| Class | Oral hypoglycaemic |
|---|---|
| Chemistry |
Meglitinide |
| Routes of administration |
Oral only |
| Absorption |
Completely absorbed, oral bioavailability 62% |
| Solubility |
pKa=4.8; poorly water-soluble, but good lipid solubility |
| Distribution |
VOD= 0.4L/kg; 97% protein bound |
| Metabolism |
Extensive hepatic metabolism |
| Elimination |
90% of the inactive metabolites are eliminated in the faeces |
| Time course of action |
Half life 60 minutes |
| Target receptor |
Sulfonylurea receptors (SUR1 and SUR2), which form a part of the ATP-sensitive potassium channel complex on pancreatic β-cells |
| Mechanism of action |
By binding to the ATP-sensitive K channel, meglitinides act like ATP (i.e. same as a rise in blood glucose), closing the channel and stopping the efflux of potassium from the cell, which promotes depolarisation. The depolarisation then leads to insulin release |
| Clinical effects |
Hypoglycaemia, but also: |
| Literature reference |
Scott, 2012 |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |