�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 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 hardly starting to understand extra kinds of inheritance like metabolic computer programming, which occurs when an insult during a critical period of development, either in the womb or soon subsequently birth, triggers permanent changes in metabolism.
In this field of study, the researchers looked at the effects of a diet high in saturated fat on mice and their young. As expected, they establish that a high-fat diet induced type 2 diabetes in the adult mice and that this upshot was transposed by stopping the diet.
However, if female mice continued a high-fat diet during pregnancy and/or suckling, their offspring too had a greater oftenness of diabetes development, even though the offspring were given a moderate-fat diet. These mice were then mated with healthy mice, and the next genesis offspring (grandchildren of the original high-fat fed generation) could develop diabetes as well.
In effect, exposing a fetal computer mouse to senior high levels of saturated fats can cause it and its materialization to assume diabetes, even if the mouse goes off the high-fat diet and its young are never straightaway exposed.
The survey used mice so it's not time to warn women to eat differently during pregnancy and breastfeeding but in the beginning research has shown that this genial of inheritance is at work in humans. For example, there is an increased risk 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 data 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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