| Literature DB >> 33358450 |
Sai P Pydi1, Luiz F Barella1, Jaroslawna Meister1, Jürgen Wess2.
Abstract
β-Arrestin-1 and -2 are intracellular proteins that are able to inhibit signaling via G protein-coupled receptors (GPCRs). However, both proteins can also modulate cellular functions in a G protein-independent fashion. During the past few years, studies with mutant mice selectivity lacking β-arrestin-1 and/or -2 in metabolically important cell types have led to novel insights into the mechanisms through which β-arrestins regulate key metabolic processes in vivo, including whole-body glucose and energy homeostasis. The novel information gained from these studies should inform the development of novel drugs, including β-arrestin- or G protein-biased GPCR ligands, that could prove useful for the therapy of several important pathophysiological conditions, including type 2 diabetes and obesity. Published by Elsevier Ltd.Entities:
Keywords: G protein-coupled receptors; diabetes; metabolism; mutant mice; obesity; β-arrestins
Mesh:
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Year: 2020 PMID: 33358450 PMCID: PMC7855863 DOI: 10.1016/j.tem.2020.11.008
Source DB: PubMed Journal: Trends Endocrinol Metab ISSN: 1043-2760 Impact factor: 12.015