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Featured Review
Cellscience Reviews Vol 4 No 4
ISSN 1742-8130 |
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Mitochondrial Oxidative Phosphorylation, Obesity and Diabetes
Bi-Dar Wang 1, Owen M. Rennert 2 & Yan A. Su 1
1 Dept. of Biochemistry & Molecular Biology & the Catherine Birch McCormick Genomics Ctr., The George Washington University School of Medicine & Health Sciences, Washington, &
2 Laboratory of Clinical Genomics, National Institute of Child Health & Human Development, NIH, Bethesda, Maryland, USA.
Received 26th February © Cellscience 2008
Mitochondria are essential for ATP synthesis via oxidative phosphorylation (OXPHOS) and their dysfunction may cause energy deficiency in cells resulting in metabolic disorders: obesity and diabetes. Obesity or excessive bodyweight with elevated free fatty acids in the blood stream affects 2.1 billion people worldwide, and one of its adverse consequences is type 2 diabetes mellitus (T2DM). T2DM is characterized by hyperglycemia resulting from insufficient production of insulin by pancreatic β-cells, and insulin resistance in target tissues (muscle, liver and fat). Lipotoxicity and glucotoxicity in obesity and T2DM induce the β-cell overexpression of uncoupling protein 2 which increases proton leakage across the mitochondrial inner membrane and decreases ATP synthesis leading to insufficient secretion of insulin. Insulin resistance in the target tissues has been related to decreased mitochondrial content, reduced fatty acid oxidation, defective OXPHOS, and poor ATP production. This review focuses on the cellular and molecular mechanisms underlying defective mitochondrial OXPHOS in obesity and T2DM.
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