Recent research has shown that the offspring of mice fed a high-fat diet are more susceptible to developing obesity and diabetes. Because of the study design, susceptibility in the offspring was not attributable to inheritable genetic variations. Rather, the results suggest that acquired metabolic disorders can be passed on epigenetically to offspring via oocytes and sperm.
For their experiments, investigators in Germany isolated gametes from parental mice that were exposed to a high-fat diet, low-fat diet, or normal standard chow for 6 weeks. All parental mice on the high-fat diet developed obesity and traits associated with type 2 diabetes. The researchers then implanted embryos derived from the isolated parental gametes via in vitro fertilization into healthy surrogate mothers. This allowed the team to exclude potential confounding variables, such as diet-induced environmental changes in utero, milk composition during lactation, and behavioral effects during postnatal care.
When exposed to a high-fat diet challenge, female offspring from obese parents gained at least 20% more body weight than female offspring from lean parents. Female offspring from 1 obese and 1 lean parent had 8% (high-fat paternal) and 14% (high-fat maternal) higher body weight averages than control offspring. These findings suggest that high-fat diets in parents can additively render female offspring more obese.
Male offspring from parents that consumed a high-fat diet tended to be heavier than their counterparts from lean parents at 15 weeks of age, but the difference in body weight was not statistically significant.
The scientists also found that high-fat diet–induced insulin resistance appeared to be more prominently epigenetically inherited via maternal than paternal gametes.