Abstract
Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.
Highlights
Diabetes is a disease considered to be a worldwide epidemic
Mitochondrial dysfunction related to Type 2 diabetes (T2D), hyperglycemia, and insulin resistance has been described in different tissues, including skeletal muscle, kidney, lung, heart, and liver [6], as well as in circulating cells such as leukocytes [7,8]
These results are in accordance with the progressive rise in oxidative stress and altered mitochondrial morphology associated with hyperglycemia in diabetic subjects
Summary
Diabetes is a disease considered to be a worldwide epidemic. The prevalence of diabetes among adults in 2017 was around 451 million cases, a number that is expected to rise to 693 million in 2045 [1]. Diabetes affects mainly developed countries, but its prevalence is increasing considerably in developing countries such as India and China [2]. Since it is a life-long condition, it represents an enormous economic burden on healthcare systems worldwide. Type 2 diabetes (T2D) involves decreased insulin secretion by β-cells, or increased insulin resistance, and represents around 95% of all cases. Mitochondrial dysfunction related to T2D, hyperglycemia, and insulin resistance has been described in different tissues, including skeletal muscle, kidney, lung, heart, and liver [6], as well as in circulating cells such as leukocytes [7,8]
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