Gastric emptying (revision 5)

Gastric emptying is the rate at which the contents of the stomach are delivered to the duodenum. It is regulated by fundic tone, antral contraction and pyloric resistance, and is modulated by feedback from nutrients already in the small intestine — the mechanism by which Glucagon-like peptide-1 and other gut hormones slow it.^[1]

Delayed emptying is one of the principal actions of GLP-1 receptor agonists. It blunts the postprandial glucose excursion by delivering carbohydrate to the absorptive surface more slowly, and it contributes to early satiety through gastric distension. In short-acting agonists it accounts for a substantial part of the postprandial glycaemic effect.^[1]

The delay attenuates with continued exposure to a long-acting agonist — a rare instance of clinically relevant tachyphylaxis in this class — which is why the glycaemic contribution of delayed emptying is larger for short-acting agents such as exenatide and lixisenatide than for weekly agents.^[2]

Liquids empty approximately exponentially and rapidly; solids empty after a lag phase during which food is triturated to particles small enough to pass the pylorus, then at an approximately linear rate. A half-emptying time of about 45–90 minutes is usual for a standard solid meal, with wide interindividual variation.^[1]

Rate is regulated to deliver nutrient to the small intestine at a roughly constant caloric rate, near 2 kcal per minute, regardless of meal composition. The regulator is feedback from nutrient sensing in the duodenum and ileum, mediated by cholecystokinin, GLP-1, peptide YY and neural reflexes — the so-called ileal brake.^[3]

Measurement methods are not interchangeable. Scintigraphy is the reference technique; the ¹³C-octanoate breath test is a validated surrogate; paracetamol absorption is convenient but measures liquid-phase emptying only. A study reporting "delayed emptying" without naming its method is not comparable with one that names a different method.