Obesity is a direct consequence of prolonged positive energy balance that occurs when energy intake (ie. calories) exceeds energy expenditure. In mammals, brown fat plays a critical role in energy metabolism due to its ability to burn energy by dissipating heat, a process known as thermogenesis. Therapeutics that target brown fat could possibly increase metabolism and correct the imbalance that leads to obesity. In this issue of the Journal of Clinical Investigation, researchers led by Matthias Tschöp identified a protein in mice, p62, that is required for brown fat thermogenesis. Mice that did not express p62 in fat cells became obese and developed glucose intolerance, key features of metabolic syndrome in humans. These findings indicate that p62 is an important regulator of metabolism and energy balance and is could potentially serve as a therapeutic target for the treatment of metabolic syndrome.
TITLE: p62 links beta-adrenergic input with mitochondrial function
Journal of Clinical Investigation