Maternal under-nutrition brings about modifications involving DNA, leading to metabolic disorders at the adult age, according to new research.
The study, published in The FASEB Journal, reports to demonstrate for the first time, that environmental influences, such as maternal nutritional stress, could induce deleterious metabolic symptoms that last for the entire life of individuals, and implying that epigenetic modifications play an important role in this process.
The animal-based study found that maternal nutritional status can have repercussions at the level of the leptin gene, the hormone that regulates satiety and metabolism. The researchers, from Centre de Recherche de l'Institut du Cerveau et de la Moelle Epinière (CRICM) and and the Unité de Nutrition Humaine (INRA), France, said that their work reveals the molecular process that takes place during the perinatal period leaves an imprint in the genes of the foetus, lasting throughout the individual's lifetime.
“We have investigated, in mice, the consequences of maternal under-nutrition during gestation and lactation on DNA methylation and expression of the leptin gene, which plays a major regulatory role in coordinating nutritional state with many aspects of mammalian biology,” wrote the researchers, led by Pierre Fafournoux from the nutrition unit at INRA.
“We show that animals born to mothers fed a low-protein-diet have a lower body weight … and exhibit a higher food intake than animals born to mothers fed a control diet. These modifications persisted throughout life … emphasizing that maternal protein-under-nutrition affects the balance between food intake and energy expenditure in adults,” said the researchers.
They added that their work could, in the longer term, have an impact on the prevention of metabolic diseases.
The researchers specifically studied the consequences of maternal nutrition during the perinatal period (gestation followed by lactation) on epigenetic modifications of the genome.
Pregnant mice were fed from the first day of gestation up to weaning either with a diet containing 22 per cent protein (control mice), or with a low protein diet containing ten per cent protein. Then, from weaning, all the baby mice were fed a control diet.
The result was that young mice whose mothers had been given a low protein diet were, as adults, thinner than the control mice and showed symptoms of metabolic disorders.
Fafournoux and his colleagues directly linked the consequences of protein deficiency during the perinatal period to demethylation at the level of the leptin gene.
They said that understanding such programming mechanisms is essential to define prevention policies for these diseases, which are a major public health issue.