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Year 1 Summative 1 > BMS07-1032/33 Integration of Metabolism > Flashcards

BMS07-1032/33 Integration of Metabolism Flashcards

1
Q

Fed state

A

Fuel comes from food your eating

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2
Q

Fasting state

A

Fuel comes from stores put down during the fed state

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3
Q

What controls how much fuel we store?

A

Hormones

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4
Q

How does starvation alter metabolism

A

Cells start metabolising different fuels

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5
Q

How do enzymes alter metabolism (3)?

A

Allosteric regulation
Covalent modification
Changing their synthesis

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6
Q

ADP + ADP =

A

ATP & AMP

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7
Q

How does AMP affect phosphofructokinase?

A

Activates it

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8
Q

What molecule does phosphofructokinase act on?

A

Phosphorylates fructose-6-phosphate

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9
Q

What will/wont the liver respond to?

A

Responds to hormones not low levels of ATP

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10
Q

What activates glycogen phosphorylase?

A

Glucagon by adding a Pi to it

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11
Q

Which 2 molecules is this enzyme related to?

A

Glycogen to glucose-1-phosphate

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12
Q

What happens when there is low cholesterol?

A

HMG coenzyme A reductase is made to make cholesterol if enough isn’t being taken in through the diet

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13
Q

The liver only takes up glucose when there is lots of it to ensure…

A

Ensures glucokinase is only made when theres lots of glucose for it to phosphorylate

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14
Q

Which hormones alter the effects of insulin? (3)

A

Adrenaline
Cortisol
Growth hormone

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15
Q

Which hormone do alpa cells release?

A

Glucagon

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16
Q

When do beta cells release insulin?

A

When glucose enters them, they have a low affinity for this so it only occurs in high concentrations

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17
Q

What type of cells are they?

A

Endocrine

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18
Q

What % are alpha cells?

A

30-40%

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19
Q

What do omega cells release?

A

Somatostatin

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20
Q

What is somatostatin?

A

Growth hormone inhibitor

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21
Q

What stimulates insulin secretion?

A

Glucose
AA
Hormones released after eating before glucose levels rise
Glucagon

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22
Q

What is the role of glucagon?

A

Fine tuning of glucose levels

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23
Q

Which hormones are released after eating?

A

Gastrointestinal hormones and secretin

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24
Q

Describe insulin secretion?

A 
AA or glucose enter the beta cell
ATP is made
ATP closes K channels
Membrane gets depolarised
Ca channels open
Insulin vesicles move
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25
Q

Compare the effects of AA and glucose on beta cells

A

AA don’t lead to as much insulin being released

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26
Q

Proinsulin is converted to…

A

Insulin and C-peptide

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27
Q

Metabolic effects of insulin

A 
Fuel storage 
Growth
Glycogen synthesis/storage
AA uptake and protein synthesis 
FA storage
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28
Q

How are fatty acids stored?

A

Acetyl coenzyme A is converted to malonyl coenzyme A which is involved in protein synthesis

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29
Q

What makes up the bottom half of the insulin receptor?

A

Tyrosine kinase

Insulin receptor substrate docking site

30
Q

What happens at her IRS docking site?

A

It gets phosphorylated which activates a kinase which continues to activate other kinase by phosphorylation until the active protein kinase is reached

31
Q

What does active protein kinase do? (2)

A

Kinase moves the GLUT4 receptor to the membrane

Phosphorylate glucose synthase kinase making it inactive so glycogen synthase doesn’t get phosphorylated so its active and can form glycogen

32
Q

How does insulin affect lipolysis?

A

Inhibits protein kinase A by removing the cAMP activator using phosphodiesterase which active protein kinase activated

This means hormone sensitive lipase isn’t activated by protein kinase A so FA aren’t stored

33
Q

How does insulin affect gene expression?

A

The receptor is phosphorylated due to the presence of insulin
This activated RAS which activates kinases and then MAPK which influences transcription factors

34
Q

When is RAS active and inactive?

A

Active has GTP bound

Inactive has GDP

35
Q

Whats special about the GLUT4 receptor in the brain, liver, RBC and pancreas?

A

They aren’t insulin dependant so glucose can be uptaken even when in low concentration

36
Q

What stimulates the release of glucagon?

A

Low blood glucose
High AA
Adrenaline

37
Q

What happens when there are high AA?

A

Releases both insulin and glucagon

38
Q

What does adrenaline do?

A

Supress insulin secretion
Mobilises fuel in stress
Glucose secretion
FA release

39
Q

What does glucagon do?

A 
Mobilise fuel 
Maintains glucose in fasting
Glycogenolysis
Gluconeogensis
AA uptake at the livere
FA release
FA oxidation
Ketone body formation in the liver
40
Q

How do GI hormones get to the liver?

A

In the pancreatic vein

41
Q

How does glucose get to peripheral tissue?

A

Travel down the hepatic vein

42
Q

What do GI hormones do?

A

Stimulate Islets of Langerhans

43
Q

What does cortisol do?

A

Glyconeogensis
FA release
AA mobilisation from the muscle

44
Q

What does insulin inhibit and what are the consiquences of this?

A

Protein kinase so glycogen isn’t made

45
Q

When isn’t the liver in glycogensis?

A

Fasting state

46
Q

Why does the liver have a low affinity for glucose?

A

So it doesn’t compete with the brain

47
Q

What is gluconeogenesis?

A

Breaking down of non sugars for energy e.g. lactate, glycerol and AA

48
Q

Glycogensis

A

Breaking down glycogen

49
Q

Glycolysis

A

Making glycogen

50
Q

What activates glycolysis?

A

Glucokinase/pyruvate kinase/ phosphofructokinase

51
Q

What happens to glycogen in the fasting state?

A

It is broken down

52
Q

What happens to glycogen synthase in the fasting state?

A

Inhibited, phosphorylase is inhibited so it cant turn the enzyme on

53
Q

How are fatty acids prevented from being esterified?

A

Malonyl coenzyme A inhibits carnitine transferase so FA cat enter the mitochondria to be oxidised

54
Q

What is activated to prevent FA synthesis?

A

Acetyl coenzyme A carboxylase

55
Q

What has a greater uptake in the fasting state in muscles?

A

AA, so protein synthesis

56
Q

What activates lipoprotein lipase and what does this cause?

A

Insulin so FA can enter adipose tissue for esterification

57
Q

The inhibition of which enzyme results in FA being broken down?

A

Hormone sensitive lipase

58
Q

After how long will all glycogen stores have been used up?

A

24hrs

59
Q

What inhibits pyruvate dehydrogenase to stop pyruvate being converted to…

A

Glucagon inhibits and insulin activates so its not converted to acetyl coenzyme A and its used to make glucose

60
Q

What happens to an excess of acetyl coenzyme A?

A

Put into FA synthesis when acetyl A carboxylase is activated, this means glucose formation is favoured

61
Q

What metabolism is useful for long term starvation?

A

Ketone

62
Q

Where are ketone bodies sent and why?

A

Into circulation as the liver cant use them

63
Q

What makes ketone bodies?

A

Acetyl coenzyme A

64
Q

Which tissues oxidise FA and ketone bodies?

A

Most

65
Q

How can the brain use ketone bodies?

A

They are small and lipid soluble so they can cross the barrier

66
Q

What do ketone bodies do?

A

Get beta cells to make insulin and inhibit the breakdown of AA

67
Q

Give 2 examples of ketone bodies

A

Acetoacetate and beta hydroxybutyrate

68
Q

What do muscles use in extreme starvation?

A

Fatty acids

69
Q

What happens to the concentration of ketone bodies and fatty acids?

A

FA plateu but ketone bodies continue to increase

70
Q

Complications of type 2 diabetes

A

Blindness
Foot ulcers
Thickened basement membrane
Kidney failure

71
Q

Treating type 2 diabetes

A

Biguanides (increase GLUT4 receptors), sulphonylureas (insulin secretion) and oral hypoglycaemic

72
Q

What happens in type 1 diabetes?

A

Insulin cant prevent the breakdown of protein and fat
Similar to starvation
Ketone bodies are made

Year 1 Summative 1 (56 decks)

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