Dab2 protein is also involved in fat storage
In a paper published online in Scientific Reports, researchers of University of Miami Miller School of Medicine report that a protein termed Disabled-2 (Dab2) is involved in fat storage.
Previous studies have linked Dab2 with cancer. This protein is a widely expressed clathrin binding endocytic adaptor protein, and regulates the Ras-MAPK pathway. Mutations in this pathway can lead to uncontrolled cell growth.
The finding that Dab2 plays a role in fat storage is a new discovery. Professor Xiang-Xi Xu, lead researcher of the study, found this protein over two decades ago. Since then, he has been delving into the connection between cancer and Dab2. His latest research showed that juvenile mice that did not express Dab2 did not gain weight when fed a high-fat diet.
Dab2-deficient mice appeared mostly normal. But they maintained lean body composition even when they ate a high fat and high caloric diet. Notably, this phenomenon was found only in juvenile but not in mature mice.
Looking into the underlying mechanism, Xu's team found that in normal mice, Dab2 inhibits Ras-MAPK, which in turn increases a protein termed PPAR that helps fat stem cells develop into mature fat cells. Further experiments confirmed that Dab2 promotes adipocyte differentiation. Adipocytes, also known as adipocytes and fat cells, are cells that are specialized for the storage of fat. So loss of Dab2 may impact adipocyte differentiation and fat storage. This may help explain why juvenile Dab2 knockout mice were resistant to high fat diet-induced weight gain.
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