A region of the brain that is responsible for powerful emotions may also play a part in overeating. Researchers at Cold Spring Harbor Laboratory (CSHL) report they have found that a group of neurons in the amygdala drives mice to eat fatty or sugary foods—even when they’re not hungry. The new findings may lead to new treatments for obesity with minimal side effects.

The research is published in the journal Nature Neuroscience in an article titled, “Neurotensin neurons in the extended amygdala control dietary choice and energy homeostasis,” and led by CSHL professor Bo Li, PhD.

“Obesity is a global pandemic that is causally linked to many life-threatening diseases. Apart from some rare genetic conditions, the biological drivers of overeating and reduced activity are unclear,” noted the researchers. “Here, we show that neurotensin-expressing neurons in the mouse interstitial nucleus of the posterior limb of the anterior commissure (IPAC), a nucleus of the central extended amygdala, encode dietary preference for unhealthy energy-dense foods.”

“Even if the animal is supposed to stop eating because they are already full, if those neurons are still active, it can still drive those animals to eat more,” Li explained.

“The medications currently available to aid weight management can cause significant side effects. So, a more targeted approach is needed,” Li said. “Identifying the brain circuitry that controls eating is important for developing better treatment options for people who struggle to control their weight.”

The researchers switched off the specific neurons and observed the mice weren’t drawn to the fatty, sugary foods that had tempted them before.

“They just happily ate and stayed healthy,” Li said. “They not only stopped gaining weight, but also seemed to be much healthier overall.” Switching these neurons off reduced overeating and protected against obesity. It also boosted the animals’ physical activity, leading to weight loss and better metabolic health.

Li and his team are exploring ways to manipulate the neurons that trigger hedonic eating. The next step, he said, is to map out how these neurons respond to different types of food and see what makes them so sensitive. He hopes this collaboration will lead to new strategies for effective anti-obesity therapeutics.

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