SAN DIEGO — New research may help explain why chronic stress, sleep deprivation and other disruptions in the body’s daily rhythms are linked to obesity.
Chronic exposure to stress hormones stimulates growth of fat cells, Mary Teruel of Stanford University reported December 16 at the annual meeting of the American Society for Cell Biology. Normally, stress hormones, such as cortisol, are released during waking hours in regular bursts that follow daily, or circadian, rhythms. Those regular pulses don’t cause fat growth, Teruel and colleagues discovered. But extended periods of exposure to the hormones, caused by such things as too little sleep, break up that rhythm and lead to more fat cells.
Even though only about 10 percent of fat cells are replaced each year, the body maintains a pool of prefat cells that are poised to turn into fat. “If they all differentiated at once, you’d be drowning in fat,” Teruel said.
Previous studies have shown that a protein called PPAR-gamma controls the development of fat cells and that stress hormones turn on production of PPAR-gamma. Teruel’s team discovered that prefat cells with levels of PPAR-gamma below a certain threshold don’t transform into fat in laboratory tests. Steady hormone exposure eventually allowed the precursor cells to build up enough PPAR-gamma to cross the threshold into fat making. But in cells given the same total amount of stress hormone in short pulses, PPAR-gamma levels rose and fell.
The stress hormone works like pushing on a car’s accelerator. Steadily increasing pressure eventually puts the car over the speed limit, while pulses effectively take the foot off the gas pedal, causing periodic slowdowns that fall short of the fat-making threshold. Pulses shorter than 12 hours didn’t make extra fat, while longer pulses, such as those that may be caused by sleep deprivation, overeating or other disruptions in circadian rhythms, increased the number of precursor cells that became fat cells.