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Developmental biology - Brown Fat

Brown fat flexes its muscle

Brown fat works much like muscle...


Scientists at the University of California, Berkeley, have discovered that the same kind of fat cells that help newborn babies regulate their body temperature could be a target for weight-loss in adults.

Brown fat cells, which help mammals regulate their body temperature, work much like muscle cells, researchers discovered. When the brain sends a signal to brown fat it starts burning energy and generating heat. The cells stiffen, which triggers a biochemical pathway. The multidisciplinary team of bioengineers and metabolic researchers teased apart the many steps in this pathway identifying a possible means to activate adult brown fat cells.

"We figured out the pathway that triggers brown fat tissue to consume calories from fat and sugars then radiate it away as heat," explains Andreas Stahl, professor and chairman of the Department of Nutritional Sciences and Toxicology at Berkeley. "Understanding of how brown fat is activated could unlock new ways to combat obesity."

The research published March 6 in the journal Cell Metabolism. The work was funded by the National Institutes of Health and the American Diabetes Association.
When cold, the human body shivers to produce heat in an attempt to maintain a body temperature of 98.6 degrees Fahrenheit. Newborn babies, who can't shiver just yet, have a large patch of brown fat between their shoulder blades. Its job is to absorb nutrients and burn their energy to produce heat for regulating body temperature. Brown fat cells decrease in number as babies grow, until upon reaching adulthood, they have a very small number of not very active brown fat cells.

Here's how brown fat works: When the body senses cold, our brain releases norepinephrine, which is detected by a receptor on brown fat cells. This triggers a cascade of biochemical signals leading to production of a protein called Uncoupling Factor-1 also known as Mitochondrial uncoupling protein (UCP1). UCP1 then fuses into the mitochondria within brown fat cells.

In a normal cell, mitochondria act much like batteries. They convert nutrients from our diet into energy and then store it, primarily, in ATP molecules. But in brown fat cells, UCP1 creates heat instead of ATP. With UCP1 made active in mitochondria, brown fat cells soak up fat and sugars to burn for heat.

Previous research found brown fat shares some characteristics of muscle, particularly in the myosin proteins, which act like little motors. In muscle, myosin contracts the muscle cells, but what myosin did in brown fat cells was unknown. So researchers stimulated brown fat and measured how much the cell flexed by measuring the tension of the cell wall. Cell walls became roughly twice as stiff when stimulated. But, when researchers disabled myosin they found brown fat cells reduced stiffness by a factor of about two significantly softer.
"Our finding that the muscle-like myosin is responsible for stiffening brown fat cells was really unexpected, no one has ever observed that before."

Andreas Stahl PhD, Program for Metabolic Biology, Department of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, California, USA.

The study found that UCP1's activity is directly tied to the increase in cell tension. When that tension in activated brown fat cells caused a 70 percent reduction in UCP1 and generated less heat. Researchers were then able to identify the molecules in the cell that respond to increased tension which triggers activation of UCP1. In experiments in mice, they disrupted these molecules to find that brown fat cells lose their function and physically look more like white fat cells, where excess energy is stored.

"Now that we better understand how brown fat cells work, we can think about ways to stimulate muscle-like myosin in brown fat to increase thermogenesis and burn calories," Stahl said. "Drugs to stimulate muscle-like myosin in existing brown fat would probably create more active brown fat cells in adults."

"This study offers a remarkable example of how mechanical and other physical forces can influence physiology and disease in powerful, unexpected ways," explains Sanjay Kumar, Berkeley professor of bioengineering and a co-author of the study. "We hope that our work will aid in the design of therapeutic biomaterials and other technologies geared towards enhancing brown fat function."

Highlights
BAT adrenergic stimulation induces an actomyosin-based mechanical response
Modulation of actomyosin responses alters oxidative metabolism in adipocytes
Thermogenic gene expression in adipocytes is in part regulated by YAP/TAZ

Summary
The activation of brown/beige adipose tissue (BAT) metabolism and the induction of uncoupling protein 1 (UCP1) expression are essential for BAT-based strategies to improve metabolic homeostasis. Here, we demonstrate that BAT utilizes actomyosin machinery to generate tensional responses following adrenergic stimulation, similar to muscle tissues. The activation of actomyosin mechanics is critical for the acute induction of oxidative metabolism and uncoupled respiration in UCP1+ adipocytes. Moreover, we show that actomyosin-mediated elasticity regulates the thermogenic capacity of adipocytes via the mechanosensitive transcriptional co-activators YAP and TAZ, which are indispensable for normal BAT function. These biomechanical signaling mechanisms may inform future strategies to promote the expansion and activation of brown/beige adipocytes.

Authors: Kevin M. Tharp, Michael S. Kang, Greg A. Timblin, Jon Dempersmier, Garret E. Dempsey, Peter-James H. Zushin, Jaime Benavides, Catherine Choi, Catherine X. Li, Amit K. Jha, Shingo Kajimura, Kevin E. Healy, Hei Sook Sul, Kaoru Saijo, Sanjay Kumar and Andreas Stahl.


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Jun 29, 2018   Fetal Timeline   Maternal Timeline   News   News Archive




Illustration of a brown/beige adipose tissue (BAT) cell metabolism - and the induction
of uncoupling protein 1 (UCP1). Image; University of California Berkeley.


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