The same proteins that moderate nicotine dependence in the brain may be involved in regulating metabolism by acting directly on certain types of fat cells, new research from the University of Michigan Life Sciences Institute shows.
Previous research by LSI research assistant professor Jun Wu and others identified a new type of fat cell in mice and humans, in addition to the white fat cells that store energy as lipids. These thermogenic, or “beige,” fat cells can be activated to burn energy through a process called thermogenesis.
To better understand what makes beige fat unique, Wu and her colleagues analyzed activated beige fat and uncovered a molecule directly linked to thermogenesis in these cells: CHRNA2 (for cholinergic receptor nicotinic alpha 2), a type of receptor that is best known for regulating nicotine dependence in brain cells.
Their findings, scheduled to be published May 21 in Nature Medicine, reveal that CHRNA2 functions in mouse and human beige fat cells, but not in energy-storing white fat cells–indicating that this protein plays a role in energy metabolism.
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