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Obesity is a pathology that affects more than one billion people in the world and is considered by the World Health Organization as a priority in the field of public health. In addition, it constitutes a risk factor for different diseases, which represents limitations in the life expectancy and quality of the affected people. Identifying the molecular factors involved is essential for the development of therapies that allow their regulation and control. A study led by the Higher Council for Scientific Research (CSIC) and in which the URJC has participated has discovered that the Dido1 protein is key in the development of adipose tissue and has the ability to prevent obesity even in situations of feeding with enriched diets. in fats. The work, which describes the functions of Dido1 in the development of adipose tissue, is published in the journal Proceedings of the National Academy of Sciences (PNAS).
By generating genetically modified mice, the authors identify the ability of this gene to prevent obesity. Thierry Fischer, CSIC researcher at the National Center for Biotechnology (CNB-CSIC), gives the keys to the study. "The focus of our laboratory - he points out - is the development of stem cells and in previous work on the function of Dido1 we had observed that mice with mutations in the amino terminal end of the protein presented a differential phenotype: they were thinner than mice. wild mice.” “For this reason we decided to check what the differences were in their metabolism,” Fischer continues.
Adipose tissue is the main fat storage organ and plays a fundamental role in the regulation of systemic metabolism and obesity-related diseases. “Dysfunctional adipose tissue can induce excess or reduction in body fat (also called lipodystrophy). In this study, we identified that the thinness of the mutant mice is due to a decrease in adipose tissue and a low presence of lipids in the blood, even when their feeding conditions include a high-fat diet,” explains the CSIC researcher.
Furthermore, Gema Medina-Gómez, a scientist at the Rey Juan Carlos University, comments: “We have seen that, when studies are carried out on the energy expenditure and intake of animals in metabolic cages, the mutated mice have more difficulties in using lipids from the diet efficiently. “They prefer to use carbohydrates.” Another of the interesting findings of the study for Guadalupe Sabio, researcher at the National Center for Cardiovascular Research (CNIC) is that "the alteration of fat, in addition to causing thinness, results in slight hypothermia in these animals."
These results, although they have been obtained in experimental mice, may have important therapeutic implications in metabolic pathologies. This model differs from other previously published lipodystrophic mouse models and could constitute a new system for the research and development of targeted therapeutic interventions. “The development of this model can be very useful to better understand the regulation of fat storage and distribution," explains María Ángeles García-López, also a CNB-CSIC researcher and first author of the research.
Obtaining this data has been achieved through the combination of different cutting-edge technologies, and the collaboration with the research groups of Guadalupe Sabio at the National Center for Cardiovascular Research and Gema Medina-Gómez at the Faculty of Health Sciences of the URJC, Alcorcón Campus.