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Diabetes > T1DM > Flashcards

T1DM Flashcards

1
Q

what are different islet endocrine cells?

A

α-cells secrete glucagon
* β-cells secrete insulin
* δ-cells secrete somatostatin
* PP-cells secrete pancreatic
polypeptide(PP)
* ε-cells secrete Ghrelin

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2
Q

what is the role of the KATP channel in the beta cell?

A

At low glucose, the KATP channel is open,
maintaining a hyperpolarised plasma
membrane.

At high glucose, closure of the KATP channel depolarises the PM, triggering insulin secretion.

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3
Q

what is the mechanism of action of sulphonylureas?

A

Sulfonylureas bind the SUR1 subunit of the KATP channel, closing the channel and triggering insulin secretion irrespective of glucose concentrations.

very good at treating monogenic diabetes

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4
Q

what happens to the phases of insulin secretion in T2DM?

A

insulin secretion is biphasic but this is somewhat lost in T2DM

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5
Q

what happens to beta cells in T2DM?

A
  • Beta cell apoptosis increased during T2D
    (TUNEL stained, insulin+ cells).

another study suggested degranulation or dedifferentiation of beta cells during type 2
diabetes, rather than beta cell loss.

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6
Q

what do GLP1s do

A

GLP1 potentiates insulin secretion in depolarised beta cells, via elevations in cAMP leading to activation of PKA and EPAC.

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7
Q

how does glucose stimulate insulin secretion in beta cells?

A

via a coupling pathway involving oxidative glucose metabolism, ATP production, KATP channel closure, membrane depolarisation, calcium influx and insulin vesicle exocytosis.

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8
Q

what do beta cells do?

A

Beta cells respond to numerous nutrients and hormones besides glucose to coordinate insulin secretion.

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9
Q

what are the 5 subtypes of diabetes?

A

severe insulin deficient (high HBA1C low C peptides)
severe insulin resistant (older, high C peptides)
mild obesity (young and obese)
mild age related diabetes (older)
T1DM

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10
Q

what are factors leading to failure to reach glycaemic targets?

A

younger
femlae
obese
not at BP/ lipid targets
2 or 3 drugs
poor adherences to meds/ lifestyles/ targets

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11
Q

what do incretins do?

A

cause intestinal secretion of insulin (GIP from K cells, GLP-1 form L cells)

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12
Q

describe GLP-1

A

cleaved from proglucagon in the intestinal L cell

direct stimulus by nutrients such as carbohydrate and fats largely via G protein coupled receptors

they are taken up by portal veins and act on pancreatic betas cells, enterocytes and other enteroendicrine cells

activate vagal afferents and the neteric nervous system

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13
Q

describe sulphonylureas

A

Act via Triggering Pathway
Close KATP channels – the ‘master’ switch for insulin secretion
Membrane depolarisation & Calcium influx triggers insulin release
Insulin release happens whatever the blood glucose – so can result in hypoglycaemia
Potentiating (amplifying) pathways can work to increase insulin secretion
e.g. Glucose
e.g. GLP-1

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14
Q

describe incretins (and incretin like drugs)

A

Act via Amplifying Pathway
Act via the GLP-1/GIP receptor – G Protein coupled
Increase in cAMP acts in many ways (not fully understood) to:

close KATP channel (PKA)
Modulate calcium currents (PKA)
Directly on Insulin secretory mechanism via EPAC/Rim/Piccolo

The net result is primarily augmentation of insulin secretion when the pathway is triggered (by glucose or sulphonylureas)

no hypoglycaemia

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15
Q

what drugs act on the incretin axis?

A

DPP4 inhibitors (gliptins)
GLP-1 receptor agonists
Metformin
bile acids

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16
Q

what does metformin do?

A

Metformin may reduce hepatic glucose production but this is only a small part of its action

Metformin works primarily in the gut; increases GLP-1 concentrations

Metformin does not need to get into the liver to work (in patients with T2DM)

Intraduodenal Metformin>Portal Metformin>intravenous metformin

Delayed release metformin is effective, yet systemic metformin levels are low

17
Q

what are benefits of GLP-1RA? (exenatide, liraglutide)

A

Promote insulin secretion from pancreas without hypoglycaemia

Suppress glucagon (which is increased in T2DM)

Decrease gastric emptying – early satiety

Act on hypothalamus – reduce appetite – resulting weight loss (~3kg)

Cardiovascular Benefits

18
Q

what are down sides of GLP-1RA?

A

Nausea – usually resolves in most by 6-8 weeks

Injectable

Pancreatitis?

19
Q

describe DPP4i

A

DPP4i increase GLP-1 concentrations (by inhibiting breakdown). Weight neutral. Increase insulin secretion (glucose regulated). Not potent. CV neutral.

20
Q

what has CV benefit?

A

SGLT2i
GLP-1
pioglitazone

21
Q

what happens to the incretin effect in T2DM?

A

The incretin effect is mediated via incretin peptides GIP and GLP-1 and is lost in T2DM; most likely due to impaired incretin action at the beta-cell

Diabetes (8 decks)

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