- Researchers investigated the neural activity underlying the consumption of fatty and sugary foods and activity levels.
- They looked at the effect of a specific cluster of neurons in the brain’s emotional center—the amygdala— on energy consumption and energy expenditure.
- They tested this by turning these brain cells ‘on’ and ‘off’ in genetically engineered mice.
- The researchers say that their findings could provide a basis for new anti-obesity treatments.
According to the World Health Organization, obesity has almost tripled since 1975.
While obesity has multiple possible
Pharmaceutical interventions may eventually prove useful for treating obesity, although many that are currently available cause significant side effects due to the pathways on which they work.
Research seeking to identify brain networks that shape dietary choice and self-control is thus critical for understanding mechanisms to develop new treatment approaches to obesity.
Recently, researchers discovered that a group of neurons in the amygdala—a part of the brain involved in experiencing emotions and decision-making—may also trigger hedonic eating.
The study was published in
“The identification of the neuronal substrates mediating overeating could provide new molecular targets for devising new anti-obesity treatments,” Alessandro Furlan, assistant professor at the Department of Neuroscience at Karolinska Institutet, Sweden, one of the study’s authors, told Medical News Today.
“If this information can be translated to people, then specific biochemical targets or psychotherapy services may produce real results for people in need,”
— Jordan Taylor, clinical neurologist and chief of the Neurology Section and associate clinical service line director at the University of Michigan Health-West
For the study, the researchers conducted several experiments on mice to observe their neuronal behavior.
From the first set of experiments, they observed their neural activity in response to eating regular chow or a high-fat diet (HFD) after food restriction.
After an HFD, but not chow, the researchers noted higher activity levels among certain neurons in a part of the amygdala known as the interstitial nucleus of the posterior limb of the anterior commissure (IPAC).
The findings, they wrote, indicated that certain neurons of the IPAC may be activated following the consumption of palatable food, and not necessarily an energy deficit.
Further tests demonstrated that these IPAC neurons could also be activated in the presence of fatty and sugary food and smells in the absence of hunger.
The researchers next conducted an experiment to see whether activating these neurons would lead to overfeeding. They found that ‘switching’ these neurons on increased sated mice’s intake of all foods and liquids.
The effect, however, was larger for coconut and olive oil-flavored HFDs and white chocolate than for chow and dark chocolate. Meanwhile, switching the neurons off then resulted in reduced feeding.
Lastly, the researchers investigated whether inhibition of the neurons in the IPAC could prevent obesity. To do so, they inhibited IPAC activity in some mice, and not others, and then fed them an obesity-inducing diet over several weeks.
After 6 weeks of eating in a ‘diet-inducing obesity’, control mice became obese, whereas other mice remained lean.
They further found that those with inhibited IPAC activity had a higher lipid oxidation rate- the speed at which fat is burned, higher energy expenditure, and engaged in more exercise. IPAC-inhibited mice also had lower blood sugar levels than controls.
The researchers concluded that the inactivation of specific neurons in the IPAC protects against obesity and related health conditions by promoting metabolic changes that benefit energy expenditure.
“It is definitely a possibility. [The neurons observed in this study] in the IPAC receive inputs from the central amygdala. This area has been implicated in the regulation of fear and anxiety,” he said.
Dr. Taylor explained to MNT how the amygdala may play a part:
“The amygdala is a complex bit of brain anatomy that interacts with other structures of the limbic system to regulate emotional learning and behavior. It is not a stretch to consider that the amygdala plays a role in an emotional connection to eating. Overeating has diverse contributions and causes, but this structure may modulate and reinforce pathways. For instance, appetitive behavior that encourages overeating.”
“Stress and emotionally significant experiences can rewire or induce plasticity through the amygdala, which can have long-term consequences in a variety of behaviors. Eating patterns may be one of those leading to an increase in consuming foods [that] “fill the need”—hyperpalatable foods. This, in turn, can contribute to obesity.”
— Jordan Taylor
When asked about the study’s limitations, Dr. Taylor pointed out that it was a mouse study.
“[I]t is difficult to know how it will translate to humans, but there are many other studies linking the mechanisms of the amygdala to overeating and obesity. It definitely makes it a really interesting structure to focus on,” he said.
“Future studies should address the heterogeneity of [the neurons observed in this study] and the networks they form with other brain areas. For instance, it is possible that energy intake and expenditure effects that we found might be mediated by distinct [neuronal] subgroups, projecting to distinct brain areas,” Dr. Furlan added.