1 results match your criteria: "Ludgwig-Maximilians-University Munich[Affiliation]"
Loss of GIPR in LEPR cells impairs glucose control by GIP and GIP:GLP-1 co-agonism without affecting body weight and food intake in mice.
Mol Metab
May 2024
Institute for Diabetes and Obesity, Helmholtz Munich, Neuherberg, Germany; German Center for Diabetes Research (DZD), Neuherberg, Germany; Walther-Straub-Institute for Pharmacology and Toxicology, Ludgwig-Maximilians-University Munich, Germany. Electronic address:
Objective: The glucose-dependent insulinotropic polypeptide (GIP) decreases body weight via central GIP receptor (GIPR) signaling, but the underlying mechanisms remain largely unknown. Here, we assessed whether GIP regulates body weight and glucose control via GIPR signaling in cells that express the leptin receptor (Lepr).
Methods: Hypothalamic, hindbrain, and pancreatic co-expression of Gipr and Lepr was assessed using single cell RNAseq analysis.