Washington, USA (PRWEB) July 19, 2013
In an article found on Sciencedaily.com, researchers from the Spanish National Cancer Research Centre (CNIO) discovered the key role of the gene RAP1, a gene that protects telomeres – the ends of chromosomes – and it’s link to obesity.
"We still don't know what evolutionary significance to attach to it, but it is at the very least interesting that a telomere gene is related to obesity," says Maria Blasco, CNIO director and co-author of the study published today in the journal Cell Reports.
RAP1 forms part of what’s called the shelterin complex, which is a group of proteins that makes up the protective hood of telomeres. Telomeres are found at the end of the chromosomes that shortens with each celluar division and thus, measures the ageing of the organism. Studies show that RAP1 is not essential for the survival of the organism, but that won’t mean it doesn’t have its importance in the body. When comparing the genomes of different species, it was shown that RAP1 is the most conserved shelterin of all. RAP1 has not changed at all, despite the long history of evolutionary change. But what is the role in the organism?
The researchers at CNIO found that RAP1 is also present in the rest of the chromosome, not just at in telomeres. They felt that it acts as a regulation for the action of the other genes. CNIO researchers created a lineage of mice without RAP1, and found that they had a model for obesity. In other words, mice lacking RAP1 will gain more weight than those with the RAP1 gene.
"Mice -- especially female mice -- without RAP1 do not eat more, but do gain weight. They suffer from metabolic syndrome, accumulate abdominal fat and present high glucose and cholesterol levels, amongst other symptoms," says Paula Martínez, first-author of the study.
The importance of RAP1 is the regulation of genes involved in metabolism. In the next step, researchers will study if RAP1 also plays a role in human obesity. "This discovery adds an element to the obesity equation, and opens up a possible new link between metabolic dysfunction and ageing, via a protein present in telomeres," says Blasco.
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