Secretion of glucagon-like peptide-1 (GLP-1) in type 2 diabetes: what is up, what is down

• Published in: Diabetologia Vol. 54; no. 1; pp. 10 - 18
• Main Authors: Nauck, M. A, Vardarli, I, Deacon, C. F, Holst, J. J, Meier, J. J
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Berlin/Heidelberg : Springer-Verlag 2011; Springer-Verlag; Springer; Springer Nature B.V
• Subjects: Animals; Biological and medical sciences; Diabetes; Diabetes Mellitus, Type 2 - metabolism; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Glucagon; Glucagon-Like Peptide 1 - metabolism; Glucagon-Like Peptide 1 - secretion; Glucagon-like peptide-1; Glucose; Gut hormones; Hormones; Human Physiology; Humans; Hypotheses; Incretin hormones; Incretins - metabolism; Insulin; Internal Medicine; L-cell; Meals; Medical sciences; Medicine; Medicine & Public Health; meta-analysis; Meta-Analysis as Topic; Metabolic Diseases; Models, Biological; Pathophysiology; Peptides; Proteins; Review; Germany; Glucagon-like peptide-1; Gut hormones; Pathophysiology; Incretin hormones; L-cell; Review; Meta-analysis; Endocrinopathy; Type 2 diabetes; Immunopathology; Incretin; Digestive system; Secretion; Gut; Autoimmune disease; Metabolic diseases; Glucagon like peptide 1; Gastrointestinal hormone; Type 1 diabetes
• ISSN: 0012-186X; 1432-0428; 1432-0428
• DOI: 10.1007/s00125-010-1896-4

The incretin hormones gastric inhibitory polypeptide and especially glucagon-like peptide (GLP) have an important physiological function in augmenting postprandial insulin secretion. Since GLP-1 may play a role in the pathophysiology and treatment of type 2 diabetes, assessment of meal-related GLP-1 secretory responses in type 2 diabetic patients vs healthy individuals is of great interest. A common view states that GLP-1 secretion in patients with type 2 diabetes is deficient and that this applies to a lesser degree in individuals with impaired glucose tolerance. Such a deficiency is the rationale for replacing endogenous incretins with GLP-1 receptor agonists or re-normalising active GLP-1 concentrations with dipeptidyl peptidase-4 inhibitors. This review summarises the literature on this topic, including a meta-analysis of published studies on GLP-1 secretion in individuals with and without diabetes after oral glucose and mixed meals. Our analysis does not support the contention of a generalised defect in nutrient-related GLP-1 secretory responses in type 2 diabetes patients. Rather, factors are identified that may determine individual incretin secretory responses and explain some of the variations in published findings of group differences in GLP-1 responses to nutrient intake.