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SM Endocrine > Insulin Secretion and Signalling > Flashcards

Insulin Secretion and Signalling Flashcards

1
Q

What type of cells are in found i the pancreas

A

Alpha
Beta
S cells
PP cells

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2
Q

What do the beta cells do

A

Secrete insulin

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3
Q

What do alpha cells do

A

Secrete glucagon

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4
Q

What do the S cells do

A

Secrete somatostatin

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5
Q

What do the PP cells do

A

Secrete pancreatic polypeptide

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6
Q

Where and how is the insulin peptide structure synthesised

A

Int he RER of pancreatic beta cells as a larger single chain preprohormone - preproinsulin

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7
Q

Insulin peptide structure is cleaved to form what

A

Insulin

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8
Q

What does the insulin peptide structure contain

A

2 polypeptide chains linked by disulphide bonds

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9
Q

What type of product is the c peptide

A

A waste product with no known physiological function

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10
Q

Describe the variation in insulin amino acid sequence from species to species

A

Very little variation

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11
Q

What is used to avoid the problem of antibody formation

A

Human insulin instead of other animal insulin

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12
Q

How does Glucose enter the beta cells

A

Throughout he GLUT2 glucose transporter

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13
Q

What happens to the glucose when it enters the cell

A

it is phosphorylated by glucokinase

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14
Q

What cells sense the glucose levels in the blood

A

beta cells

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15
Q

Describe the relationship between the intracellular concentration to the extracellular concentration of glucose

A

Directly proportional

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16
Q

What will phosphorylate glucose at low concentrations

A

Hexokinase

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17
Q

What does a change of glucose concentration lead to

A

A dramatic change in glucokinase activity

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18
Q

An increased metabolism of glucose leads to what

A

An increase in intracellular ATP concentration

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19
Q

How many ATP molecules are produced per glucose molecule

A

36

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20
Q

What does ATP inhibit

A

The ATP sensitive K+ channel (KATP)

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21
Q

If the KATP is inhibited, what does this do to the levels of K+ in the cells

A

It increases it and causes depolarisaiton which will then result in the opening of the voltage gated claim channels.

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22
Q

If calcium is coming into the cell, what will be allowed

A

A release of insulin into the blood.

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23
Q

Inhibition of what leads to depolarisation of the cell membrane

A

Inhibition of KATP

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24
Q

What results in the opening of voltage-gated Ca2+ channels

A

Depolarisaiton of the cell membrane

25
Q

What does an increase in internal Ca2+ concentration lead to

A

fusion of secretory vesicles within the cell membrane and release of insulin

26
Q

what is the term used to describe the release of insulin

A

Biphasic

27
Q

What is the RRP

A

Readily releasable pool of insulin

28
Q

How much insulin granules are immediately available for release

A

5%

29
Q

What 2 proteins do KATP channels consist of

A

Kir6.1 (inward rectifier subunit

SUR1 (a sulphonylurea receptor)

30
Q

What are both Kir6.1 and SUR1 required for

A

To form a functional channel

31
Q

How does intracellular ATP elicit depolarisation

A

By inhibiting KATP

32
Q

KATP is directly inhibited by what class of drug

A

Sulphonylurea e.g tolbutamide or glibenclamide

33
Q

KATP is stimulated by what? What does this do to insulin secretion

A

Diazoxide - it inhibits insulin secretion

34
Q

If a patient has an overactive KATP channel, what are they most likely to have

A

Profound neonatal diabetes

35
Q

If a patient has an inactive KATP channel, what are they most likely to be

A

Hyperinsulinaemic

36
Q

What does MODY stand for

A

Mature onset Diabetes of the Young

37
Q

What causes MODY

A

Mutations in at least 6 different genes

38
Q

What play key roles in pancreas foetus development and neogenesis

A

HNF transcription factors

39
Q

What else do HNF transcription factors do

A

Regulate beta cell differentiation and function

40
Q

what is the main difference in treatment between MODY and type 1

A

Type 1 is treated with insulin

MODY is treated with sulphonylurea

41
Q

What is the main problem in MODY

A

defective gluose sensing in the pancreas and/or loss of insulin secretion

42
Q

What is the main problem in Type 1 diabetes

A

Loss of insulin secreting beta cells

43
Q

What is the main problem in type 2 diabetes

A

Initially hyperglycemia with hyperinsulinaemia so primary problem is reduced insulin sensitivity in tissues

44
Q

What is one of the major functions that regulates protein function in the cell

A

Protein phosphyorylation

this provides a reversible method for altering protein function

45
Q

Where can proteins get phosphorylated

A

On any hydroxyl group

46
Q

Insulin receptor is a what

A

Dimeric tyrosine kinase

47
Q

Binding of insulin to the alpha subunits causes what

A

Beta subunits to phosphorylate themselves, thus activating the catalytic activity of the receptor

48
Q

What is done through eh GLUT 4 pathway

A

Glucose transport into muscle and into fat

49
Q

In what patients does the GLUT4 pathway not occur

A

Those with diabetes

50
Q

What 7 different things does insulin effect

A 
Amino acid uptake in muscle 
DNA synthesis 
Protein synthesis 
Growth responses 
Glucose uptake in muscle and adipose tissue 
Lipogenesis in adipose tissue and liver 
Glycogen synthesis in liver and muscle
51
Q

Where are ketone bodies formed

A

In liver mitochondria

52
Q

What are ketone bodies derived from

A

Acetyl-coA from beta oxidation

53
Q

Why are ketone bodies important physiologically

A

They are molecules of energy metabolism for heart muscle and renal cortex

54
Q

What are oxidised when glucose is not available

A

Fatty acids

55
Q

What is converted to ketone bodies

A

Excess acetyl co-A

56
Q

What can lead to acidosis

A

Accumulation of ketone bodies

57
Q

What does a high glucose excretion cause

A

Dehydration and exacerbates acidosis

58
Q

What can ketosis result in

A

Coma or death

59
Q

What type of diabetes is ketoacidosis most associated with

A

type 1

SM Endocrine (27 decks)

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