Lixisenatide requires a functional gut-vagus nerve-brain axis to trigger insulin secretion in controls and type 2 diabetic mice

• Published in: American journal of physiology: Gastrointestinal and liver physiology Vol. 315; no. 5; pp. G671 - G684
• Main Authors: Charpentier, Julie, Waget, Aurélie, Klopp, Pascale, Magnan, Christophe, Cruciani-Guglielmacci, Céline, Lee, Shin Jae, Burcelin, Rémy, Grasset, Estelle
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.11.2018
• Subjects: Animal models; Blood glucose; Brain stem; c-Fos protein; Diabetes; Diabetes mellitus; Firing rate; Gastric emptying; Glucagon; Glucagon-like peptide 1; Glucose; High fat diet; Insulin; Insulin resistance; Insulin secretion; Laboratory animals; Life Sciences; Secretion; Solitary tract nucleus; Vagus nerve; vagus nerve; autonomic nervous system; GLP-1 receptor agonist; GLP-1 analogs; incretin; PEPTIDE-1 RECEPTOR; CELLS; ACTIVATION; TRUNCALLY VAGOTOMIZED SUBJECTS; FOOD-INTAKE; GLUCOSE; INCREASES; GLP-1 RECEPTOR AGONIST; SENSOR; EXPRESSION

Endogenous glucagon-like peptide-1 (GLP-1) regulates glucose-induced insulin secretion through both direct β-cell-dependent and indirect gut-brain axis-dependent pathways. However, little is known about the mode of action of the GLP-1 receptor agonist lixisenatide. We studied the effects of lixisena...