Unexpected New Clues to Fighting Obesity: Scientists Identify Brain Circuit That May Help Burn Fat

A newly discovered brain circuit links motion sickness with metabolism, offering potential for obesity treatments.

Motion sickness is a common condition affecting approximately one in three people, yet the underlying brain mechanisms remain poorly understood. In a new study published in Nature Metabolism, researchers from Baylor College of Medicine, the University of Texas Health Science Center at Houston, and the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital have identified a previously unknown brain circuit involved in motion sickness.

This circuit also plays a role in regulating body temperature and metabolic balance. The discovery could lead to unconvential approaches for treating obesity.

“When Dr. Longlong Tu, a postdoctoral fellow in my lab, proposed to investigate the brain circuits involved in motion sickness, a condition for which he is highly susceptible, I was not very excited about the idea because it’s not one of the main interests of my lab,” said corresponding author of the work, Dr. Yong Xu, professor of pediatrics – nutrition and associate director for basic sciences at the USDA/ARS Children’s Nutrition Research Center at Baylor. “However, I became more interested and supported Tu’s idea when he explained the emerging evidence suggesting a link between motion sickness and metabolic balance, which is one of my research interests.”

A Mouse Model to Study Motion Sickness

The Xu lab works with mouse models to investigate how the brain regulates metabolism and how this may be related to obesity and inform the development of more effective obesity drugs. Mouse models offer an abundance of molecular and genetic tools, as well as relevant behavioral assays to elucidate the neural mechanisms underlying physiological responses. But there was a challenge – mice are incapable of vomiting, one of the main manifestations of motion sickness in people.

Interestingly, mice and humans subjected to motion sickness stimuli, such as experiencing horizontal motion back and forth for some time, show hypothermia, a reduction in body temperature. “This allowed us to develop a mouse model of motion sickness in which we measured core body temperature, physical activity, and brain activity as the animals experienced motion stimuli,” Xu explained.

The team found that motion activates glutamatergic neurons – neurons that produce glutamate, the primary excitatory neurotransmitter in the central nervous system – in the medial vestibular nucleus parvocellular part (MVePC^Glu) of the brain. Activation of these neurons is required and sufficient to mediate motion-induced thermal adaptations. The researchers validated the model by showing that motion sickness-induced hypothermia does not occur when the mice are given the anti-nausea drug scopolamine.

Linking the Vestibular System to Metabolic Health

“We further studied this motion sickness circuit by inhibiting the MVePC^Glu neurons in the absence of motion stimuli,” Xu said. “Inhibiting these neurons led to an increase in body temperature, along with increased physical activity. These physiological alterations suggest that chronic inhibition of MVePC^Glu neurons may result in a higher energy expenditure in mice.”

When the researchers investigated the potential metabolic benefits of the chronic inhibition of MVePC^Glu neurons they found that, although the mice ate more, they gained less weight and exhibited better glucose tolerance and enhanced insulin sensitivity, physiological responses associated with better health. “These results highlight the underappreciated function of the brain’s vestibular system in metabolic balance, and further raise the possibility that better understanding of the neural basis for thermoregulation during motion sickness may provide unconventional targets for the treatment of obesity,” Xu said.

And for first author Tu, the findings offer hope that a better understanding of the brain circuit for motion sickness could also lead to improved medications for his condition.

Reference: “Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice” by Longlong Tu, Xing Fang, Yongjie Yang, Meng Yu, Hailan Liu, Hesong Liu, Na Yin, Jonathan C. Bean, Kristine M. Conde, Mengjie Wang, Yongxiang Li, Olivia Z. Ginnard, Qingzhuo Liu, Yuhan Shi, Junying Han, Yi Zhu, Makoto Fukuda, Qingchun Tong, Benjamin Arenkiel, Mingshan Xue, Yang He, Chunmei Wang and Yong Xu, 21 March 2025, Nature Metabolism.
DOI: 10.1038/s42255-025-01234-9

This study was supported by grants from the NIH (P01DK113954, R01DK115761, R01DK117281, R01DK125480 and R01DK120858, R01DK104901, R01DK12665, R01MH117089), USDA/CRIS (51000-064-01S, 51000-064-02S, 3092-51000-062-04(B)S, 1F32DK13868501A1), the McKnight Foundation and an American Heart Association Postdoctoral Fellowship (2020AHA000POST000204188).

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