Search Results
Search for other papers by Maria Sörhede Winzell in
Google Scholar
PubMed
Search for other papers by Bo Ahrén in
Google Scholar
PubMed
the islet β-cell: augmentation of cell proliferation and inhibition of apoptosis . Endocrinology 144 5145 – 5148 . Drucker DJ 2006 The biology of incretin hormones . Cell Metabolism 3 153 – 165 . Drucker DJ Nauck MA 2006 The incretin system
Laboratory for Molecular Dynamics of Mental Disorders, RIKEN Center for Brain Science, Wako-shi, Saitama, Japan
Search for other papers by Takumi Nakamura in
Google Scholar
PubMed
Search for other papers by Kazuki Harada in
Google Scholar
PubMed
Search for other papers by Taichi Kamiya in
Google Scholar
PubMed
Search for other papers by Mai Takizawa in
Google Scholar
PubMed
Search for other papers by Jim Küppers in
Google Scholar
PubMed
Search for other papers by Kazuo Nakajima in
Google Scholar
PubMed
Search for other papers by Michael Gütschow in
Google Scholar
PubMed
Search for other papers by Tetsuya Kitaguchi in
Google Scholar
PubMed
Search for other papers by Kunihiro Ohta in
Google Scholar
PubMed
Search for other papers by Tadafumi Kato in
Google Scholar
PubMed
Search for other papers by Takashi Tsuboi in
Google Scholar
PubMed
Introduction Glucagon-like peptide-1 (GLP-1) is a member of the incretin family and is secreted by the gastrointestinal endocrine L cells ( Harada et al. 2017 , 2018 a , b , Drucker 2018 ). GLP-1 regulates the increase in insulin
Laboratory of Experimental Hormonology, Brussels Free University, Brussels, Belgium
Search for other papers by Verónica Sancho in
Google Scholar
PubMed
Laboratory of Experimental Hormonology, Brussels Free University, Brussels, Belgium
Search for other papers by María V Trigo in
Google Scholar
PubMed
Laboratory of Experimental Hormonology, Brussels Free University, Brussels, Belgium
Search for other papers by Nieves González in
Google Scholar
PubMed
Laboratory of Experimental Hormonology, Brussels Free University, Brussels, Belgium
Search for other papers by Isabel Valverde in
Google Scholar
PubMed
Laboratory of Experimental Hormonology, Brussels Free University, Brussels, Belgium
Search for other papers by Willy J Malaisse in
Google Scholar
PubMed
Laboratory of Experimental Hormonology, Brussels Free University, Brussels, Belgium
Search for other papers by María L Villanueva-Peñacarrillo in
Google Scholar
PubMed
incretin ( Creutzfeldt 2001 ) modulates the glucose transporter levels in 3T3-L1 adipocytes ( Wang et al. 1997 ) and in liver, fat tissue and skeletal muscle of normal and diabetic rats ( Villanueva-Peñacarrillo et al. 2001 b ). In fat tissue
Clayton Foundation Laboratories for Peptide Biology, Cellular and Metabolic Research Section, Salk Institute, 10100 North Torrey Pines Road, La Jolla, California 92037, USA
Search for other papers by Lykke Blaabjerg in
Google Scholar
PubMed
Search for other papers by Gitte L Christensen in
Google Scholar
PubMed
Search for other papers by Masahito Matsumoto in
Google Scholar
PubMed
Search for other papers by Talitha van der Meulen in
Google Scholar
PubMed
Search for other papers by Mark O Huising in
Google Scholar
PubMed
Search for other papers by Nils Billestrup in
Google Scholar
PubMed
Search for other papers by Wylie W Vale in
Google Scholar
PubMed
class B G-protein-coupled receptors (GPCRs), as do receptors for incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP1) ( Brubaker & Drucker 2002 ). This subclass of receptors couples with Gαs and
Search for other papers by Srividya Vasu in
Google Scholar
PubMed
Search for other papers by R Charlotte Moffett in
Google Scholar
PubMed
Search for other papers by Neville H McClenaghan in
Google Scholar
PubMed
Search for other papers by Peter R Flatt in
Google Scholar
PubMed
al . 2011 , Kielgast et al . 2011 , Unger 2013 ). Recent investigations together with our unpublished observations have revealed that disturbances in the intestinal L-cell population may contribute to the loss-of-functional incretin response in
Search for other papers by Özlem Erdogdu in
Google Scholar
PubMed
Search for other papers by Linnéa Eriksson in
Google Scholar
PubMed
Search for other papers by Hua Xu in
Google Scholar
PubMed
Search for other papers by Åke Sjöholm in
Google Scholar
PubMed
Search for other papers by Qimin Zhang in
Google Scholar
PubMed
Search for other papers by Thomas Nyström in
Google Scholar
PubMed
). Exendin-4, a stable incretin mimetic and GLP1 receptor agonist, has been shown to promote glucose-dependent insulin secretion in vitro ( Parkes et al . 2001 ). Besides its insulinotropic action, exendin-4 may also exert direct beneficial effects on
Search for other papers by Franziska Boess in
Google Scholar
PubMed
Search for other papers by Cristina Bertinetti-Lapatki in
Google Scholar
PubMed
Search for other papers by Sannah Zoffmann in
Google Scholar
PubMed
Search for other papers by Catherine George in
Google Scholar
PubMed
Search for other papers by Thomas Pfister in
Google Scholar
PubMed
Search for other papers by Adrian Roth in
Google Scholar
PubMed
Search for other papers by Serene M L Lee in
Google Scholar
PubMed
Search for other papers by Wolfgang E Thasler in
Google Scholar
PubMed
Search for other papers by Thomas Singer in
Google Scholar
PubMed
Search for other papers by Laura Suter in
Google Scholar
PubMed
Introduction Glucagon-like peptide 1 (GLP1) is an incretin hormone that promotes glucose-dependent stimulation of insulin and suppression of glucagon secretion, delays gastric emptying, and reduces energy intake. GLP1 also increases β-cell mass via
Search for other papers by Patricia K Russell in
Google Scholar
PubMed
Search for other papers by Michele V Clarke in
Google Scholar
PubMed
Search for other papers by Jarrod P Skinner in
Google Scholar
PubMed
Search for other papers by Tammy P S Pang in
Google Scholar
PubMed
Search for other papers by Jeffrey D Zajac in
Google Scholar
PubMed
Search for other papers by Rachel A Davey in
Google Scholar
PubMed
, which encodes dipeptidyl peptidase 4 (DPP4). DPP4 plays a major role in glucose metabolism by degrading incretins, the gastrointestinal hormones that increase insulin secretion from β-cells after eating, before the rise in blood glucose ( Drucker & Nauck
Search for other papers by Sushi Jiang in
Google Scholar
PubMed
Endoscopy Center, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China
Search for other papers by Hening Zhai in
Google Scholar
PubMed
Search for other papers by Danjie Li in
Google Scholar
PubMed
Search for other papers by Jiana Huang in
Google Scholar
PubMed
Search for other papers by Heng Zhang in
Google Scholar
PubMed
Search for other papers by Ziru Li in
Google Scholar
PubMed
Department of Surgery, University of Michigan Medical Center, Ann Arbor, Michigan, USA
Search for other papers by Weizhen Zhang in
Google Scholar
PubMed
Search for other papers by Geyang Xu in
Google Scholar
PubMed
sitagliptin as monotherapy on glycemic control in patients with type 2 diabetes . Diabetes Care 29 2632 – 2637 . ( doi:10.2337/dbib6-0703 ) Baggio LL Drucker DJ 2007 Biology of incretins: GLP-1 and GIP . Gastroenterology 132 2131 – 2157
Centre of Membrane Proteins and Receptors (COMPARE), Universities of Birmingham and Nottingham, Birmingham, UK
Search for other papers by Aqfan Jamaluddin in
Google Scholar
PubMed
Centre of Membrane Proteins and Receptors (COMPARE), Universities of Birmingham and Nottingham, Birmingham, UK
Search for other papers by Caroline M Gorvin in
Google Scholar
PubMed
Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory peptide, GIP) are gut-derived hormones known as incretins, as they promote the secretion of insulin. GLP-1 is processed from the pro