Under pathophysiological conditions such as obesity, excessive oxidation of nutrients may induce mitochondrial stress, leading to mitochondrial unfolded protein response (UPR(mt)) and initiation of a retrograde stress signaling pathway. Defects in the UPR(mt) and the retrograde signaling pathways may disrupt the integrity and homeostasis of the mitochondria, resulting in endoplasmic reticulum stress and insulin resistance. Improving the capacity of mitochondria to reduce stress may be an effective approach to improve mitochondria function and to suppress obesity-induced metabolic disorders such as insulin resistance and type 2 diabetes.
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