β-Arrestins as Important Regulators of Glucose and Energy Homeostasis.

Autor: Pydi SP; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, US Department of Health and Human Services, Bethesda, Maryland, USA; email: jurgenw@niddk.nih.gov.; Current affiliation: Department of Biological Sciences and Bioengineering, The Mehta Family Centre for Engineering in Medicine, Indian Institute of Technology, Kanpur, India., Barella LF; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, US Department of Health and Human Services, Bethesda, Maryland, USA; email: jurgenw@niddk.nih.gov., Zhu L; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, US Department of Health and Human Services, Bethesda, Maryland, USA; email: jurgenw@niddk.nih.gov., Meister J; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, US Department of Health and Human Services, Bethesda, Maryland, USA; email: jurgenw@niddk.nih.gov., Rossi M; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, US Department of Health and Human Services, Bethesda, Maryland, USA; email: jurgenw@niddk.nih.gov.; Current affiliation: Department of Applied Clinical and Biotechnology Sciences, University of L'Aquila, L'Aquila, Italy., Wess J; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, US Department of Health and Human Services, Bethesda, Maryland, USA; email: jurgenw@niddk.nih.gov.
Jazyk: angličtina
Zdroj: Annual review of physiology [Annu Rev Physiol] 2022 Feb 10; Vol. 84, pp. 17-40. Date of Electronic Publication: 2021 Oct 27.
DOI: 10.1146/annurev-physiol-060721-092948
Abstrakt: β-Arrestin-1 and -2 (also known as arrestin-2 and -3, respectively) are ubiquitously expressed cytoplasmic proteins that dampen signaling through G protein-coupled receptors. However, β-arrestins can also act as signaling molecules in their own right. To investigate the potential metabolic roles of the two β-arrestins in modulating glucose and energy homeostasis, recent studies analyzed mutant mice that lacked or overexpressed β-arrestin-1 and/or -2 in distinct, metabolically important cell types. Metabolic analysis of these mutant mice clearly demonstrated that both β-arrestins play key roles in regulating the function of most of these cell types, resulting in striking changes in whole-body glucose and/or energy homeostasis. These studies also revealed that β-arrestin-1 and -2, though structurally closely related, clearly differ in their metabolic roles under physiological and pathophysiological conditions. These new findings should guide the development of novel drugs for the treatment of various metabolic disorders, including type 2 diabetes and obesity.
Databáze: MEDLINE