Author:
Oliveira de Souza Camila,Sun Xuenan,Oh Dayoung
Abstract
Seven transmembrane receptors (7TMRs), often termed G protein-coupled receptors (GPCRs), are the most common target of therapeutic drugs used today. Many studies suggest that distinct members of the GPCR superfamily represent potential targets for the treatment of various metabolic disorders including obesity and type 2 diabetes (T2D). GPCRs typically activate different classes of heterotrimeric G proteins, which can be subgrouped into four major functional types: Gαs, Gαi, Gαq/11, and G12/13, in response to agonist binding. Accumulating evidence suggests that GPCRs can also initiate β-arrestin-dependent, G protein-independent signaling. Thus, the physiological outcome of activating a certain GPCR in a particular tissue may also be modulated by β-arrestin-dependent, but G protein-independent signaling pathways. In this review, we will focus on the role of G protein- and β-arrestin-dependent signaling pathways in the development of obesity and T2D-related metabolic disorders.
Funder
National Institute of Diabetes and Digestive and Kidney Diseases
American Heart Association
Subject
Endocrinology, Diabetes and Metabolism
Reference131 articles.
1. Mechanisms Linking Obesity to Insulin Resistance and Type 2 Diabetes;Kahn;Nature,2006
2. The Epidemic of Obesity and Diabetes: Trends and Treatments;Barnes;Texas Heart Institute J,2011
3. Beta Cell Dysfunction and Insulin Resistance;Cerf;Front Endocrinol,2013
4. Islet Beta Cell Failure in Type 2 Diabetes;Prentki;J Clin Invest,2006
Cited by
10 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献