Abstract
Diabetes mellitus is rapidly becoming the world’s most dangerous serial killer. Type 1 diabetes (T1D) is a currently incurable autoimmune disease marked by progressive, and eventually exhaustive, destruction of the insulin-producing pancreatic beta cells. Type 2 diabetes (T2D) describes the combination of insulin resistance in peripheral tissue, insufficient insulin secretion from the pancreatic beta cells, and excessive glucagon secretion from the pancreatic alpha cells. T1D as well as severe cases of T2D are treated with insulin replacement, which can merely be considered as life support for the acute phases of the disease. Islet replacement of insulin-producing pancreatic beta cells represents a potential treatment method for both insulin-depleted diabetes (T1D) and insulin-resistant diabetes (T2D) and may shift diabetes management from life saving measures to a cure. One of the key challenges in islet transplants is the generation of reactive oxygen species (ROS) and the associated oxidative stress, which restricts graft longevity. A major leak of ROS takes place during oxidative phosphorylation at mitochondrial electron transport chain (ETC). Additionally, hyperglycemia-induced superoxide (O2•-) production has been linked to the development and progression of diabetic complications, both macrovascular and microvascular. Decreasing ROS in diabetic patients may prevent the incidence of long term diabetes complications. This review provides an overview of the role of mitochondria in diabetes, introducing them as a possible target for future treatment of diabetes.
Highlights
The definite etiology of type 1 diabetes (T1D) is still obscure, but considered to root in a mixture of genetic predisposition and environmental factors, leading to continued autoimmunity.[1]
Type 2 diabetes (T2D) has been linked to "metabolic syndrome", which is defined by the International Diabetes Federation (IDF) as central obesity with two of the following: elevated blood pressure, elevated fasting plasma glucose, high serum triglycerides, and low high-density cholesterol (HDL) levels (Available from: http://www.idf.org/metabolic-syndrome, updated 2014 Oct 23; cited 2015 Jan 21)
A study by Barton and colleagues compared the efficacy of allogenic islet transplantation in T1D patients in different periods between 1999 and 2010.9 They analyzed 677 T1D patients who had received islet transplants, with the aim to examine the differences in transplant efficacy between the early (1999-2002), mid (2003-2006), or recent (2007-2010) transplant era
Summary
The definite etiology of type 1 diabetes (T1D) is still obscure, but considered to root in a mixture of genetic predisposition and environmental factors, leading to continued autoimmunity.[1]. The aims of diabetes management are primarily to save life in the short term and secondarily to prevent the development of diabetic complications in the long term. Both can be achieved by improving glycemic control, aiming for a glycated hemoglobin (HbA1c) between 6.5%-7.0%.4. Islet replacement of insulin-producing pancreatic beta cells represents a potential treatment method for both insulin-depleted and insulin-resistant diabetes.[8] Following islet transplantation the patients benefit from a decrease of hypoglycemic events, and spectacular improvement of HbA1c levels and stabilization of fasting blood glucose, without exposing themselves to the risk of major surgery as in whole pancreas transplantation.[8] A study by Barton and colleagues compared the efficacy of allogenic islet transplantation in T1D patients in different periods between 1999 and 2010.9 They analyzed 677 T1D patients who had received islet transplants, with the aim to examine the differences in transplant efficacy between the early (1999-2002), mid (2003-2006), or recent (2007-2010) transplant era. Barton and colleagues suggested that the Submission: Aug 24, 2014 Acceptance: Jan 26, 2015 Publication Feb 22, 2015 Process: peer-reviewed
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