Fathers under psychological stress could pass on an increased risk of type 2 diabetes to their children, a study on mice finds.
Researchers at the Shanghai Jiao Tong University School of Medicine report that stress hormones lead to epigenetic changes in sperm that gives offspring high blood sugar. However, blocking a father’s stress hormones could prevent this change.
While the study was conducted on mice, the Shanghai team believe the findings could apply to humans as well.
The researchers confined male mice in plastic tubes for two hours a day for two weeks to induce stress. The animals’ glucose levels were slightly increased, but the mice gained weight more slowly and had increased levels of glucocorticoids, a stress hormone, in their blood.
The male mice were then mated with unstressed female mice, and their offspring had higher blood glucose levels than normal. Raised blood glucose levels are characteristic of prediabetes, which can increase the risk of type 2 diabetes.
A gene called Sfmbt2 was response for the increased blood sugar, according to the researchers. During the rise in glucocorticoids, extra methyl groups were added to the Sfmbt2 gene in the sperm of the male mice.
The microRNA in Sfmbt2, which plays a key role in the regulation of gene expressio, helps control sugar production in the liver, which is where the changes in stress levels were observed. But when mammals reproduce, Sfmbt2 is deactivated in the egg from the mother, meaning its offspring only inherits working copy from the father’s sperm.
Professor Xiaoying Li explained: “Epidemiological studies have demonstrated the association of psychological stress with incident diabetes. Paternal psychological stress can result in hyperglycemia in offspring in mice. We are curious about whether the effect can be passed down through generations.”
Li added that by understanding the mechanism involved, researchers could inhibit the effects of glucocorticoids on the sperm. This could be achieved by injecting male mice with a molecule which prevents the Sfmbt2 gene from being overly methylated.
“It is potentially possible for our study to be translated into the treatment of hyperglycemia in human beings in the future,” Li said.
The findings were published in the journal Cell Metabolism.