Methylglyoxal (MGO), advanced glycation end products (AGEs) and reactive oxygen species (ROS) alter protein structure and are damaging in diabetes.
ROS formation is strongly implicated in the relationship between mitochondrial dysfunction and insulin resistance. ROS generation occurs mainly in complexes I and III of ETCs and increases when ETCs cannot cope with excessive electron input.
Under these circumstances, as a result of nutrient overload, the electron supply to the mitochondrial ETC increases and excess electrons transfer to oxygen to produce O2- and then hydrogen peroxide. Mitochondrially-generated ROS oxidize residues of proteins, damaging protein structure and impairing their function, ultimately leading to cell death.
ROS species also damage DNA and membrane lipids, thereby promoting mitochondrial dysfunction.
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