Scientists have found how genes link a mother's diet to the risk of obesity in her offspring.
New research suggests that epigenetic methylation blocks expression of the Pomc gene, leadings to delayed satiety response and increased food intake.
Many studies have made it clear that a mother's eating habits prior to pregnancy, during pregnancy and during lactation have a profound impact on her offspring and their propensity for developing weight problems, including obesity.
However, until now, the mechanisms behind this phenomenon were unclear.
Scientists using an animal model found an epigenetic link between a mother's diet and an offspring's risk of future obesity.
This link hinges on the blocked expression of a gene called Pomc, which manages a discrete area of the brain that controls feeding behaviour.
Excess methylation on the DNA sequence blocks the ability to express this gene, leading to a late satiety response, increased food intake and eventually to obesity.
"Parental obesity and diet can affect the children's likelihood to overeat and develop obesity. Changes in epigenetic programming have been implicated as one of the mechanisms underlying this phenomenon," said Asaf Marco, a researcher from the Faculty of Life Sciences at Bar Ilan University in Ramat Gan, Israel.
"We observed a clear correspondence between a specific epigenetic mechanism and weight gain, potentially allowing for early detection and prevention of obesity," said Marco.
Marco and colleagues fed female rats either a high-fat diet or a standard diet from post-weaning to adulthood and in separate groups, throughout pregnancy and lactation.
All offspring, including those of the high-fat treated rats, received standard food after weaning until adulthood.
Blood was analysed for hormone levels and brain sections for epigenetic modification on the specific DNA sequence of interest.
Results showed that unmated female rats, chronically fed a high-fat diet, presented obesity associated with disruptions in an epigenetic mechanism that controls the production of Pomc.
However, due to the sharp weight loss during lactation, rats who consumed a high-fat diet presented normal weight and a normalised epigenetic mechanism.
Because methylation on the genes is typically considered stable and relatively permanent, this opens the door for future drug development.
Researchers found that epigenetic malprogramming induced by maternal high-fat diet had a long-term effect on the offspring's vulnerability to develop obesity.
The study was published in The FASEB Journal.
