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CEP > L13: Drug treatment of diabetes > Flashcards

L13: Drug treatment of diabetes Flashcards

1
Q

How is insulin released from beta cells when blood glucose levels rise?

A

1) glucose enters the beta cells by a transporter molecule
2) glucose gets metabolised by the mitochondria inside the beta cells
3) ATP levels rise inside
4) ATP binds to ATP-sensitive potassium channels which block potassium from leaving the cell
4) this causes depolarisation
5) depolarisation triggers voltage-gated calcium channels to open
6) calcium influx occur
7) calcium promotes enzymes such as DAG to process and package insulin into vesicles
8) calcium also causes exocytosis of vesicles containing insulin
9) insulin is released

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2
Q

In a non-diabetic patient when is insulin released?

A

Insulin is released during the 1st and 2nd phase

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3
Q

In a type 1 diabetic patient when is insulin released?

A

Insulin is an autoimmune disease so beta cells are destroyed and insulin is never released. This means that 1st and 2nd phase do not occur.

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4
Q

In a type 2 diabetic patient, when is insulin released?

A

Insulin is only released during the 2nd phase. 1st phase does not occur.

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5
Q

Where are insulin receptors found?

A

On liver, muscle and fat membrane

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6
Q

How many insulin molecules have to bind to insulin receptors to activate it ?

A

2 insulin molecules because the receptor is a dimer.

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7
Q

What is a dimer?

A

The receptor is made of 2 components: alpha and beta subunits.

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8
Q

What is the alpha subunit

A

The binding site for insulin

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9
Q

What is the beta subunit

A

Intracellular portion that has the tyrosine kinase domain

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10
Q

What happens when insulin binds to insulin receptors?

A

1) two insulin molecules bind to the alpha subunit
2) the tyrosine kinase is activated in the beta subunit
3) tyrosine kinase is an enzyme which causes the phosphorylation of IRS proteins
4) this triggers second messenger pathway that lead to other enzyme activation for transcription of genes for the expression of GLUT-4
5) GLUT-4 is a transporter molecule of glucose that allows glucose uptake. The expression of GLUT-4 therefore increases glucose uptake
6) glucose is taken up and metabolised by the mitochondria
7) glycogen synthesis increases

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11
Q

What is type 1 diabetes

A

An autoimmune disease that causes the loss of beta cells completely so that they cannot produce insulin

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12
Q

What is the treatment for type 1 diabetes?

A

Diet, insulin injections, and metformin (only if BMI is greater than 25)

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13
Q

What is insulin

A

A peptide

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14
Q

How is insulin administered to a patient

A

Intravenous injection

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15
Q

What is achieved with the treatment

A

Hba1C less than 42mmol/mol

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16
Q

What are the types of insulin

A
  • short acting

- long acting

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17
Q

Why does insulin act short

A

Because it is soluble

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18
Q

Why does insulin act long

A

Insulin molecules can associate with each other to from complexes and this delays insulin from going into the blood quick

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19
Q

What is type 2 diabetes

A

This is when you get insulin resistance due to the dysfunction of IRS proteins that link to insulin receptors by association of beta subunits.

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20
Q

What is the treatment for type 2 diabetes

A

Diet, excercise, drugs and may need insulin

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21
Q

What is metformin

A

A drug mainly to treat type 2 diabetes

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22
Q

What is the mechanism of metformin

A

This drugs requires insulin to work

It acts on tissues of liver and muscle to promote muscle uptake

23
Q

How does metformin act on the liver

A
  • gluconeogenesis decreases

- this is due to activation of AMP activated protein kinase which decrease gene expression

24
Q

What are the side effects of metformin

A
  • no hypoglycaemia
  • no increase in appetite
  • lactic acidosis
25
Q

what is sulphonylurea

A

A drug type to treat diabetes

26
Q

Give example of sulphonylurea drugs

A
  • tolmutamide
  • gilbenclamide
  • gliclazide
27
Q

What is the mechanism of sulphonylureas

A

1) sulphonylurea drugs bind to ATP- sensitive potassium channels
2) an example of an ATP-sensitive potassium channel is SU receptors
3) this causes the blockage of pottasium and causes depolarisation
3) depolarisation triggers the release of insulin vesicles by exocytosis
4) tissues also become sensitive to insulin

28
Q

Which sulphonylurea drug has the longest half life

A

Glibencalmide

29
Q

Which sulphonylurea drug has the shortest half life?

A

Tolmutamide

30
Q

What is an SUR

A

An example of ATP-sensitive potassium channel

31
Q

What is an SUR modulator

A

A drug type that has the same actions as sulphonylurea (binds to SU) to cause the release of insulin

32
Q

What is the difference of SUR modulator from sulphonylureas

A

SUR modulators do no have the same moiety as sulphonylureas

33
Q

What are the effects of SUR modulators

A
  • hypoglycaemia
  • stimulate appetite
  • contraindicated in pregnancy/ breastfeeding as the dug can pass to the infant.
34
Q

Give an example of SUR modulator

A

Repaglinide

35
Q

What is thiazolidinediones

A

A type of drug to treat diabetes

36
Q

What is the mechanism of thizaolidinediones

A
  • Binds to transcription factors which affect gene expression (similar to metformin)
  • Primary action: increases fatty acid uptake (lipogenesis) in adipose tissue
  • secondary action: decreases plasma fatty acid and increase glucose uptake
37
Q

What are the side effects of thiazolidinediones

A
  • liver toxicity

- heart failure by fluid retention

38
Q

What are incretins?

A

Gi hormones which increase insulin release when you eat

39
Q

What is dipeptidyl peptidase-4 ?

A

An enzyme that breaks down incretins

40
Q

What are the drugs called that are based on incretin action

A
  • gliptins

- exenatide

41
Q

How does gliptins work?

A

Inhibit dipeptidyl peptidase-4 so incretins are not brocken down and insulin is released

42
Q

How does exenatide work

A

Exenatide act as incretin agonist which will bind to receptors on the beta cells

43
Q

Give an example of incretin

A

GLP-1

44
Q

What is an acarbose ?

A

A drug that that inhibits the enzyme alpha glucosidase which decreases carbohydrate absorption from the gut

45
Q

What are SGLT2 inhibitors

A

A drug that inhibits sodium- glucose transporter 2 in the kidney at the proximal convoluted tubule

46
Q

Mechanism of SGLT2 inhibitors

A

Bind to SGLT2 and cause loss of glucose and sodium in the urine

47
Q

What are the side effects of SGLT2 inhibtors

A
  • ketoacidosis

- peripheral vascular disease

48
Q

Give an two examples of incretin based drugs

A
  • gliptins (enzyme inhbitor)

- exenatide (agonist)

49
Q

Give an example of incretin

A

GLP-1

50
Q

Examples of sulphonylureas

A
  • tolbutamide
  • glibencalmide
  • Gliclazide
51
Q

What is an acarbose

A

It is an alpha glucosidase (enzyme) inhibitor which decreases the uptake of carbohydrate

52
Q

Give an example of SGLT2 inhibitors

A

Canaglifozin

53
Q

Give an example of a SUR modulator

A

Repaglinide

CEP (12 decks)

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