β-Cells are the core effector of glycemic control, and when largely lost in the course of type 1 diabetes, glycemic control is no longer guaranteed. Although glycemic control can be established by insulin injections, diabetic patients still suffer from microvascular (nephropathy, retinopathy, neuropathy) and macrovascular (ischemic heart disease, cerebrovascular disease, peripheral vascular disease) complications, resulting in a lower life expectancy (1). Therefore, islet transplantation has been implemented as one therapeutic means to achieve a more physiologic form of glycemic control. Although high rates of insulin independence can be achieved shortly after transplantation, the rate of insulin independence after longer time intervals remains suboptimal, especially in view of the potential complications of immunosuppressive treatment (2). One of the reasons for the limited clinical success of islet transplantation is the exposure of the islets to stress prior to and in the first weeks after transplantation. The liver may actually not be an optimal transplantation site (although it connects the islets to the blood flow from the portal vein). Also, it has been shown that islet grafts will only be fully vascularized after 1–2 weeks, reaching the final state of vascularization even later (3). As a consequence of the lack of nutrients and hypoxia, together with other factors such as hyperglycemia and immunosuppressant toxicity, to name only two of them, a considerable proportion of the transplanted β-cells will undergo apoptosis, further limiting the success of islet transplantation. In order …
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Martin Gotthardt (2011) studied this question.
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