Signals in the pancreatic islet microenvironment influence β‐cell proliferation. (September 2017)

• Record Type: Journal Article
• Authors: Aamodt, Kristie I.; Powers, Alvin C.
• Other Names: Cerasi Erol guestEditor.; Accili Domenico guestEditor.; Ahrén Bo guestEditor.; Boitard Christian guestEditor.; Seino Susumu guestEditor.; Thorens Bernard guestEditor.
• Is Part Of: Diabetes, obesity & metabolism. Volume 19(2017)Supplement 1
• Page Start: 124
• Page End: 136
• Publication Date: 2017-09
• Subjects: beta‐cell -- islets; Diabetes -- Periodicals; Obesity -- Periodicals; Metabolism -- Disorders -- Periodicals; Clinical pharmacology -- Periodicals; 616.462
• DOI: 10.1111/dom.13031
• Languages: English
• ISSNs: 1462-8902

Abstract

Abstract : The progressive loss of pancreatic β‐cell mass that occurs in both type 1 and type 2 diabetes is a primary factor driving efforts to identify strategies for effectively increasing, enhancing or restoring β‐cell mass. While factors that seem to influence β‐cell proliferation in specific contexts have been described, reliable stimulation of human β‐cell proliferation has remained a challenge. Importantly, β‐cells exist in the context of a complex, integrated pancreatic islet microenvironment where they interact with other endocrine cells, vascular endothelial cells, extracellular matrix, neuronal projections and islet macrophages. This review highlights different components of the pancreatic microenvironment, and reviews what is known about how signaling that occurs between β‐cells and these other components influences β‐cell proliferation. Future efforts to further define the role of the pancreatic islet microenvironment on β‐cell proliferation may lead to the development of successful approaches to increase or restore β‐cell mass in diabetes.