Regenerative Medicine News and General Information
Discovery of a New Molecule that Boosts Fat Burning
Jul
In a recently published study, researchers at the University of Bonn have identified a key molecule named inosine that is capable of burning fat. Their results were published in the journal Nature.
There are 2 main types of fat tissue, brown and white adipose tissue. In brown fat cells energy is dissipated as heat, and it serves as a biological heater. This is how newborns can stay warm, and in human adults, brown fat activation positively correlates with cardiometabolic health.
Researchers have been evaluating ways to stimulate brown fat to increase fat burning for many years.
According to Prof. Alexander Pfeifer from the Institute of Pharmacology and Toxicology at the University of Bonn, our body’s own furnaces are hardly needed anymore due to the use of clothes, heaters, and the consumption of increasingly energy-dense diets. These factors are, according to him, poison to brown fat cells, leading them to cease function and die.
A New Way to Stimulate Fat Burning
For the study, the team studied brown fat cells subjected to severe stress, so that the cells were virtually dying, and found that they secrete the purine inosine in larger quantities, which then activated intact brown fat cells that were in the vicinity. Also, white fat cells converted to their brown siblings.
The team used a mice model and found that mice fed with a high-energy diet that were treated with inosine remained leaner compared to control animals and were protected from diabetes.
Their results suggest that inosine regulates thermogenesis in human brown fat cells and that substances that interfere with the activity of the transported could potentially be used for the treatment of obesity.
Source:
University of Bonn. “Molecule boosts fat burning: Study identifies a new signaling molecule that increases the energy consumption of brown fat cells.” ScienceDaily. ScienceDaily, 5 July 2022. <www.sciencedaily.com/releases/2022/07/220705112250.htm>.
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