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CVDM > Incretin Islet Axis > Flashcards

Incretin Islet Axis Flashcards

1
Q

What is the incretin effect?

A

Beta cells don’t produce as much insulin when given IV glucose as when given oral glucose

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2
Q

The incretin effect is lost early/late in T2DM?

A

Early

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3
Q

What are incretins?

A

Intestinal secretion of insulin

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4
Q

What are incretins secreted in response to?

A

Nutrient stimuli

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5
Q

Name the two incretins and where they are secreted from

A

GIP - secreted from K cells
GLP-1 - secreted from L cells

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6
Q

Incretins are broken down quickly/slowly

A

Quickly

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7
Q

What breaks down incretins?

A

DPP-4

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8
Q

GIP is more/less potent than GLP-1

A

Far less potent

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9
Q

What is the function of GIP?

A

To promote glucose dependent insulin secretion

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10
Q

What is GLP-1?

A

Glucagon-like peptide I
1

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11
Q

What is GLP-1 cleaved from?

A

Proglucagon in the intestinal L cels

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12
Q

Where are L cells found?

A

Distal ileum and colon (some in jejunum and duodenum)

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13
Q

How does glucose stimulate GLP-1 secretion?

A

Co-transported with sodium which causes sodium influx and depolarisation, calcium influx and hormonal release

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14
Q

Names of some non-glucose nutrients that stimulate GLP-1

A

Amino acids
Short chain fatty acids
Long chain fatty acids

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15
Q

What happens to GLP-1 after it is secreted?

A

It is taken up by portal vein and acts on pancreatic beta cells
Acts on enterocytes and other enteroendocrine cells
Activates vagal afferents and the enteric nervous system

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16
Q

Effects of GLP-1 on different organs

A

Pancreas (can cause pancreatitis)
Brain - appetite regulation
Stomach - reduction in gastric emptying
The heart - increases heart rate

17
Q

What type of receptor is the GLP-1 receptor?

A

G-protein coupled receptor

18
Q

What pathway do incretin drugs act on?

A

The amplifying pathway - which augments insulin secretion

19
Q

What pathway do sulphonylurea drugs and glucose act on?

A

Triggering pathway

20
Q

What do sulphonylureas do?

A

Close the KATP channel which is the master switch for insulin secretion.
The membrane depolarises and calcium influx triggers insulin release

21
Q

Is the insulin release caused by sulphonylureas dependent on glucose?

A

No - it triggers insulin release no matter the glucose level and so can cause hypoglycaemia

22
Q

Is the insulin release caused by incretin drugs dependent on glucose?

A

Yes - they result in augmentation of insulin secretion when the pathway is triggered by glucose and so there is no hypoglycaemia

23
Q

What do DPP-4 inhibitors do?

A

Prevent the breakdown of GLP-1 and GIP, resulting in modest rise of GLP-1 and GIP.
But reliant on levels of GLP-1 and GIP so can only boost levels a little

24
Q

What are GLP-1 receptor agonists?

A

Modified GLP-1 molecules that avoid breakdown by DPP-4, resulting in supraphysiological GLP-1 action

25
Q

How does metformin work?

A

By lowering hepatic glucose production

26
Q

Benefits of GLP-1 receptor agonists

A

Promote insulin secretion from pancreas without hypoglycaemia
Suppress glucagon
Decrease gastric emptying - early satiety
Act on hypothalamus to reduce appetite resulting in weight loss
CV benefits

27
Q

Disadvantages of GLP-1 receptor agonists

A

Nausea (but usually resolves 6-8 weeks)
Injectable
May cause pancreatitis?

28
Q

Examples of GLP-1 receptor agonists

A

Semaglutide
Liraglutide
Exenatide
Dulaglutide

29
Q

Which GLP-1 receptor agonist can be given orally?

A

Semaglutide

30
Q

Benefits of DPP-4 inhibitors

A

Promote insulin secretion from pancreas without hypoglycaemia
Suppress glucagon
Weight neutral
Limited side effects

31
Q

Disadvantages of DPP-4 inhibitors

A

Not that potent
No weight loss
No CV benefit
May cause pancreatitis

32
Q

What do SGLT2 inhibitors do?

A

Work on the kidney specific isoform of SGLT causing glycosuria and weight loss

33
Q

Example of SGLT2 inhibitor

A

Dapagliflozin

CVDM (16 decks)

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