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Diet, energy metabolism and mitochondrial biogenesis

Civitarese, Anthony E; Smith, Steven R; Ravussin, Eric

Current Opinion in Clinical Nutrition & Metabolic Care: November 2007 - Volume 10 - Issue 6 - p 679–687
doi: 10.1097/MCO.0b013e3282f0ecd2
Nutrition and physiological function: Edited by Wim H.M. Saris

Purpose of review This review highlights some recent findings regarding nutritional and endocrine regulators of mitochondrial mass and function and their association with insulin resistance.

Recent findings Insulin resistance is central to many chronic metabolic diseases, including obesity, type 2 diabetes, dyslipidemia, and hypertension. Insulin resistance in skeletal muscle is associated with lower mitochondrial mass and reduced oxidative phosphorylation. Part of the mitochondrial dysfunction can be triggered by adverse nutrition. Increased fatty acid exposure, resulting from high fats diets or overfeeding, is linked to both decreased mitochondrial number and markers of oxidative phosphorylation. Caloric restriction and the adiponectin signaling pathway, however, can stimulate mitochondrial biogenesis by elevating the transcriptional machinery that regulates mitochondrial mass, improving mitochondrial efficiency, activating the peroxisome proliferator-activated receptor coactivator 1α mediated reactive oxygen species scavenging mechanism, and lowering reactive oxygen species production.

Summary States of insulin resistance are characterized by defects in lipid and carbohydrate metabolism. Abnormalities in oxidative capacity, however, can be partially normalized by caloric restriction by modulating mitochondrial mass in an insulin sensitizing manner.

Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA

Correspondence to Anthony E. Civitarese, Skeletal Muscle Metabolism Laboratory, Human Physiology, Pennington Biomedical Research Center, 6400 Perkins Rd, Baton Rouge, LA 70808, USA E-mail:

© 2007 Lippincott Williams & Wilkins, Inc.