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So, for the new study, which was published in March in the Journal of Applied Physiology, scientists at the University of Virginia School of Medicine and other institutions first gathered a large group of mice. Some of the animals, male and female, were allowed to gorge on a high-fat, high-calorie diet, inducing obesity and metabolic problems, while others remained on normal chow, at their usual weight.
Next, the mice hooked up, with obese animals of both genders mating with normal-weight mice, so that, in theory, one parent in each pairing could bequeath unhealthy habits and metabolism to the young. A few normal-weight animals without metabolic problems also mated, to produce control offspring.
Finally, some mothers, including the obese, jogged on little running wheels throughout the resulting pregnancies, voluntarily covering up to seven miles a week in the early stages of their three-week gestations.
Afterward, the researchers tracked the metabolic health and underlying genetic activity of the offspring, until they reached adulthood. This second generation ate normal chow and led normal, lab-mouse lives.
Many, though, developed multiple metabolic problems as adults, including obesity, insulin resistance and other disruptions of their blood-sugar control. These conditions were most pronounced in the male children of obese mothers and in both the male and female children born to obese fathers.
Interestingly, the underlying genetics of their conditions differed by parental gender. Mice born to obese mothers displayed unusual activity in a set of genes known to be involved in inflammation. Those born to obese fathers did not.
In other words, the genetic legacies from mothers and fathers “operate through different biological pathways,” says Zhen Yan, a professor of medicine and director of the Center for Skeletal Muscle Research at the University of Virginia School of Medicine, who oversaw the new study.