Researchers have in past years established that some degree of transmission of environmental information takes place from generation to generation. The epigenetic response to environmental factors such as abundance of food is partially passed on to offspring to result in changes in the operation of offspring metabolism. Epigenetic and metabolic reactions to abundance of food affect pace of aging and life span, and these outcomes are also changed in offspring, even when the offspring live in a different environment with different abundance of food.
Data in mice, nonhuman primates, and in humans demonstrate that exposure to maternal obesity increases the risk of multiple diseases in offspring. However, little is known about the aging effects of maternal obesity on the offspring. This study shows that maternal obesity significantly reduced the lifespan of both male and female mice born to obese dams despite being weaned onto a healthy diet at three weeks of age.
This reduction in longevity was linked to an increase in age-related fibrotic pathology across multiple organs, e.g., liver, heart, and kidney. Gompertz analysis of the lifespan data showed that maternal obesity offspring have reduced lifespan due to detrimental changes established early during development rather than factors that modify aging later-in-life. These findings are translationally significant as they demonstrate that the growing prevalence of maternal obesity may lead to a decrease in overall lifespan and increase in age-related diseases in the next generation.
