A new study in the September issue of the Journal of Lipid Research suggests an unusual form of inheritance may have a role in the rising rate of diabetes, especially in children and young adults, in the United States.
DNA is the primary mechanism of inheritance; kids get half their genes from mom and half from dad. However, scientists are just starting to understand additional kinds of inheritance like metabolic programming, which occurs when an insult during a critical period of development, either in the womb or soon after birth, triggers permanent changes in metabolism.
In this study, the researchers looked at the effects of a diet high in saturated fat on mice and their offspring. As expected, they found that a high-fat diet induced type 2 diabetes in the adult mice and that this effect was reversed by stopping the diet.
However, if female mice continued a high-fat diet during pregnancy and/or suckling, their offspring also had a greater frequency of diabetes development, even though the offspring were given a moderate-fat diet. These mice were then mated with healthy mice, and the next generation offspring (grandchildren of the original high-fat fed generation) could develop diabetes as well.
In effect, exposing a fetal mouse to high levels of saturated fats can cause it and its offspring to acquire diabetes, even if the mouse goes off the high-fat diet and its young are never directly exposed.
The study used mice so it's not time to warn women to eat differently during pregnancy and breastfeeding but earlier research has shown that this kind of inheritance is at work in humans. For example, there is an increased risk of hypertension and cardiovascular disease in children born of malnourished mothers.
The above story is based on materials provided by American Society for Biochemistry and Molecular Biology. Note: Materials may be edited for content and length.
- Gniuli et al. Effects of high-fat diet exposure during fetal life on type 2 diabetes development in the progeny. The Journal of Lipid Research, 2008; 49 (9): 1936 DOI: 10.1194/jlr.M800033-JLR200
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