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Hypoglycaemia: difference between revisions

Diff·revision 3 → 4·10:26, 5 Sep 2024

Difference between revision 3 and revision 4 of Hypoglycaemia. 2 lines changed; the page grew by 235 bytes.

Revision 3 — 06:20, 17 Aug 2024
BiliaryBea (talk)
expand §Why glucose dependence matters
1,779 bytes ±0
Revision 4 — 10:26, 5 Sep 2024
MTC_Marisol (talk)
add the interaction with the mechanism that explains it
2,014 bytes +235
11Incretin agonists carry a low intrinsic risk because their action on [[Insulin secretion|insulin secretion]] is glucose-dependent: they amplify a response that glucose has initiated rather than initiating one. Below the glucose threshold for triggering, there is nothing to amplify.{{r|nauck2016}}11Incretin agonists carry a low intrinsic risk because their action on [[Insulin secretion|insulin secretion]] is glucose-dependent: they amplify a response that glucose has initiated rather than initiating one. Below the glucose threshold for triggering, there is nothing to amplify.{{r|nauck2016}}
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+13Risk arises when they are combined with agents that are not glucose-dependent — insulin and sulfonylureas — and the usual response on initiating an incretin agonist alongside either is to reduce the background agent.{{r|ada2024}}
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13== Why glucose dependence matters ==15== Why glucose dependence matters ==
14The beta cell distinguishes a triggering signal from an amplifying one. Glucose metabolism raises the ATP:ADP ratio, closes potassium channels and admits calcium — the trigger. Incretin signalling raises cAMP, which increases the amount of insulin released per unit of calcium — the amplifier.{{r|nauck2016}}16The beta cell distinguishes a triggering signal from an amplifying one. Glucose metabolism raises the ATP:ADP ratio, closes potassium channels and admits calcium — the trigger. Incretin signalling raises cAMP, which increases the amount of insulin released per unit of calcium — the amplifier.{{r|nauck2016}}