Mitochondrial Metabolism

The accumulation of "ectopic" triglyceride in visceral depots has suggested a defect in mitochondrial lipid oxidation in patients with type 2 diabetes, who have impaired oxidative capacity and small mitochondria in skeletal muscle (42). Peroxisome proliferator-activated receptor-gamma (PPAR-y) coactivator 1 (PGC-1), a transcription factor for genes involved in mitochondrial fatty acid oxidation and ATP synthesis, was decreased in young, lean, insulin-resistant offspring of parents with type 2 diabetes, suggesting that an inherited defect in mitochondrial oxidative phosphorylation could lead to cellular lipid accumulation (43). Gene expression profiling studies have also shown that decreased expression of PGC-1 and related gene products may affect mitochondrial function in subjects with insulin resistance and type 2 diabetes (44,45).

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