( Bjorbaek & Kahn 2004 ). Leptin also inhibits AMP-activated protein kinase (AMPK) activity in the arcuate nucleus and in the paraventricular nucleus of the hypothalamus ( Minokoshi et al . 2004 ). Glucagon-like peptide-1 (GLP1), a gastrointestinal hormone
Sayaka Akieda-Asai, Paul-Emile Poleni, Kazuya Hasegawa, and Yukari Date
Paul Millar, Nupur Pathak, Vadivel Parthsarathy, Anthony J Bjourson, Maurice O’Kane, Varun Pathak, R Charlotte Moffett, Peter R Flatt, and Victor A Gault
surge in the number of new drug classes such as glucagon-like peptide-1 (GLP-1) agonists, dipeptidylpeptidase-4 (DPP4) inhibitors and sodium glucose cotransporter-2 (SGLT2) inhibitors ( Bailey et al . 2016 ). Although these agents may be used as
Akiko Mizokami, Satoru Mukai, Jing Gao, Tomoyo Kawakubo-Yasukochi, Takahito Otani, Hiroshi Takeuchi, Eijiro Jimi, and Masato Hirata
et al. 2014 ) or indirectly through stimulation of the secretion of glucagon-like peptide-1 (GLP-1) from intestinal endocrine cells ( Mizokami et al. 2013 , 2014 ). GLP-1 is a member of the incretin family of hormones that are secreted from
Yingxin Xian, Zonglan Chen, Hongrong Deng, Mengyin Cai, Hua Liang, Wen Xu, Jianping Weng, and Fen Xu
visceral omental fat in subjects with obesity exhibit severely impaired endothelium-dependent vasodilation ( Farb et al. 2012 ). Clinical studies demonstrated that exenatide, a glucagon-like peptide 1 (GLP-1) receptor agonist, improved glycemic control
Christian Hölscher
Introduction The main hallmark of type 2 diabetes mellitus (T2DM) is insulin desensitisation. The discovery that the incretin hormone glucagon-like peptide 1 (GLP-1) facilitates insulin release during episodes of hyperglycaemia and has several
Berit Svendsen, Ramona Pais, Maja S Engelstoft, Nikolay B Milev, Paul Richards, Charlotte B Christiansen, Kristoffer L Egerod, Signe M Jensen, Abdella M Habib, Fiona M Gribble, Thue W Schwartz, Frank Reimann, and Jens J Holst
Introduction The incretin hormones, glucagon-like peptide-1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP) strongly potentiate postprandial insulin secretion and are therefore important regulators of glucose homeostasis. They are
Eun Young Lee, Shuji Kaneko, Promsuk Jutabha, Xilin Zhang, Susumu Seino, Takahito Jomori, Naohiko Anzai, and Takashi Miki
Introduction Oral ingestion of nutrients triggers the secretion of gut hormones from various enteroendocrine cells ( Ezcurra et al . 2013 , Cho et al . 2014 ). Among these, glucagon-like peptide 1 (GLP1) and glucose-dependent insulinotropic
Rebecca McGirr, Leonardo Guizzetti, and Savita Dhanvantari
al . 1994 , Furuta et al . 2001 ). By contrast, proglucagon is processed to glucagon-like peptide (GLP)-1 and GLP-2 in the intestine and brain by PC1/3 ( Dhanvantari et al . 1996 , Dhanvantari & Brubaker 1998 , Damholt et al . 1999 ). Glucagon
J C Parker, K S Lavery, N Irwin, B D Green, B Greer, P Harriott, F P M O’Harte, V A Gault, and P R Flatt
Introduction Glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are important gastrointestinal-releasing hormones involved in the regulation of postprandial nutrient homeostasis ( Meier et al
G Üçkaya, P Delagrange, A Chavanieu, G Grassy, M-F Berthault, A Ktorza, E Cerasi, G Leibowitz, and N Kaiser
that aim to improve β-cell function and survival. Glucagon-like peptide 1 (GLP-1) is a potent incretin hormone secreted by the intestinal L cells in response to food intake ( Drucker 2001 ). GLP-1 exerts multiple effects on pancreatic β
