Spanish researchers identify an important protein involved in the regulation of obesity

A study conducted by the Higher Council of Scientific Research (CSIC) found that the Dido1 protein plays a key role in the development of adipose tissue and has the ability to prevent obesity even in situations of feeding diets enriched with fats.

The work describing the functions of Dido1 in adipose tissue development was published in the journal Proceedings of the National Academy of Sciences (PNAS). Its goal is to identify the molecular factors involved, which is important for the development of treatments that can regulate and control them.

The researchers remind that obesity is a condition that affects more than one billion people worldwide and is considered a public health priority by the World Health Organization. In addition, it represents a risk factor for the development of various diseases, which limits the length and quality of life of affected people.

By creating genetically modified mice, the authors identified the ability of this gene to prevent obesity. “Our laboratory’s goal is to develop stem cells, and in previous work on Dido1 function, we observed that mice with mutations at the amino-terminal end of the protein had a differential phenotype: they were thinner than wild-type mice,” says Thierry Fischer, CSIC researcher at the National Center for Biotechnology (CNB-CSIC).

“For this reason, we decided to test what the differences were in their metabolism,” continues Fischer. Adipose tissue is the primary fat storage organ and plays a fundamental role in the regulation of systemic metabolism and obesity-related diseases.

“Dysfunctional adipose tissue can cause excess or decreased body fat (also called lipodystrophy). In this study, we determined that the leanness of the mutant mice is due to decreased adipose tissue and low blood lipids, even when their feeding conditions include a diet rich in fat,” explains the CSIC researcher.

Moreover, “we saw that when studies were done on animal energy expenditure and energy intake in metabolic cells, the mutated mice had a harder time using dietary lipids efficiently. They prefer to use carbohydrates,” says Gema Medina. Gómez, scientist at the Rey Juan Carlos University.

Another interesting finding from the study by Guadalupe Sabio, a researcher at the National Center for Cardiovascular Research (CNIC), is that “changes in fat, in addition to leanness, lead to slight hypothermia in these animals.”

These results, although obtained in experimental mice, may have important therapeutic implications for metabolic pathologies. This model differs from other previously published lipodystrophic mouse models and may represent a new system for research and development of targeted therapeutic interventions.

“The development of this model could be very useful for better understanding the regulation of fat storage and distribution,” explains Maria Angeles Garcia-Lopez, also a CNB-CSIC researcher and first author of the study.

The acquisition of these data was achieved through a combination of various advanced technologies and collaboration with the research groups of Guadalupe Sabio from the National Center for Cardiovascular Research and Gema Medina-Gomez from the Rey Juan Carlos University of Alcorcón.