Advances in the physiology of gastric emptying

Abstract

There have been many recent advances in the understanding of various aspects of the physiology of gastric motility and gastric emptying. Earlier studies had discovered the remarkable ability of the stomach to regulate the timing and rate of emptying of ingested food constituents and the underlying motor activity. Recent studies have shown that two parallel neural circuits, the gastric inhibitory vagal motor circuit (GIVMC) and the gastric excitatory vagal motor circuit (GEVMC), mediate gastric inhibition and excitation and therefore the rate of gastric emptying. The GIVMC includes preganglionic cholinergic neurons in the DMV and the postganglionic inhibitory neurons in the myenteric plexus that act by releasing nitric oxide, ATP, and peptide VIP. The GEVMC includes distinct gastric excitatory preganglionic cholinergic neurons in the DMV and postganglionic excitatory cholinergic neurons in the myenteric plexus. Smooth muscle is the final target of these circuits. The role of the intramuscular interstitial cells of Cajal in neuromuscular transmission remains debatable. The two motor circuits are differentially regulated by different sets of neurons in the NTS and vagal afferents. In the digestive period, many hormones including cholecystokinin and GLP‐1 inhibit gastric emptying via the GIVMC, and in the inter‐digestive period, hormones ghrelin and motilin hasten gastric emptying by stimulating the GEVMC. The GIVMC and GEVMC are also connected to anorexigenic and orexigenic neural pathways, respectively. Identification of the control circuits of gastric emptying may provide better delineation of the pathophysiology of abnormal gastric emptying and its relationship to satiety signals and food intake.

The novel dual glucose‐dependent insulinotropic polypeptide and glucagon‐like peptide‐1 (GLP‐1) receptor agonist tirzepatide transiently delays gastric emptying similarly to selective long‐acting GLP‐1 receptor agonists

“…Gastric emptying is one of the critical factors affecting postprandial glycaemia and food intake, which is a complex interplay involving gastric, intestinal and central neuronal and humoral mechanisms. 11 The role of GLP-1 in GE has been intensively studied. 12 Research on GIP and its effect in GE is limited.…”

Increased expression of CART, nNOS, VIP, PACAP, SP and GAL in enteric neurons of the porcine stomach prepyloric region following hydrochloric acid infusion

“…Gastric motility is regulated by neural circuits that affect smooth muscle contractility. Current studies have shown that the gastric inhibitory vagal motor circuit that comprises DMX-located preganglionic cholinergic neurons and postganglionic neurons of the myenteric plexus also mediates inhibition of gastric emptying [53]. Vagal stimulation of the myenteric neurons relaxes the smooth muscles by releasing VIP and NO [54].…”

Slowed gastric emptying and improved oral glucose tolerance produced by a nanomolar‐potency inhibitor of calcium‐activated chloride channel TMEM16A

“…The rate of gastric emptying, which depends on ingested food volume, osmolality, chemical composition, and caloric content, is an important determinant of digestion and nutrient absorption in small intestine (45). Liquids generally exit the stomach much faster than solid foods.…”

“…The rate of gastric emptying of carbohydrates and simple sugars is particularly important for postprandial elevations in blood glucose (16). In the clinical setting, measurement of gastric emptying uses a [ 13 C] or [ 99m Tc]-DTPA-labeled egg white meal with breath testing or scintigraphy readouts, respectively (45). [ 13 C] breath testing following an egg white meal is also used in mice, with time to empty half of the stomach contents generally between 60 and 90 min (38,46).…”