Voeding kan de genetische aanleg veranderen*
Mensen worden generatie op generatie dikker wat waarschijnlijk het gevolg is van genetische aanleg. In deze studie weliswaar met muizen werden drie generaties bekeken van genetisch identiek gelijke muizen met aanleg voor
overgewicht. Bij de ene groep muizen kreeg de drie generaties allemaal hetzelfde gewone dieet. Iedere generatie zag men dikker worden. In de andere groep kregen de generaties ook allemaal dit zelfde dieet nu echter aangevuld met foliumzuur, vitamine B12, betaïne en choline. Deze nutriënten staan bekend als
methylbronnen die genen kunnen uitzetten. In deze groep nu werd de tweede en derde generatie niet dikker.
Epigenetics could promote obesity in next generation
Overweight mothers give birth to offspring who become even heavier, resulting in amplification of obesity across generations, said Baylor College of Medicine researchers in Houston who found that chemical changes in the ways genes are expressed – a phenomenon called epigenetics -- could affect successive generations of mice.
"There is an obesity epidemic in the United States and it's increasingly recognized as a worldwide phenomenon," said Dr. Robert A. Waterland, assistant professor of pediatrics – nutrition at BCM and lead author of the study that appears in the International Journal of Obesity. "Why is everyone getting heavier and heavier? One hypothesis is that maternal obesity before and during pregnancy affects the establishment of body weight regulatory mechanisms in her baby. Maternal obesity could promote obesity in the next generation."
Waterland and his colleagues studied the effect of maternal obesity in three generations of genetically identical mice, all with the same genetic tendency to overeat. One group of mice received a standard diet; the other a diet supplemented with the nutrients folic acid, vitamin B12, betaine and choline. The special 'methyl supplemented' diet enhances DNA methylation, a chemical reaction that silences
genes.
"We wanted to know if, even among genetically identical mice, maternal obesity would promote obesity in her offspring, and if the methyl supplemented diet would affect this process," said Waterland. "Indeed, those on the regular diet got fatter and fatter with each generation. Those in the supplemented group, however, did not."
"We think DNA methylation may play an important role in the development of the hypothalamus (the region of the brain that regulates appetite)," said Waterland.
"Twenty years ago, it was proposed that just as genetic mutations can cause cancer, so too might aberrant epigenetic marks – so called 'epimutations.' That idea is now largely accepted and the field of cancer epigenetics is very active. I would make the same statement for obesity. We are on the cusp of understanding that," he said.
Waterland is also a researcher at the USDA/ARS Children's Nutrition Research Center at BCM and Texas Children's Hospital. Others who contributed to this research include Kajal Tahiliani, Marie-Therese Rached and Sherin Mirza of Baylor College of Medicine and the USDA/ARS Children's Nutrition Research Center in Houston and Michael Travisano of the University of Minnesota in St. Paul.
Funding for this work came from the National Institutes of Health, the March of Dimes Birth Defects Foundation and the U.S. Department of
Agriculture.
(Oktober
2008)
