Diabetes Mellitus and Mitochondria Dysfunction: Comparison
Please note this is a comparison between Version 1 by Natalia V. Belosludtseva and Version 2 by Camila Xu.

1. Definition

Diabetes mellitus is a chronic disease that is characterized by an absolute or relative deficiency of insulin, the hormone that stimulates the transport of glucose across cell membranes, which leads to an increase in blood glucose—hyperglycemia. Two main types of diabetes are distinguished. Type I diabetes mellitus (about 10% of cases of diabetes) is an autoimmune disorder that results from the progressive destruction of the insulin-producing beta cells of the pancreas by T cells and activated macrophages and eventually leads to insulin deficiency in the organism. It is well known that type I diabetes most frequently develops in childhood and causes severe long-term complications, including retinopathy, neuropathy, and nephropathy [4,5,6]. Type II diabetes or adult-onset diabetes (about 90% of cases) is characterized by an impairment of homeostasis of glucose and insulin, in particular, the development of insulin resistance of target tissues associated with compensatory hyperinsulinemia, followed by beta-cell dysfunction. Type II diabetes mellitus is accompanied by glucose toxicity, lipotoxicity, and chronic oxidative stress, which finally can result in damage to vital organs and development of life-threatening secondary complications [4,7]. Mitochondria are one of the main targets of diabetes at the intracellular level. Recent data indicate that disturbances in mitochondrial calcium transport systems and a pathophysiological phenomenon called the permeability transition pore are involved in the pathogenesis of diabetes mellitus. 

  • diabetes mellitus
  • mitochondrial dysfunction
  • calcium transport
  • mitochondrial calcium uniporter
  • mitochondrial permeability transition pore
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