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As we all know, delicious and delicious foods are usually those that are high in sugar, fat, and calories (which are more palatable).
While they satisfy our appetite, they also lead to an imbalance in the body's energy homeostasis, bringing more and more obese people
to the world.
Today, obesity is a global epidemic, and many life-threatening major diseases are associated with
obesity.
While poor dietary choices (can't keep your mouth shut) and lack of exercise (can't move your legs) are the leading causes of obesity, how our food preferences are established is still an open question
.
For now, choice seems to be more important
than effort for weight loss.
The amygdala is one of the important brain regions and is named
for its almond-shaped shape.
The amygdala plays a major role in memory processing, decision-making, and emotional responses, including fear, anxiety, and aggression, and it is thought to be part of the
limbic system.
So, what does the amygdala have to do with food choices? Like most people, mice prefer foods high in sugar and fat
.
They can even choose between
"fatal" or "desperate".
In a new study published in Nature Neuroscience, a team led by Cold Spring Harbor Laboratory (CSHL) identified a previously uncharacterized group of neurons in the amygdala that plays a key role in promoting metabolic responses through behavioral changes: this group of neurons drives mice to choose high-sugar or high-fat foods after a full meal.
Triggers "hedonic" overeating and eventually obesity
.
From a therapeutic perspective, targeting this group of neurons leads to long-term weight loss and improved
metabolic health.
The study points out that the amygdala is an ideal entry point
to unravel the complex metabolic regulatory circuits of the brain in energy homeostasis.
The anterior commismatic hindlimb interstitial nucleus (IPAC) is a major structure
of the expanded amygdala.
IPAC neurons are activated
by innate or acquired taste stimuli.
They receive dense projections
from the insular cortex, a hedonic hotspot.
However, until now, the role of IPAC in energy homeostasis has been unknown
.
In the new study, the team experimented with mice to reveal the critical role
of neurons, which express neurotensin, in IPAC, in establishing dietary choices and coordinating behaviors that affect metabolic health.
They found that IPAC (IPAC-Nts), which expresses neurotensin, encodes dietary preferences for unhealthy, energy-intensive foods
, such as high-fat and high-sugar foods.
In experiments, mice stop eating because they are full; But when the researchers used optogenetics to activate IPAC-Nts neurons in mice, the already full animals would start a new round of eating behavior, that is, hedonic eating behavior; Activated IPAC-NTS also modulated food preferences, making mice more willing to choose high-sugar and high-fat foods
.
Conversely, after the IPAC-Nts neurons were acutely inhibited, the mice were no longer attracted to the high-sugar, high-fat foods that had previously tempted them, that is, they reduced hedonic eating
.
Meanwhile, chronic inactivation of IPAC-Nts neurons also reduced taste preference in mice, enhanced exercise and energy expenditure, and showed long-term weight loss and improved
metabolic health.
In conclusion, the study reveals that the activity of a single population of neurons can regulate energy homeostasis
in both directions.
In general, on the road to weight loss, few people can control their weight
in the long term.
Over time, the body's metabolic processes reverse all previous weight loss gains
.
The group of diet-controlling neurons identified by the new study offers promising targets for the development of new strategies to prevent and treat obesity
.
The team says that deeper characterization of this brain region may reveal molecular heterogeneity
not currently found in its neurons.
While they satisfy our appetite, they also lead to an imbalance in the body's energy homeostasis, bringing more and more obese people
to the world.
Today, obesity is a global epidemic, and many life-threatening major diseases are associated with
obesity.
While poor dietary choices (can't keep your mouth shut) and lack of exercise (can't move your legs) are the leading causes of obesity, how our food preferences are established is still an open question
.
For now, choice seems to be more important
than effort for weight loss.
The amygdala is one of the important brain regions and is named
for its almond-shaped shape.
The amygdala plays a major role in memory processing, decision-making, and emotional responses, including fear, anxiety, and aggression, and it is thought to be part of the
limbic system.
So, what does the amygdala have to do with food choices? Like most people, mice prefer foods high in sugar and fat
.
They can even choose between
"fatal" or "desperate".
In a new study published in Nature Neuroscience, a team led by Cold Spring Harbor Laboratory (CSHL) identified a previously uncharacterized group of neurons in the amygdala that plays a key role in promoting metabolic responses through behavioral changes: this group of neurons drives mice to choose high-sugar or high-fat foods after a full meal.
Triggers "hedonic" overeating and eventually obesity
.
From a therapeutic perspective, targeting this group of neurons leads to long-term weight loss and improved
metabolic health.
The study points out that the amygdala is an ideal entry point
to unravel the complex metabolic regulatory circuits of the brain in energy homeostasis.
The anterior commismatic hindlimb interstitial nucleus (IPAC) is a major structure
of the expanded amygdala.
IPAC neurons are activated
by innate or acquired taste stimuli.
They receive dense projections
from the insular cortex, a hedonic hotspot.
However, until now, the role of IPAC in energy homeostasis has been unknown
.
In the new study, the team experimented with mice to reveal the critical role
of neurons, which express neurotensin, in IPAC, in establishing dietary choices and coordinating behaviors that affect metabolic health.
They found that IPAC (IPAC-Nts), which expresses neurotensin, encodes dietary preferences for unhealthy, energy-intensive foods
, such as high-fat and high-sugar foods.
In experiments, mice stop eating because they are full; But when the researchers used optogenetics to activate IPAC-Nts neurons in mice, the already full animals would start a new round of eating behavior, that is, hedonic eating behavior; Activated IPAC-NTS also modulated food preferences, making mice more willing to choose high-sugar and high-fat foods
.
Conversely, after the IPAC-Nts neurons were acutely inhibited, the mice were no longer attracted to the high-sugar, high-fat foods that had previously tempted them, that is, they reduced hedonic eating
.
Meanwhile, chronic inactivation of IPAC-Nts neurons also reduced taste preference in mice, enhanced exercise and energy expenditure, and showed long-term weight loss and improved
metabolic health.
In conclusion, the study reveals that the activity of a single population of neurons can regulate energy homeostasis
in both directions.
In general, on the road to weight loss, few people can control their weight
in the long term.
Over time, the body's metabolic processes reverse all previous weight loss gains
.
The group of diet-controlling neurons identified by the new study offers promising targets for the development of new strategies to prevent and treat obesity
.
The team says that deeper characterization of this brain region may reveal molecular heterogeneity
not currently found in its neurons.
Links to papers:
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