“We therefore asked how brown fat mass can be increased while simultaneously reducing bad white fat,” says Bonn postdoctoral researcher and first author Dr. Laia Reverte-Salisa.
Together with researchers from the University Medical Center Hamburg-Eppendorf, Helmholtz Munich and the University of Toulouse-Paul Sabatier, the Bonn team investigated the cAMP signaling pathway in fat metabolism that plays a central role in fat cells.
Using a mouse model, they discovered that the relatively unknown protein “exchange proteins directly activated by cAMP” (EPAC1), is responsible for the growth of brown fat.
In addition, EPAC1 even increases the formation of brown fat cells in white fat, which are also known as “beige” cells.
Prof. Pfeifer’s team also showed that the signaling pathway is also active in human fat cells.
In addition, they confirmed the function of EPAC1 in human organoids — organ-like microstructures that serve as a human brown fat model.
The Bonn researchers further found that a non-functional human EPAC1 gene variant is associated with an increased body mass index (BMI). “Our study shows that EPAC1 is an attractive target to increase brown fat mass and thus also energy expenditure,” says Prof. Pfeifer. In view of the worldwide increase in obesity, he hopes to develop novel therapies that help those affected to combat metabolic diseases. This study was conducted in the context of the DFG Collaborative Research Center Transregio-SFB 333 “Brown and Beige Fat — Organ Interactions, Signaling Pathways and Energy Balance (BATenergy),” which is pursuing a better understanding of the different types of adipose tissue and their role in metabolic diseases.
Sources : www.sciencedaily.com