Investigators found in animal models that pulmonary endothelial function was influenced by caloric intake rates.
Jesse Roman, MD
Past research has shown that certain maternal health habits, such as smoking, can increase an infant’s chances of developing lung disease. But a new study using a mouse model also gives indication that diet may have a bigger role.
A team of investigators found that lower caloric intake in pregnant mice caused alterations in genes that are crucial for pulmonary endothelial function.
“We wanted to look at the genetic make-up of these animals to see if somehow the malnutrition created changes in the expression of their DNA,” said lead investigator, Jesse Roman, MD, Professor and CEO of the Jane and Leonard Korman Respiratory Institute-Jefferson Health and National Health. “There is no question that there is a link between exposures, such as smoking, alcohol, and infection, and having an increased incidence of asthma. But very few think about nutrition.”
According to the World Health Organization (WHO), 15% of babies born around the globe have low birth weight, mostly in developing countries. The March of Dimes states that 1 of the risk factors for low birth weight is the mother not gaining enough weight. Respiratory issues are one of the many challenges these babies may face.
For this study, investigators performed 2 experiments. In the first, adult male mice, between 6-8 weeks old (female mice were not used to avoid hormone fluctuations), were divided into 2 groups of 6 mice each. A control group was fed the Laboratory Autoclavable Rodent Diet 5010, ad libitum. The energy-restricted (ER) group was given 65% of the food intake of the control group.
The second experiment involved 2 groups of pregnant female mice. The control was fed Autoclavable Mouse Breeder Chow Diet 5021, ad libitum, while the ER group was fed 65% of the control group’s food intake during the second and third trimesters of pregnancy.
Results showed that in offspring of the ER mice, the genes fibronectin-1 and plasminogen activator inhibitor-1 were up-regulated and the expression of the genes involved in regulating histone acetylation was significantly reduced. In addition, the global DNA methylation in the pulmonary cells of the adult male mice fed the ER diet did not change when compared with the adult male mice control group.
Roman said this study illustrates that nutrition in and of itself can change the way genes behave and may have implications on the development of chronic lung disease, yet raises many more questions. Factors such as being born to a mother who is malnourished and smokes or a premature birth and being on a ventilator for a month would be occurring in a lung that is already compromised from altered gene expression.
“So, I would think, hypothetically, that there are a significant number of people with chronic lung disease where perhaps that disease was more relevant in them because of these exposures as a baby or child,” said Roman.
With this information, research needs to now evaluate these mice at several months old to determine pulmonary function, if the changes are permanent, if biological sex matters, and how these factors are influenced by malnutrition, smoking, alcohol consumption, and prematurity, Roman noted.
The study, “Maternal undernutrition during pregnancy alters the epigenetic landscape and the expression of endothelial function genes in male progeny,” was published in the journal Nutrition Research.