for anaerobic respiration

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21
Q

how do we get glucose

A

diet intake
make glucose- gluconeogensis
degredation of glycogen

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22
Q

why is glucose from diet intake not the best

A

not always readily available and is sporadic

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23
Q

when is glucose mobilised from glycogen

A

between meals or during exercise

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24
Q

describe glycogen

A

excellent short term storage source which when required can be accessed and used immediately

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25
Q

what is the molecular mass of one molecule of glycogen

A

10^8 daltons

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26
Q

where is glycogen stored

A

in discrete cytoplasmic granules which contain most of the enzymes necessary for glycogen synthesis and degradation

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27
Q

describe glycogen

A

homopolysaccharide made from only a D GLUCOSE

multiple chains and highly branched

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28
Q

which bonds are found in glycogen

A

a 1,4 glycosidic bonding and 1,6 glycosidic bonding found at the branches

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29
Q

where does glycogen branches occur

A

8-10 glucosyl residues

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30
Q

what is the significance of branching

A

glycogen is synthesised and broken down by adding or removing glucose units from NON REDUCING ENDS

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31
Q

what does branching create

A

countless non reducing ends which means glycogen can be synthesised or broken down rapidly

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32
Q

what is the main function of liver glycogen

A

maintenance of blood glucose between meals and during early stages of fasting

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33
Q

what is the main function of muscle glycogen

A

fuel reserve for muscle contraction

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34
Q

is the glucose released from the glycogen exportable in the liver

A

is released into the blood to be used by other tissues

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35
Q

is the glucose released from the glycogen exportable in the muscle

A

cannot leave the muscle it enters glycolysis

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36
Q

what is the size of glycogen stores in liver

A

10% wet weight of liver-stores lasts about 24 hrs

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37
Q

what is the size of glycogen stores in muscle

A

1-2% of wet weight of muscle but we have more muscle than liver

38
Q

what is the hormonal control of glycogen in the liver

A

glucagon and adrenaline promote breakdown

insulin promotes synthesis

39
Q

what is the hormonal control of glycogen in the muscle

A

adrenaline promotes breakdown

insulin promotes synthesis

40
Q

when is glycogen broken down

A

from non reducing terminals when blood glucose begins to fall( in liver only)
when muscles need glucose for ATP(broken down in muscles and liver)

41
Q

how is glycogen broke down

A

glycogen (n residues) + Pi with the enzyme glycogen phosphorylase to form glucose 1 phosphate and glycogen( n-1 residues)

42
Q

when might glycogen phosphorylase be defective

A

defective in type V glycogen storage disease(effects muscle)

43
Q

what hormones does the liver respond to

A

glucagon and adrenaline

44
Q

what hormones does the muscle respond to

A

adrenaline ONLY

45
Q

describe phosphorylated glucose

A

much more energy rich molecule can glucose

46
Q

when does glycogen phosphorylase stop cleaving

A

stops 4 units to the branch point

47
Q

which enzymes do we need to cleave at the branch point

A
  1. transferase- cuts three units off and attaches to the long chain
  2. amylo- a 1,6 glucosidase
48
Q

what does transferase do

A

it cuts three units off the branch and attaches to the long chain

49
Q

what does amylo-alpha 1,6 glucosidase do

A

hydrolyses the last glucose unit and attaches it to the long chain and then glucose phosphorylase can work again

50
Q

what is the ratio of glycogen breakdown

A

generates mainly glucose 1 phosphate along with some glucose( 8:1)

51
Q

what is the pathway of glycogen breakdown in the liver

A
  1. broken down into glucose 1 phosphate(8) and glucose(1)
  2. converted into glucose 6 phosphate by phosphoglucomutase- reversible reaction
  3. glucose 6 phosphate dephosphorylated into glucose by glucose 6 phosphatase with hydrolysis
  4. glucose released into blood to maintain glucose levels
52
Q

what is the pathway of glycogen breakdown in the muscle

A
  1. glucose 1 phosphate (8) and glucose(1) rpdocued by breakdown of glycogen
  2. the small amount go glucose is converted into glucose 6 phosphate by hexokinase using ATP
  3. the glucose 1 phosphate is converted into glucose 6 phosphate by phosphoglucomutase
  4. glycolysis in the muscle generates ATP
  5. the muscle doesn’t have glucose 6 phosphatase and cannot convert glucose 6 phosphate INTO GLUCOSE. trapped in the muscle for glycolysis
53
Q

what is produced in the pentose phosphate pathway

A

ribose and NADPH

54
Q

how do we regulate the glycogen metabolism

A

controlled by hormones

allosteric control regulates glycogen metabolism

55
Q

give an example of allosteric control of glycogen metabolism

A

amp allosterically stimulates glycogen breakdown while ATP inhibits glycogen breakdown

56
Q

what does adrenaline and and glucagon do in the liver

A

stimulates muscle glycogen breakdown ready for fight or flight

57
Q

what does glucagon do

A

signals low blood glucose but muscles ignores this as muscle serves glycogen for its own needs

58
Q

how does the hormone signalling work

A

1.adrenaline works in muscle and liver
2.glucagon only works in liver
3.binding of the hormones leads to activation of adenylate cyclase
4.catalyses formation of cAMP from ATP
5.activates protein kinase A ( in the cytosol)
6.the catalytic site phosphorylates phosphorylase kinase
7.phosphorylase kinase phosphorylates glycogen phosphorylase
8. we then get glycogen breakdown
this is regulated by glycogen synthase( inactive) which can be activated by protein kinase A

59
Q

when is phosphorylase kinase most active

A

in the presence of PKA

or when muscles are contracted ( high levels of calcium ions present)

60
Q

what is the hormonal control of glucagon and adrenaline known as

A

an amplification cascade

61
Q

when is insulin released

A

when blood glucose is elevated( after a meal) and stimulates glycogen synthesis whilst inhibiting breakdown

62
Q

how does the hormone signalling work

A

1.adrenaline works in muscle and liver
2.glucagon only works in liver
3.binding of the hormones leads to activation of adenylate cyclase
4.catalyses formation of cAMP from ATP
5.activates protein kinase A ( in the cytosol)
6.the catalytic site phosphorylates phosphorylase kinase
7.phosphorylase kinase phosphorylates glycogen phosphorylase
8. we then get glycogen breakdown
this is regulated by glycogen synthase( inactive) which can be activated by protein kinase A

63
Q

what else does active phosphoprotein phosphatase 1 do

A

hydrolyses glycogen phosphorylase a( active) into glycogen phosphorylase b( inactive)
glycogen switched off

64
Q

what is the hormonal control of glucagon and adrenaline known as

A

an amplification cascade

65
Q

what tissue is affected in von gierkes disease

A

liver
intestine
kidney

66
Q

what tissue is affected in pompe disease

A

liver muscle heart

67
Q

what tissue is affected in forbes disease

A

liver muscle

due to abnormal glycogen structure

68
Q

what tissue is affected by andersen disease

A

liver

abnormal glycogen structure

69
Q

what tissue is affected in McArdlie disease

A

muscle only

70
Q

what tissue is affected in pompe disease

A

liver muscle heart

71
Q

what tissue is affected in forbes disease

A

liver muscle

due to abnormal glycogen structure

72
Q

what tissue is affected by andersen disease

A

liver

abnormal glycogen structure

73
Q

what tissue is affected in McArdlie disease

A

muscle only

74
Q

what enzyme is defected in von gierke disease

A

glucose 6 phosphatase

75
Q

what enzyme is defected in pompe disease

A

lysosomal a glucosidase

76
Q

what enzyme is defected in forbes disease

A

amylo 1,6 glucosidase

77
Q

what enzyme is defected in andersen disease

A

1,4 a glucan branching enzyme

78
Q

what enzyme is defected in McArdlie disease

A

phosphorylase

79
Q

what tissue do we need for diagnosis of von gierkes disease

A

liver

80
Q

what tissue do we need for diagnosis of pompe disease

A

leukocytes
liver
muscle

81
Q

what tissue do we need for diagnosis of forbes disease

A

leukocytes
liver
muscle

82
Q

what tissue do we need for diagnosis of andersen disease

A

leukocytes
liver
muscle

83
Q

what tissue do we need for diagnosis of McArdlie disease

A

muscle

84
Q

what is the outcome for patients with McArdle disease

A

normal lifespan exercise must be avoided

85
Q

what is NASH

A

non alcoholic steatohepatitis-

86
Q

what is the outcome for patients with forbes disease

A

good prognosis

87
Q

what is the outcome for patients with andersen disease

A

death in first 3 years

88
Q

what are the symptoms of NASH

A

silent or non specific making it difficult to diagnose- remain unaware till late stages of the disease

89
Q

what is NASH

A

non alcoholic steatohepatitis-

90
Q

describe NASH

A

defined as liver manifestation fo metabolic disorder and most severe form of non alcoholic fatty liver disease

91
Q

what else might people suffer with if they have NASH

A

obesity
pre diabetic
diabetes

92
Q

what are the symptoms of NASH

A

silent or non specific making it difficult to diagnose

intro to biomedical sciences IBMS (35 decks)

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