Nicotine Receptors Might Help Fat Cells Burn Energy

Nicotine receptor proteins might help fat cells in burning energy, according to a study conducted on May 21, 2018.

This study was conducted by the researchers at the University of Michigan. Earlier research by professor Jun Wu and others had led to the discovery of a new type of fat cell in mice and humans, apart from 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 the uniqueness of beige fat, the activated beige fat was analyzed by the research team. They discovered a molecule that was directly linked to thermogenesis in these cells. It was called as CHRNA2 (cholinergic receptor nicotinic alpha 2), a type of receptor that is best known for regulating nicotine dependence in brain cells. The results of the study showed that CHRNA2 functions in mouse and human beige fat cells, but not in energy-storing white fat cells.

It has been found that appetite can be suppressed by nicotine. By identifying how nicotine affects metabolism directly, this study may open the door to more novel approaches to combating the weight gain that often occurs when individuals stop smoking. From the researches, it was found that CHRNA2 receptor proteins can be activated both by nicotine and by acetylcholine molecules produced by nearby immune cells. When the CHRNA2 protein receives the acetylcholine or nicotine, it stimulates the beige fat cells to start burning energy.

By analyzing the mice that lacked the gene, which was needed to make this protein, the role of CHRNA2 in metabolism was further tested. Mice without the genes exhibited no differences when they were given regular diet. However, when they were fed with high-diet fat, the mice gained weight and high body fat content. According to Wu, understanding the specific CHRNA2 signaling pathway in beige fat will be beneficial in developing drugs that can treat obesity and metabolic syndrome.

 

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