Thu. May 23rd, 2024

A new signalling molecule that boosts brown fat cells’ energy consumption has been discovered through research

Purine inosine is a chemical that has been linked to increased fat oxidation in brown adipocytes, according to a study. 

The mechanism was found in mice, but it most likely also exists in humans: The mice maintain their substantial leanness despite consuming a high-fat diet if an inosine transporter is less active.

Energy is kept in fat cells. Energy is released as heat within brown fat cells, acting as a biological heater. It is a system found in most mammals. In adults, brown fat activation is positively correlated with cardio-metabolic health in humans because it keeps infants warm.
As per Dr. Alexander Pfeifer from the University of Bonn, our bodies no longer really need their own furnaces. In addition to moving much less than our ancestors, we are eating a diet that is getting more and more energy-dense. Brown fat cells are poisoned by these three elements. They eventually stop functioning completely and even pass away. People who are extremely overweight are becoming more prevalent worldwide.

Therefore, Pfeifer says, “Research teams all over the world are seeking for compounds that promote brown fat and thereby improve fat burning.”

Inosine is a crucial chemical that has been discovered by researchers at the University of Bonn to be capable of burning fat. According to Dr. Birte Niemann of Pfeifer’s study team, “it is known that dying cells emit a mixture of messenger molecules that affect the function of their neighbours.” She organised and carried out the study’s key experiments with the assistance of her colleague Dr. Saskia Haufs-Brusberg. “We were curious as to whether brown fat was likewise subject to this process.”

Therefore, the researchers looked at brown fat cells that had been under extreme stress to the point where the cells were almost dead. According to Niemann, “We observed that they secrete huge amounts of purine inosine.”

In this situation, the inosine transporter protein in the cell membrane, which transports inosine into the cell and lowers the extracellular levels, appears to be crucial. As a result, inosine is no longer able to promote combustion.

According to Pfeifer, a researcher at the University of Bonn who is also a member of the transdisciplinary research areas “Life and Health” and “Sustainable Futures,” there is a medication that was really created for coagulation disorders but also inhibits the inosine transporter. When we administered this medication to mice, they expended more energy. Inosine transporters are also present in humans. It is less active in two to four percent of persons due to a genetic difference. Pfeifer notes that 900 individuals have undergone genetic analysis by our colleagues at the University of Leipzig. On average, the participants with the less active transporter were noticeably thinner.

These findings imply that inosine controls thermogenesis in human brown fat cells as well. Therefore, drugs that prevent the transporter from functioning properly may be useful for treating obesity. A good place to start would be the medication that has already been approved for coagulation problems.

“However, further studies in humans are needed to clarify the pharmacological potential of this mechanism,” Pfeifer says. Neither does he believe that a pill alone will be the solution to the world’s rampant obesity pandemic. “But the available therapies are not effective enough at the moment,” he stresses. “We therefore desperately need medications to normalize energy balance in obese patients.”

The German Research Foundation (DFG) recently approved a Transregional Collaborative Research Center in which the Universities of Bonn, Hamburg, and Munich perform focused research on brown adipose tissue, underscoring the crucial role played by the body’s own heating system.

By Editor

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