Can We Delay or Even Reverse Diabetic Complications By Islet Transplantation?

Introduction

Hyperglycemia is the predominant alteration of diabetes and plays a central role in the initiation and progression of diabetic complications (2, 3). The Diabetes Control and Complications Trial (DCCT) was one of the first studies showing that intensive glycemic treatment, obtained by multiple daily insulin injections, reduces the incidence of vascular complications and slows their progression when compared to conventional therapy (4). After the original trial, most participants of the DCCT continued to be followed up in the Epidemiology of Diabetes Interventions and Complications (EDIC) study, which demonstrated the long-term benefits of close glycemic control. The EDIC results demonstrated that the reduced rate of progressive retinopathy and nephropathy, as a result of intensive therapy, persist beyond the period of strictest intervention (5, 6). Although the incidence of clinical neuropathy during DCCT was low, polyneuropathy and cardiovascular autonomic neuropathy emerged during EDIC, suggesting the attainable intensive glycemic control is necessary but perhaps insufficient to prevent adverse nervous system effects (7).

Abstract

Treatment of diabetes is of crucial importance not only for glycemic control but also for the prevention of complications that causes irreversible damage to peripheral nerves, heart, kidney, and eyes. Despite a major effort to obtain prolonged metabolic control, diabetes complication can only be delayed in time. In a recent publication we investigated the effect of islet transplantation on diabetic complications in a rat model of streptozotocin-induced diabetes (1). We reported that islet transplantation induced an amelioration of impaired nociceptive threshold and normalization of nerve conduction velocity in diabetic rats. Cardiomyocyte loss was also reduced by islet transplantation and the observed mild kidney damage of diabetic rats was prevented. We concluded that transplantation of pancreatic islets, besides controlling glycemia, induced regression of neuropathy and prevented cardiovascular alterations, which was always there supporting the potential of islet transplantation. In this review we compare our recently published data with previous reports on prevention and regression of diabetic neuropathy, cardiovascular disease, nephropathy, and retinopathy with a particular attention to those on animal models of diabetes. In details, the potential of islet transplantation in inducing the regression of diabetic complications is discussed.

Keywords

islet transplantation, diabetic complications, neuropathy, retinopathy, nephropathy, cardiovascular disease