| Class | Pancreatic hormone analog |
|---|---|
| Chemistry |
Peptide hormone (29 amino acids) |
| Routes of administration |
IV, subcutaneous, IM |
| Absorption |
Essenially zero oral bioavailability. Absorbed well from subcutaneous depot, with onset of effect within about 20 minutes |
| Solubility |
pKa of around 7.1; poor water solubility at high concentrations (because it self-associates into a trimer) |
| Distribution |
VOD=0.25 L/kg; minimally protein bound |
| Metabolism |
30% metabolised in the liver, 30% metabolised in the kidney, the rest degraded by (probably) the reticuloendothelial system |
| Elimination |
Minimal free drug is eliminated in the urine |
| Time course of action |
Half life is about 20-30 minutes |
| Target receptor |
Glucagon receptors - G-protein (Gs and Gq) coupled receptors which activate adenylyl cyclase and therefore produce increased cAMP. |
| Mechanism of action |
By increasing intracellular cAMP, glycogen stimulates cAMP-dependent protein kinases and therefore activates pathways of glycogen breakdown and glucose release (among many metabolic pathways) |
| Clinical effects |
Mainly hepatic effects: Increased glycogenolysis, decreased glycogen synthesis, increased gluconeogenesis, decreased synthesis of VLDLs and increased β-oxidation of fatty acids, leading to ketosis. Also decreased release of insulin, decreased appetite, increased basal energy expenditure. In high doses, increased cardiac contractility and heart rate |
| Literature reference |
Müller et al, 2017 |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |