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Ruijun Han of the University of Minnesota Medical School's Department of Integrative Biology and Physiology will present the findings at a meeting of Experimental Biology, April 9-13, 2011, in Washington, DC.
The Minnesota team focused on the behavior of the neuropeptide Y (NPY), a neurotransmitter found in the brain and autonomic nervous system. NPY is associated with appetite stimulation and the storage of energy as fat. Building on prior research, the team undertook two studies, one involving mice and the other mouse embryonic stem cells.
In the first study, they wanted to determine if prenatal and postnatal stress exerted long-term effects on the activation of NPY and its Y2 receptor (Y2R) that would create fat cells and promote obesity.
First, they exposed pregnant mice to stress by feeding them a low-protein diet. This caused low birth weight in the offspring. Female offspring of the mice stressed during pregnancy and lactation grew faster after weaning when they were fed a high-fat diet. Within 2 months they developed abdominal fat, prediabetes (impaired glucose tolerance) and increased upregulation of Y2R in their fat tissue.
Although male offspring of stressed mothers also had low birth weight, they did not develop obesity and had lower Y2R expression and better metabolic health, even when fed a high-fat diet.
"This indicates that maternal stress during pregnancy and lactation could induce gender-specific abdominal obesity and impaired glucose metabolism associated with increased plasma NPY and fat Y2R," says Dr. Han.
Dr. Zofia Zukowska, professor of physiology and the senior researcher of the study, says stress may affect NPY and Y2R in several ways.
"It could be that the mother's poor nutrition or other type of stress can affect fetal development by depriving the fetus of necessary nutrients or exposing it to levels of stress hormones such as cortisol, norepinephrine and epinephrine [adrenaline], which in turn up-regulates the NPY-Y2R system to affect metabolism and fat growth of the offspring."
The team sought to tease out these effects in the second study by observing how mice embryonic stem cells behave when over-exposed to stress hormones at a critical point during differentiation.
Embryonic stem cells that are treated with insulin and dexamathasone (synthetic glucocorticoid) will differentiate into fat cells. So the team exposed embryonic stem cells with epinephrine in a test dish and watched this process as the cells increased fat-cell formation and NPY expression.
The former stem cells also decreased DNA methylation, along the NPY promoter region. Through an non-genetic process, they altered expression of the NPY peptide in each cell inducing the cell to "remember" its new type (i.e., stem cells will remain committed to fat cell lineage and give rise to fat cells, instead of becoming or giving rise to another kind of cell).
"All of this data suggests that stress may induce epigenetic changes in NPY and its receptor genes and program [the offspring's DNA] for the future development of abdominal obesity and metabolic syndrome," says Dr. Han.
Although mice are not people, the Minnesota team's research sheds light on the process by which fat cell volume and the number of fat cells are created, says Dr. Han.
"Adipocyte number before adolescence is a major determinant [of a person's risk of obesity], so intervention during pregnancy and childhood might be an efficient way to prevent adult obesity."
Original article: Maternal stress during pregnancy may affect child's obesity