A new study has found an epigenetic link between a mother's diet and risk of future obesity in her offspring.
Scientists used an animal model and found that this link hinges on the blocked expression of a gene called Pomc, which manages a discrete area of the brain that controls feeding behavior. 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.
To make this discovery, the team 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 analyzed 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 controlled 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 normalized epigenetic mechanism. Because methylation on the genes is typically considered stable and relatively permanent, it opened 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 effects were not reprogrammed by providing standard food to the pups after weaning and the offspring maintained their obesogenic phenotype until adulthood.
The study is published in the in The FASEB Journal.
