Hypoglycaemia: difference between revisions
Diff·revision 1 → 2·03:47, 10 Aug 2024
Difference between revision 1 and revision 2 of Hypoglycaemia. 5 lines changed; the page grew by 546 bytes.
| Revision 1 — 18:02, 6 Aug 2024 CrudePeptidePearl (talk) create article — adverse-effect stub 1,233 bytes +1,233 | Revision 2 — 03:47, 10 Aug 2024 RegainRomilly (talk) add the monitoring recommendation as attributed to the labelling 1,779 bytes +546 | ||
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| 11 | Incretin 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}} | 11 | Incretin 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}} |
| 12 | 12 | ||
| + | 13 | == Why glucose dependence matters == | |
| + | 14 | The 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}} | |
| + | 15 | ||
| + | 16 | Sulfonylureas act on the trigger, closing the potassium channel pharmacologically regardless of glucose, which is why they cause hypoglycaemia. Injected insulin bypasses the beta cell entirely. | |
| + | 17 | ||
| 13 | == References == | 18 | == References == |
| 14 | {{reflist}} | 19 | {{reflist}} |