May 16, 2014
Science Daily/University of Chicago Medical Center
Poor-quality sleep during the third trimester of pregnancy can increase the odds of weight gain and metabolic abnormalities in offspring once they reach adulthood. The effects, caused by epigenetic modifications, impose lasting consequences on the next generation.
The researchers linked the excess weight and changes in metabolism to epigenetic modifications that reduce expression of the gene for adiponectin -- a hormone that helps regulate several metabolic processes, including glucose regulation. Lower levels of adiponectin correlate with increased body fat and reduced activity.
"Disrupted sleep is a common problem during the final trimester of a pregnancy," said study director, sleep specialist David Gozal, MD, the Herbert T Abelson professor of pediatrics at the University of Chicago. "For some women, sleep fragmentation, especially sleep apnea, can be profound. We wanted to devise a system that enabled us to measure the potential impact of fragmented sleep on the fetus, which is uniquely susceptible so early in life."
Adiponectin is usually a "beneficial hormone," Gozal said. "It can reduce cholesterol, make you more sensitive to insulin, protect your heart." As adiponectin levels in adults go up, body-fat percentage tends to go down. Expression of the adiponectin gene was reduced in the offspring of sleep-fragmented mothers, especially in their visceral fat cells.
A closer look revealed epigenetic changes, such as methylation and histone modification, which shut down selected genes, often in response to environmental stresses.
"We found that the offspring of sleep-deprived mothers had largely inactivated AdipoQ, the adiponectin gene," Gozal said. "Such changes may affect other genes as well; we haven't studied all the potential targets yet. Even so, this is the first example of a perturbation during pregnancy that translates into a genetic risk, in midlife, for the next generation."
"This is kind of scary," he added. "Will this generation, the sons of sleep-deprived mice, who are already at increased risk for metabolic syndrome and type 2 diabetes, transmit this inherited risk, perhaps compounded by new stresses, to their offspring?"