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GLP‐1R and amylin agonism in metabolic disease: complementary mechanisms and future opportunities
Author(s) -
Roth Jonathan D,
Erickson Mary R,
Chen Steve,
Parkes David G
Publication year - 2012
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2011.01537.x
Subject(s) - amylin , exenatide , incretin , glucagon like peptide 1 , agonism , gastric emptying , hormone , liraglutide , endocrinology , receptor , medicine , insulin , diabetes mellitus , type 2 diabetes , bioinformatics , biology , islet , stomach , politics , political science , law
The discoveries of the incretin hormone glucagon-like peptide-1 (GLP-1) and the β-cell hormone amylin have translated into hormone-based therapies for diabetes. Both classes of molecules also exhibit weight-lowering effects and have been investigated for their anti-obesity potential. In the present review, we explore the mechanisms underlying the physiological and pharmacological actions of GLP-1 and amylin agonism. Despite their similarities (e.g. both molecular classes slow gastric emptying, decrease glucagon and inhibit food intake), there are important distinctions between the central and/or peripheral pathways that mediate their effects on glycaemia and energy balance. We suggest that understanding the similarities and differences between these molecules holds important implications for the development of novel, combination-based therapies, which are increasingly the norm for diabetes/metabolic disease. Finally, the future of GLP-1- and amylin agonist-based therapeutics is discussed.