Rapid Gastric Emptying in Diabetes Mellitus: Pathophysiology and Clinical Importance
Overview
Affiliations
Although slow gastric emptying (gastroparesis) is a well-known complication of chronic hyperglycemia in diabetes mellitus (DM), it recently has become clear that rapid gastric emptying also is a frequent and important diabetic complication. In contrast, acute hyperglycemia causes slow gastric emptying, and acute hypoglycemia causes rapid gastric emptying. Rapid gastric emptying is frequent in T2DM; however, it may also occur in T1DM, particularly in the early stages of the disease, but may persist even into late stages. Recent studies suggest that usually, the stomach restricts the emptying of nutrients to 1-4 kcals/min. This restriction is due to the action of the gastric 'braking' hormones such as GLP-1, leptin, and amylin acting via the gastric inhibitory vagal motor circuit (GIVMC). Disruption of this braking system leads to rapid gastric emptying. Acute hyperglycemia also slows gastric emptying by stimulating the GIVMC, while acute hypoglycemia causes rapid gastric emptying by stimulating the gastric excitatory vagal motor circuit (GEVMC). In contrast, chronic hyperglycemia causes rapid gastric emptying by inducing oxidative stress in the stomach wall that disrupts inhibitory neuromuscular transmission and increases the contractility of the smooth muscle, while chronic hyperglycemia may also cause slow gastric emptying via severe inflammatory stress caused by proinflammatory macrophages and reduce contractility of the smooth muscle. There is a bidirectional relationship between blood glucose and gastric emptying. Thus, rapid gastric emptying may lead to a sizeable postprandial spike, and slow gastric emptying may blunt it. Postprandial hyperglycemia is involved in the development, progression, and complications of DM. Correction of fast gastric emptying involves agents that activate GIVMC and the use of gastric 'braking' hormones or their analogs. Recognition and treatment of rapid gastric emptying may contribute to better management of postprandial hyperglycemia and prevention of some diabetic complications.
Inan S, Erdivanli B J Clin Med. 2025; 14(2).
PMID: 39860647 PMC: 11766326. DOI: 10.3390/jcm14020641.
Robinson-Papp J, Mehta M, Mueller B, Neupane N, Zhao Z, Cedillo G medRxiv. 2024; .
PMID: 39399020 PMC: 11469347. DOI: 10.1101/2024.09.25.24314370.
Manipulation of Post-Prandial Hyperglycaemia in Type 2 Diabetes: An Update for Practitioners.
Shibib L, Al-Qaisi M, Guess N, Miras A, Greenwald S, Pelling M Diabetes Metab Syndr Obes. 2024; 17:3111-3130.
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Rieck J, Heidinger H, Schloricke E, Schmidt N, Krause S Langenbecks Arch Surg. 2024; 409(1):94.
PMID: 38472479 DOI: 10.1007/s00423-024-03283-2.
Gunther R, Banks K, McWhorter N J Nucl Med Technol. 2024; 52(1):52-54.
PMID: 38443110 PMC: 10924154. DOI: 10.2967/jnmt.123.266808.