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.