New research from the University of Bonn adds weight to the idea that a child’s future health may be shaped long before birth.
In a mouse study published in Nature, researchers found that obesity during pregnancy may “reprogram” liver cells in the developing fetus, making the offspring more likely to develop metabolic conditions, including fatty liver disease, even if they eat a healthy diet later in life.
The study focused on special immune cells called Kupffer cells, which live in the liver and help regulate its function. In the offspring of obese mice, these cells sent altered signals that caused fat to build up in liver tissue, despite no change in diet.
“We were able to show that the offspring of obese mothers frequently developed a fatty liver shortly after birth,” said Dr. Hao Huang, a researcher in the lab of study leader Professor Elvira Mass. “And this happened even when the young animals were fed a completely normal diet.”
The team traced the cause to a metabolic “switch” flipped in the womb. This switch, a transcription factor, was triggered by molecules circulating in the mother’s body and changed the way liver cells functioned in the offspring.
When the researchers disabled that switch during pregnancy, the fatty liver symptoms did not occur, suggesting this pathway might one day be targeted to prevent disease.
While this study was done in mice, the researchers believe the findings may help explain why children born to mothers with obesity have a higher risk of metabolic disorders, even when raised in healthier environments.
“Our study is one of the few to explain in detail how this early programming can happen,” said Prof. Elvira Mass, senior author and spokesperson for the University of Bonn’s Life & Health research area.
The research was supported by the German Research Foundation, the European Research Council and other European scientific institutions.