INTRODUCTION: Glucagon-like peptide 1 (GLP-1), a gastrointestinal peptide and central mediator of glucose metabolism, is secreted by L cells in the intestine in response to food intake. Postprandial secretion of GLP-1 is triggered by nutrient sensing via transporters and G protein-coupled receptors (GPCRs). GLP-1 secretion may be lower in adults with obesity (OW) or type 2 diabetes mellitus (T2DM) than in those with normal glucose tolerance (NGT), but these findings are inconsistent. Because of the actions of GLP-1 on stimulating insulin secretion and promoting weight loss, GLP-1 and its analogs are used in pharmacological preparations for the treatment of T2DM. However, physiologically stimulated GLP-1 secretion through the diet might be a preventive or synergistic method for improving glucose metabolism in individuals who are OW, or have impaired glucose tolerance (IGT) or T2DM.

RATIONALE: This narrative review focuses on fasting and postprandial GLP-1 secretion in individuals with different metabolic conditions and degrees of glucose intolerance. Further, the influence of relevant diet-related factors (e.g., specific diets, meal composition and size, phytochemical content, and gut microbiome) that could affect fasting and postprandial GLP-1 secretion are discussed.

RESULTS: Some studies showed a diminished glucose- or meal-stimulated GLP-1 response in participants with T2DM, IGT, or OW compared to those with NGT, whereas other studies have reported an elevated or unchanged GLP-1 response in T2DM or IGT. Meal composition, especially the relationship between macronutrients and interventions targeting the microbiome can impact postprandial GLP-1 secretion, although it is not clear which macronutrients are strong stimulants of GLP-1. Moreover, glucose tolerance, antidiabetic treatment, grade of overweight/obesity, and sex were important factors influencing GLP-1 secretion.

CONCLUSION: The results presented in this review highlight the potential of nutritional and physiological stimulation of GLP-1 secretion. Further research on fasting and postprandial GLP-1 levels and the resulting metabolic consequences under different metabolic conditions is needed.