Queen Mary University of London in the United Kingdom led a research that revealed how a mother’s diet during pregnancy could permanently affect her child’s attributes. This could also explain how diseases such as type 2 diabetes and obesity are inherited. It also was shown that attributes, such as weight, could be shaped by genetic variation in an unexpected area of the genome. Genetic studies have been unable to interpret the process by which some diseases such as type 2 diabetes and obesity are inherited until now. The discovery was published in Science, which was co-authored by University of Cambridge and King’s College London. This discovery could provide the missing link in the conundrum of disease inheritance. The research demonstrates that the genetic variation of ribosomal DNA could be guiding how the environment within the womb determines an offspring’s attributes.
The lead researcher from Queen Mary University of London, Prof. Vardhman Raakyan, says that the face genetic variation of ribosomal DNA that seems to play such a major role, suggests that many human genetics studies could be missing a key part of the puzzle. Studies never looked at ribosomal DA, only at a single copy part of individuals’ genomes.
Diet, stress and smoking are environmental factors that work alongside genetic factors in the in-utero environment to influence the attributes of offspring as adults. At this stage the developmental programming could contribute to the increase in obesity. The epigenetics refer to external modifications to DNA that turn genes on or off and do not change the DNA sequence, but affect how they are expressed.
Tagging DNA with chemical compounds called methyl groups is one modification that determines which genes are or are not expressed. A low-protein diet of 8% protein and a normal diet of 20% protein affected the offspring of pregnant mice.
After the team analyzed the ribosomal data differently, they found huge epigenetic differences. For example, when cells are stressed the nutrient levels are low and they alter protein production as a survival strategy. Offspring of the low-protein mice mothers had methylated rDNA, which slowed the expression of their rDNA and could be influencing the function of ribosomes and resulting in smaller offspring.
These effects occurring in a critical timeframe of the offspring’s development in-utero are permanent effects through adulthood. Offspring from others fed on the low-protein diets had only one form of rDNA that seemed to experience methylation and affect weight.
Findings also show that mice provided with a high-fat diet had offspring with increased rDNA methylation which would suggest that methylation could be a general stress response and may also explain the rise in obesity worldwide.
– Dr Fredda Branyon