Diet, energy metabolism and mitochondrial biogenesis

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

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 1alpha mediated reactive oxygen species scavenging mechanism, and lowering reactive oxygen species production.

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.