Human and animal studies suggest that nutritional imbalances occurring during fetal and early postnatal periods can have long-term consequences on health, including obesity and diabetes, and appear to be at least partly caused by changes in genomic expression.
Genomes can integrate and translate environmental changes into stable modifications of gene expression by altering epigenetic marks. Epigenetic marks like DNA methylation are particularly important, because they are highly dependent on the availability of methyl donors that are supplied by the diet. Our hypothesis is that the mechanism involved in the long-term effects of nutrition is mediated by changes in the degree of DNA methylation, that in turn, cause permanent changes in gene expression.
We propose to determine the genome-wide methylation profiling of liver samples from a mouse model of fetal undernutrition by using microarrays specific for CpG islands, because these are chromosomic regions that are susceptible to methylation and are physically associated to gene regulatory regions. We will also explore the role of diets supplemented with nutrient methyl donors in preventing/attenuating the phenotypes associated with fetal malnutrition.
The presence of a link between nutrition, changes in DNA methylation and gene expression can have great clinical relevance, since the possibility of using dietary intervention to maintain the right degree of DNA methylation in order to prevent the deleterious metabolic effects, may become feasible.
Field of science
- /natural sciences/biological sciences/genetics and heredity/genome
- /medical and health sciences/clinical medicine/endocrinology/diabetes
- /natural sciences/biological sciences/genetics and heredity/dna
- /medical and health sciences/health sciences/nutrition
- /medical and health sciences/clinical medicine/obstetrics and gynaecology/obstetrics/postnatal
- /natural sciences/biological sciences/genetics and heredity/epigenetics
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