Vascular pericytes and the broader vasculature play a critical, underappreciated role in insulin secretion, islet function, and peripheral insulin delivery in the pathogenesis of type 2 diabetes.
The pathogenesis of type 2 diabetes is intimately intertwined with the vasculature. Insulin must efficiently enter the bloodstream from pancreatic beta-cells, circulate throughout the body, and efficiently exit the bloodstream to reach target tissues and mediate its effects. Defects in the vasculature of pancreatic islets can lead to diabetic phenotypes. Similarly, insulin resistance is accompanied by defects in the vasculature of skeletal muscle, which ultimately reduce the ability of insulin and nutrients to reach myocytes. An underappreciated participant in these processes is the vascular pericyte. Pericytes, the smooth muscle-like cells lining the outsides of blood vessels throughout the body, have not been directly implicated in insulin secretion or peripheral insulin delivery. Here, we review the role of the vasculature in insulin secretion, islet function, and peripheral insulin delivery, and highlight a potential role for the vascular pericyte in these processes.
Richards et al. (Tue,) conducted a review in Type 2 diabetes and insulin resistance. Vascular pericytes and endothelial cells was evaluated. Vascular pericytes and the broader vasculature play a critical, underappreciated role in insulin secretion, islet function, and peripheral insulin delivery in the pathogenesis of type 2 diabetes.