Duodenal fat, acid, hypertonicity and protein all slow emptying
Expansion
Slowed by (all duodenal feedback)
- Fat, the most potent inhibitor, via cholecystokinin
- Acid, via secretin
- Hypertonicity
- Protein and amino acids
- Distension of the duodenum, via the enterogastric reflex
Slowed by other factors: sympathetic activity, pain, anxiety, opioids, anticholinergics, diabetic autonomic neuropathy, pregnancy, and critical illness.
Accelerated by: gastric distension, gastrin, liquids as opposed to solids, and prokinetics such as metoclopramide and erythromycin.
Emptying is roughly exponential for liquids and linear after a lag phase for solids, with indigestible solids cleared later by the migrating motor complex.
Two clinical consequences: gastroparesis in diabetes causes early satiety, vomiting and erratic glycaemic control; and after gastric surgery the loss of this feedback causes dumping syndrome, with rapid delivery of hyperosmolar chyme producing fluid shift and vasomotor symptoms early, and reactive hypoglycaemia later.