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Keeping fat cells in check

Published online 22 July 2019

Two proteins work together to maintain a healthy balance of fat cell formation.

Islam Elkholi

A mouse missing Arid5a (left) weighed twice as much as a wild-type control mouse (right).
A mouse missing Arid5a (left) weighed twice as much as a wild-type control mouse (right).
Tadamitsu Kishimoto /Jaya Prakash Chalise
Two proteins work together to keep fat tissue formation in check. The finding sheds light on the molecular processes involved in the formation of fat cells, which could lead to effective interventions against obesity.

Researchers from Japan, India, the USA, and Jordan investigated the role of the protein Arid5a in fat tissue formation. This protein is known for having a variety of roles, including one related to the inflammatory process.

Immunologist, Tadamitsu Kishimoto, of Osaka University, in Japan, along with his colleagues, found that mice missing the Arid5a protein weighed twice as much as normal mice. Mice with an excess of Arid5a were half the weight of normal mice when they were all fed a high fat diet.

The team found that Arid5a and a protein called Ppar-γ2, a master regulator of fat cell formation, counteract each other. Ppar-γ2 inhibits Arid5a during fat cell formation. Once enough fat cells are formed, mature fat cells along with resident immune cells secreting pro-inflammatory proteins, including one called interleukin-6, prompt Arid5a to suppress this process. Arid5a and Ppar-γ2 thus work together to maintain a healthy balance of fat cell formation. 

“The secretion of inflammatory proteins by immune cells inside metabolic tissues can lead to different consequences,” says Kishimoto. “Revealing the molecular actors provoked by these inflammatory proteins will provide promising strategies to address metabolic disorders, such as obesity,” he says. 

doi:10.1038/nmiddleeast.2019.105


Chalise J. P. et al. Feedback regulation of Arid5a and Ppar-γ2 maintains adipose tissue homeostasis. PNAS https://doi.org/10.1073/pnas.1906712116 (2019).