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brown fat heat production mechanism

Breakthrough in Brown Fat Research: New Mechanism of Heat Production Revealed

Researchers at LMU University Hospital have uncovered a novel mechanism governing heat generation within mitochondria. Special fat cells, known as brown adipocytes, play a crucial role in regulating body temperature by converting calorie-rich nutrients into heat, a process that mitigates weight gain and metabolic disorders.

A global team led by Professor Alexander Bartelt from the Institute for Cardiovascular Prevention (IPEK) has decoded a mechanism that amplifies respiration and metabolic activity in brown fat cells. This breakthrough may pave the way for innovative methods to combat metabolic diseases using brown fat. Their findings were recently published in The EMBO Journal.

Brown adipocytes target fat reserves

The activation of these fat-burning cells results in weight loss. In colder environments, brown adipocytes draw their fuel from stored fat since thermogenesis demands substantial calories. “Individuals who regularly expose their brown fat to cold tend to be leaner and less susceptible to diabetes and cardiovascular conditions,” notes Bartelt.

Brown fat cells contain an abundance of mitochondria, the cell’s energy factories. Yet, the exact mechanism by which these cells enhance metabolism remains elusive, hindering the development of targeted therapies.

brown fat heat production mechanism: Cold induces thermogenesis

The secret weapon of brown fat cells is uncoupling protein-1, which enables heat production rather than the usual ATP output from cellular respiration. “We postulated that cold exposure regulates this high metabolic activity of brown fat cells,” Bartelt explains, “particularly in terms of ATP production.”

Collaborating with researchers from São Paulo, the team identified a molecule called “inhibitory factor 1,” which ensures that ATP production is sustained rather than shifting toward thermogenesis. As temperatures drop, the level of inhibitory factor-1 decreases, allowing thermogenesis to proceed. Artificially raising the levels of this factor disrupts brown fat activation in cold conditions.

These insights emerged from experiments involving isolated mitochondria, cultured cells, and animal models. “While we’ve uncovered a significant aspect of thermogenesis, clinical applications remain distant,” remarks Dr. Henver Brunetta, a key figure in the research. According to the team, many people underutilize their brown fat, causing it to become inactive.

The study suggests the existence of molecular switches that can enhance mitochondrial function in brown fat cells. Bartelt and his colleagues plan to expand on this discovery. “In the long term, we hope to identify ways to rejuvenate mitochondria in white fat cells as well, given that most individuals have an excess of them,” Bartelt concludes.

Reference

“IF1 is a cold-regulated switch of ATP synthase hydrolytic activity to support thermogenesis in brown fat” by Henver S Brunetta, Anna S Jung, Fernando Valdivieso-Rivera, Stepheny C de Campos Zani, Joel Guerra, Vanessa O Furino, Annelise Francisco, Marcelo Berçot, Pedro M Moraes-Vieira, Susanne Keipert, Martin Jastroch, Laurent O Martinez, Carlos H Sponton, Roger F Castilho, Marcelo A Mori, and Alexander Bartelt, The EMBO Journal, 16 September 2024.
DOI: 10.1038/s44318-024-00215-0.