�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, particularly in children and offspring adults, in the United States.
DNA is the primary mechanism of inheritance; kids get half their genes from mamma and half from pa. However, scientists are just starting to understand additional kinds of inheritance wish metabolic programing, 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 establish 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 contemporaries) could develop diabetes as well.
In burden, 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 like a shot exposed.
The survey used mice so it's not meter to warn women to eat other than during pregnancy and breastfeeding but before research has shown that this kind of inheritance is at work in humans. For example, thither is an increased risk of exposure of high blood pressure and cardiovascular disease in children born of malnourished mothers.
From the article: "Effects of High Fat Diet Exposure During Fetal Life on Type 2 Diabetes Development in the Progeny" by Donatella Gniuli, Alessandra Calcagno, Maria Emiliana Caristo, Alessandra Mancuso, Veronica Macchi, Geltrude Mingrone, and Roberto Vettor.
Article link: http://www.jlr.org/cgi/content/abstract/M800033-JLR200v1
Corresponding Author: Donatella Gniuli, Istituto di Medicina Interna, Universita' Cattolica del Sacro Cuore, Rome
Source: Nick Zagorski
American Society for Biochemistry and Molecular Biology
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