A crummy diet can obviously have a lasting impact on the waistline—but for parents, it may also have a lasting impact on DNA and the family line, a new study suggests.

Compared with skinny mice on a standard or low-fat diet, genetically similar mice that became obese on a high-fat, high-calorie diet were more likely to have obese offspring at risk of developing type 2 diabetes. While researchers have noted such a familial influence on metabolic disorders before, the new study took the extra steps of producing the pups by in vitro fertilization of the sperm and eggs from the obese parents, implanted in slim, surrogate mothers. This experimental setup eliminates confounding influences from mom and dad, such as chemicals in seminal fluid, molecular signals in utero, microbiome transfers, and components of breast milk.

The finding, published Monday in Nature Genetics, provides clean support for the theory that poor diet and/or obesity in parents produces epigenetic changes—chemical tags and other molecular switches of DNA that alter how the genetic code is read and translated, rather than the code itself. And those changes can get passed down to offspring and influence their metabolism and health.

Though the work was done in mice, researchers speculate that similar epigenetic changes may occur in humans and other mammals, which could help explain the recent worldwide boom in obesity and type 2 diabetes. Indeed, previous data has found that lean and obese men have different epigenetic tags in their sperm.

For the mouse study, researchers raised genetically similar mice for six weeks on one of three diets: standard mouse chow, a low-fat diet, or a high-fat, high-calorie diet. The latter became obese and developed severe glucose intolerance (a precursor to type 2 diabetes), while the other mice stayed slim.

Harvesting the eggs and sperm from mice in each of the diet groups, the researchers then used in vitro fertilization to make specific, controlled crosses. All of the embryos were transferred to healthy, skinny foster mothers. To see if the diet of their biological parents affected their metabolism, all of the pups were challenged with a high-fat, high-calorie diet.

Unsurprisingly, the female pups with two obese parents had a high degree of insulin resistance and gained at least 20 percent more weight than the offspring of parents on standard or low-fat diets. Female pups with only one obese parent, either the mother or the father, also gained more weight than the control groups—but only between 8 and 14 percent. The result suggests that the metabolic influence of each parent may be additive.

But in a puzzling finding, the male pups didn’t have the same pattern. The male pups of obese parents did tend to be a bit heavier than those from the control groups, but the difference wasn’t statistically significant, the authors report. They did, however, also have a high degree of insulin resistance.

Examining the glucose intolerance more closely, the researchers noted that offspring (both male and female) tended to have more severe glucose intolerance if their mothers were obese. This backs up epidemiological data in humans that suggests a stronger maternal influence over type 2 diabetes development.

If the results hold up in further studies, the researchers hope to figure out what exactly the epigenetic factors are that are getting passed down, how they develop, and how many generations they last.

Nature Genetics, 2015. DOI: 10.1038/ng.3527 (About DOIs).