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Arch Physiol Biochem. 2011 Jul;117(3):177-87. doi: 10.3109/13813455.2011.584538.

Mitochondrial pathophysiology and type 2 diabetes mellitus.

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Diabetes and Obesity Laboratory, Institute for Biomedical Research August Pi i Sunyer (IDIBAPS) and Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Barcelona, Spain.


Over the last decades, substantial progress has been made in defining the molecular events and relevant tissues controlling insulin action and the potential defects that lead to insulin resistance and later on Type 2 diabetes mellitus (T2DM). Mitochondrial dysfunction has been postulated as a common mechanism implicated in the development of insulin resistance and T2DM aetiology. Since then there has been growing interest in this area of research and many studies have addressed whether mitochondrial function/dysfunction is implicated in the progression of T2DM or if it is just a consequence. Mitochondria are adjusted to the specific needs of the tissue and to the environmental interactions or pathophysiological state that it encounters. This review offers a current state of the subject in a tissue specific approach. We will focus our attention on skeletal muscle, liver, and white adipose tissue as the main insulin sensitive organs. Hypothalamic mitochondrial function will be also discussed.

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