Side by side

1. 1.Slows gastric emptying, so glucose from a meal arrives more gradually.
2. 2.Suppresses glucagon release in a glucose-dependent manner, reducing hepatic glucose output after meals.
3. 3.Signals satiety centres in the hindbrain, reducing intake.
4. 4.Works alongside insulin rather than replacing it, smoothing the post-meal glucose curve.
5. 5.Amylin receptors are formed from calcitonin receptor plus receptor-activity-modifying proteins.

• Type 1 diabetes as an adjunct to insulin
• Type 2 diabetes on insulin therapy
• Postprandial glucose control
• Weight change in insulin-treated diabetes
• Gastric emptying research

• HbA1c reductions of roughly 0.3 to 0.6 percentage points
• Clearly blunted post-meal glucose rise
• Weight loss of about 1 to 2 kg in trials
• Increased fullness and reduced intake
• Frequent nausea limits dose escalation for some people

• Nausea, very common and dose-related
• Vomiting and anorexia
• Headache
• Hypoglycaemia, particularly in type 1 diabetes
• Injection-site reactions
• Reduced appetite severe enough to affect nutrition

Research context only - prescription medicine. US labelling starts at 15 micrograms subcutaneously before major meals in type 1 diabetes (60 micrograms in type 2) and escalates in 15-microgram steps to a maximum of 60 micrograms as tolerated, with mealtime insulin usually reduced to avoid hypoglycaemia. Trial durations ran 26 to 52 weeks.

Research context only