�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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