The β-Cell/EC Axis: How Do Islet Cells Talk to Each Other?
- Heshan Peiris1⇑,
- Claudine S. Bonder2,
- P. Toby H. Coates3,4,
- Damien J. Keating1 and
- Claire F. Jessup1,3
- 1Department of Human Physiology, Centre for Neuroscience, Flinders University of South Australia, Adelaide, Australia
- 2Vascular Biology and Cell Trafficking Laboratory, Centre for Cancer Biology, South Australia Pathology, Adelaide, Australia
- 3Australian Islet Consortium, Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, Adelaide, Australia
- 4Centre for Clinical and Experimental Transplantation, The University of Adelaide, Adelaide, Australia
- Corresponding author: Claire F. Jessup, .
Within the pancreatic islet, the β-cell represents the ultimate biosensor. Its central function is to accurately sense glucose levels in the blood and consequently release appropriate amounts of insulin. As the only cell type capable of insulin production, the β-cell must balance this crucial workload with self-preservation and, when required, regeneration. Evidence suggests that the β-cell has an important ally in intraislet endothelial cells (ECs). As well as providing a conduit for delivery of the primary input stimulus (glucose) and dissemination of its most important effector (insulin), intraislet blood vessels deliver oxygen to these dense clusters of metabolically active cells. Furthermore, it appears that ECs directly impact insulin gene expression and secretion and β-cell survival. This review discusses the molecules and pathways involved in the crosstalk between β-cells and intraislet ECs. The evidence supporting the intraislet EC as an important partner for β-cell function is examined to highlight the relevance of this axis in the context of type 1 and type 2 diabetes. Recent work that has established the potential of ECs or their progenitors to enhance the re-establishment of glycemic control following pancreatic islet transplantation in animal models is discussed.
- Received April 18, 2013.
- Accepted September 7, 2013.
- © 2014 by the American Diabetes Association.
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