Inter-relationships between gastric emptying and glycaemia: Implications for clinical practice

Abstract

Gastric emptying (GE) exhibits a wide inter-individual variation and is a major determinant of postprandial glycaemia in health and diabetes; the rise in blood glucose following oral carbohydrate is greater when GE is relatively more rapid and more sustained when glucose tolerance is impaired. Conversely, GE is influenced by the acute glycaemic environment acute hyperglycaemia slows, while acute hypoglycaemia accelerates it. Delayed GE (gastroparesis) occurs frequently in diabetes and critical illness. In diabetes, this poses challenges for management, particularly in hospitalised individuals and/or those using insulin. In critical illness it compromises the delivery of nutrition and increases the risk of regurgitation and aspiration with consequent lung dysfunction and ventilator dependence. Substantial advances in knowledge relating to GE, which is now recognised as a major determinant of the magnitude of the rise in blood glucose after a meal in both health and diabetes and, the impact of acute glycaemic environment on the rate of GE have been made and the use of gut-based therapies such as glucagon-like peptide-1 receptor agonists, which may profoundly impact GE, in the management of type 2 diabetes, has become commonplace. This necessitates an increased understanding of the complex inter-relationships of GE with glycaemia, its implications in hospitalised patients and the relevance of dysglycaemia and its management, particularly in critical illness. Current approaches to management of gastroparesis to achieve more personalised diabetes care, relevant to clinical practice, is detailed. Further studies focusing on the interactions of medications affecting GE and the glycaemic environment in hospitalised patients, are required.

Keywords: Glycaemia; Gastric emptying; Clinical practice; Glucagon-like peptide-1

Core Tip: Gastric emptying (GE) is a major determinant of postprandial glycaemia in health, diabetes and critical illness. Acute hyperglycaemia slows GE while insulin-induced hypoglycaemia accelerates it. Gastroparesis occurs frequently in diabetes and critical illness with a weak correlation between gastrointestinal symptoms and GE. Accordingly, diagnosis of gastroparesis should ideally be made after measuring GE with an optimal technique. Glucagon-like peptide-1 receptor agonists, commonly used in the treatment of type 2 diabetes and increasingly in obesity, may profoundly impact GE. We explore the rationale for current glycaemic targets and the implications of dysglycaemia and its management in hospitalised and critically ill populations.