2024-01-24 06:45:45
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 life 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) in Spain 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 diets enriched in fat.
By generating genetically modified mice, the authors of the new study identify the ability of this gene to prevent obesity. Thierry Fischer, CSIC researcher at the National Center for Biotechnology (CNB), gives the keys to the study. “The focus of our laboratory 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 wild-type mice. For this reason we decided to check what the differences were in their metabolism,” explains Fischer.
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 of Spain, 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 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) of Spain, is that “the alteration of fat, in addition to causing thinness, results in slight hypothermia in these animals.”
Here we observe the development of adipocytes (green fluorescence) in adipose tissue from a mouse with mutations in the DIDO protein. (Image: María Ángeles García / CNB / CSIC)
These results, although they have been obtained in experimental mice, may have important therapeutic implications in metabolic pathologies suffered by humans. 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 researcher and first author of the research.
The study is titled “DIDO is necessary for adipogenesis that promotes diet-induced obesity”. And it has been published in the academic journal Proceedings of the National Academy of Sciences (PNAS). (Source: CNB / CSIC)
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