Molecule fuels fat burning – DocCheck

Current medications for the treatment of obesity are usually only marginally effective. The use of a specific nucleoside could enable a new therapy in the future.

A study led by the University of Bonn has identified a molecule that fuels fat burning in brown fat cells. The mechanism was discovered in mice but probably also exists in humans. If a transporter for the signaling substance is less active in them, they remain significantly slimmer despite eating a high-fat diet. The work is now in the journal Nature appeared.

Too warm, too unhealthy, too inactive

Normally, fat cells store energy. In brown fat cells, on the other hand, it dissipates as heat – so brown fat serves as biological heating, so to speak. In cold conditions, this is not only practical, but essential for survival. The activation also protects against cardiovascular diseases.

“Nowadays we are cozy and warm even in winter,” explains Prof. Dr. Alexander Pfeifer from the Institute for Pharmacology and Toxicology at the University of Bonn. “Our body’s own incinerators are hardly needed anymore.” At the same time, we eat more and more energy and move far less than our ancestors. These three factors are poison for brown fat cells: they gradually cease to function and eventually even die. On the other hand, the number of severely overweight people is increasing all over the world. “Working groups around the world are therefore looking for active ingredients that stimulate brown fat and thus increase fat burning,” says Pfeifer.

Human brown adipocytes. Credit: Laia Reverte Salisa

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Dying fat cells fuel combustion in their neighbors

Together with colleagues, the team from the University of Bonn has now identified a central molecule that is able to do this. “It is known that dying cells often give off a mix of messenger substances that influence the behavior of their neighbors,” explains Dr. Birte Niemann from Pfeifer’s working group. Together with her colleague Dr. Saskia Haufs-Brusberg, she planned and carried out the central experiments of the study. “We wanted to know if it’s the same with brown fat.”

The researchers therefore examined murine brown fat cells, which they had stressed so much that they were practically on their way to death. “We discovered that they release a molecule called inosine in large quantities,” says Niemann. What was more interesting, however, was how intact brown fat cells reacted to the molecular call for help: They were activated by the inosine – or simply by dying cells in their vicinity. White fat cells also turned into brown ones. Mice fed a high-energy diet and injected with inosine also remained leaner than their peers and were protected from diabetes.

The inosine transporter seems to play an important role in this context: This protein in the cell membrane transports inosine into the cell and thus reduces the concentration of the messenger substance on the outside. The signal molecule can probably no longer develop its combustion-promoting effect.

Drug inhibits the inosine transporter

“There is a drug that was actually developed against coagulation disorders, but also inhibits the inosine transporter,” says Pfeifer. “We gave it to mice, which made them use more energy.” We also have an inosine transporter. In two to four percent of all people, it is less active due to a genetic change. “Our colleagues at the University of Leipzig genetically analyzed 900 people,” explains Pfeifer. “Those with the less active transporter were significantly slimmer on average.”

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The results indicate that inosine also regulates the burning of brown fat cells in us. Substances that interfere with the activity of the transporter could therefore possibly be suitable for the concomitant treatment of obesity. The already approved active substance against coagulation disorders could serve as a starting point. “However, further studies in humans are needed to clarify the pharmacological potential of this mechanism,” says Pfeifer. Nor does he believe that a single pill will be the solution to the obesity pandemic raging around the world. “However, the available therapies are currently not effective enough,” he emphasizes. “Therefore, we absolutely need drugs to normalize the energy balance in obese patients.”

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This article is based on a press release from the Rheinische Friedrich-Wilhelms-Universität Bonn. The original publication can be found here and in the text.

Image source: Diana Polekhinaunsplash



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