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endocrine > The endocrine pancreas > Flashcards

The endocrine pancreas Flashcards

1
Q

Give a summary of the glucostatic theory

A

Our drive to eat is driven by our glucose levels

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2
Q

Give a summary of lipostatic theory

A

Our drive to eat is driven by fat stores

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3
Q

What is the function of leptin

A

Peptide hormone driven by fat stores which depresses feeding activity through its affect on the hypothalamus

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4
Q

What are the 3 categories of energy output

A

cellular work - transporting molecules across membranes, growth and repair, storage of energy

mechanical work - movement using muscle

heat loss - associated with cellular and mechanical work

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5
Q

what are Anabolic pathways

A

Building up of larger molecules from smaller ones
(remember anabolic steroids - build up muscle therefore anabolic pathways build up bigger molecules)

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6
Q

What are catabolic pathways

A

Degradation of large molecules into smaller ones which releases energy

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7
Q

What is an absorptive state

A

Ingested nutrients supply the energy the body needs and the the excess is stored (anabolic phase)

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8
Q

When does an absorptive state occur

A

After eating

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9
Q

What is a post absorptive state

A

(fasting state)
Rely on body stores to provide energy (catabolic phase)

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10
Q

When does a post absorptive state occur

A

Between meals and overnight

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11
Q

What does it mean to be an obligatory glucose utiliser and give an example

A

It can only use glucose for energy for example the brain

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12
Q

What is the normal range of blood glucose

A

3.2-6.3 mM

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13
Q

What organ has first access to glucose in the blood

A

The brain

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14
Q

What is excess glucose converted into

A

fat stores or glycogen

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15
Q

What is glucagon

A

Catabolic hormone which breaks down glycogen stores and activates enzymes to break down amino acids into glucose

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16
Q

What is insulin

A

Anabolic hormone which stimulates production of fat and glycogen from glucose

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17
Q

Why is glucose excreted in the urine in diabetics

A

They don’t have enough insulin to deal with increased blood glucose levels so when the blood gets to the glomerulus, the kidneys have too much glucose to deal with so the excess gets excreted

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18
Q

What organ releases insulin and glucagon

A

pancreas

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19
Q

How much of the pancreas has endocrine function and where in the pancreas are insulin and glucagon produced

A

1% is endocrine and insulin and glucagon are produced in the islets of langerhans

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20
Q

What do alpha cells of the islets of langerhans produce

A

glucagon

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21
Q

What do the beta cells of the islets of langerhans produce

A

insulin

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22
Q

What do the delta cells of the islets of langerhans produce

A

Somatostatin

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23
Q

When is glucagon released into the plasma

A

When the blood glucose levels decrease

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24
Q

When is insulin released into the plasma which causes glucose to be up taken into cells to decrease plasma blood glucose

A

When the blood glucose in the plasma is very high
And when amino acids enter the blood from the GI tract

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25
Q

Describe how insulin is synthesised

A

It is synthesised as a large preprohormone - preproinsulin which is then converted into proinsulin
Proinsulin is then packaged into secretory Vesicles which has enzymes which cleave the proinsulin into insulin and C peptide insulin

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26
Q

Why os C peptide a good marker for pancreatic health

A

it resists degradation and persists in the plasma, longer than insulin

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27
Q

Which hormone dominates the absorptive state

A

Insulin (anabolic)

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28
Q

What is glucose stored as in liver and muscle

A

Glycogen

29
Q

What is glucose stored as in liver and adipose tissue

A

Triacylglycerols

30
Q

What causes beta cells to release insulin

A

They have a special Katp channel which is sensitive to ATP

When glucose is abundant, it enters cells through the GLUT transported and metabolism increases which causes more ATP to be produced in the cell which causes the channel to close. Intracellular potassium then rises which depolarises the cell which causes voltage gated calcium channels to open and triggers insulin to be exycytosed from their vesicles to be released into the circulation

31
Q

What is the primary action of insulin

A

Binds to tyrosine kinase receptors on the cell membrane of insulin dependent tissues to increase the glucose uptake in that cell

32
Q

How does insulin increase glucose uptake in cells

A

Mobilisation of GLUT-4 which is normally in the cytoplasm but migrates to the membrane which allows more glucose to be up taken into the cell

33
Q

What are the insulin dependent cell types

A

Muscle and fat

34
Q

What GLUT transporter is insulin dependant

A

GLUT-4

35
Q

What transporter does the liver use for glucose uptake

A

GLUT 2 which is insulin independent

36
Q

How does insulin indirectly alter glucose transport in hepatocytes

A

It breaks down glucose into glucose-6-phosphate which keeps the glucose concentration in the hepatocyte low which maintains the gradient for more glucose to enter the cell

37
Q

What is the effect of insulin on glycogen synthesis in muscle and liver

A

Stimulates glycogen synthesis and inhibits glycogen phosphorylase

38
Q

What is the effect of insulin on amino acid uptake

A

Increases it which promotes protein synthesis

39
Q

What is the effect of insulin on triaglycerol synthesis

A

Increases it in adipocytes and liver by stimulating lipogenesis

40
Q

What is the effect of insulin on gluconeogenesis in the liver

A

inhibits it

41
Q

What is the relation between insulin and growth hormone

A

Permissive effect - insulin is required for Growth hormone to be active and working

42
Q

What is the effect of insulin on potassium entry

A

Stimulates sodium potassium ATPase so increases potassium entry into the cell

43
Q

What happens to insulin receptors after the effects of insulin are completed

A

The receptors are endocytosed and destroyed by insulin protease

44
Q

Why does glucose given orally cause bigger release of insulin then IV glucose

A

Because the release of GI hormones causes release of insulin as well as blood glucose and in IV glucose these hormones will not be released

45
Q

What is the effect of vagal activity on insulin release

A

Increased vagal activity causes insulin release

46
Q

What is the main target organ for glucagon

A

Liver

47
Q

What are the hormones which are part of the glucose counter-regulatory system

A

Epinephrine, cortisol, growth hormone and glucagon

48
Q

What does glucagon cause

A

Increased glycogenolysis
Increased gluconeogenesis
Formation of ketones from fatty acids

49
Q

What does the brain use instead of glucose in severe cases of starvation

A

Ketones

50
Q

What are potent stimulus for glucagon secretion

A

Amino acids but they also increase insulin levels

51
Q

What is the effect of somatostatin on insulin and glucose release

A

Somatostatin inhibits both glucagon and insulin release

52
Q

Why do cushings patients appear diabetic

A

They have high cortisol which inhibits insulin

53
Q

What is the main function of somatostatin

A

Inhibit the GI tract

54
Q

What occurs if insulin and glucagon are both inhibited

A

Blood glucose rises as there are multiple hormones which increase blood glucose but only insulin reduces blood glucose

55
Q

What is the effect of insulin on glucagon

A

Inhibits glucagon

56
Q

What is the effect of glucagon on insulin

A

stimulates insulin release

57
Q

What is the effect of exercise on blood glucose

A

Decreases blood glucose because it increases glucose entry into muscle cells even in absence of insulin which causes increase in GLUT-4 transporters

It also increases insulin sensitivity

58
Q

What happens during starvation with regards to production of energy

A

Adipose tissue is broken down and fatty acids are released - these are readily used by most tissues to produce energy

59
Q

What does the liver convert free fatty acids into during starvation

A

Ketone =bodies which can be used by muscle and brain

60
Q

What is ketone body uptake dependant on

A

insulin

61
Q

What happens in type one diabetes

A

Autoimmune destruction of the pancreatic beta cells of the islets of langerhans which compromises ability to produce insulin

62
Q

What do type one patients have an absolute need for

A

Insulin - without it they become excessively wasted and develop ketoacidosis

63
Q

How does ketoacidosis occur in type 1 diabetes

A

No insulin results in a starvation like state due to glucose not being up taken into cells
This results in adipose being broken down into fatty acids and the excess free fatty acids converted into ketone bodies
Ketone bodies rely on insulin for their up take so without the insulin they stay in the plasma and due to their acidity cause acidosis

64
Q

How are ketones detected

A

In the urine and can smell acetone in the breath

65
Q

What happens in type 2 diabetes

A

Peripheral tissues become insensitive to insulin

66
Q

What is type 2 diabetes associated with

A

obesity - chronic levels of exposure of high insulin due to their high glucose diets - this eventually builds an insulin resistance

67
Q

How is diabetes detected

A

Glucose tolerance test - patients ingest glucose after fasting blood glucose is measured - the blood glucose should return to normal fasting levels within an hour - anything over 2 hours is indicative of diabetes

68
Q
A

endocrine (30 decks)

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