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Singularity Cake recently encountered a problem
.
A friend of Singularity Cake finally determined to lose weight, from "mouth" to "legs"
.
As his strong backing and leading by example, this cake also followed the control of food intake, mainly based on light diets such as round lettuce and broccoli, and refused high-fat food (legs are really immobile)
.
However, the good times are not long
.
Singularity Cake only lasted for three days.
On the fourth day, it broke the defense directly at 9 o'clock in the evening, and dragged him to eat kebabs, grilled small waist, grilled chicken crispy bones, grilled leeks, grilled plate tendons, and grilled steamed buns.
That's right.
, Add a portion of roasted trotters and roasted brain flower
.
The scene was a joy~ After the storm was inhaled, Singularity Cake couldn't help but patted his belly and roared-Is there any way to control this appetite? Recently, J.
Nicholas Betley and her colleagues from the University of Pennsylvania in the United States published an article in the journal “Nature” to clarify the singularity
.
Our cerebellum is the key to suppressing appetite! They found that after eating, signals from the intestine activate the glutamatergic neurons in the deep cerebellar nucleus (aDCN-Lat).
The activation of these neurons will increase the basal release level of dopamine and reduce the intensity caused by eating.
The short-term stimulation peak weakens the reward value brought about by extra food and reduces the food intake [1]
.
Screenshot of the paper's homepage It is often said that we must be the masters of desire! However, one of the strongest desires in nature-dry rice, is really hard to control
.
(Tired, tears) To elaborate on the desire for dry rice, it can be divided into "want to eat" and "want to eat"[2]
.
"To eat" is a "life event" necessary for basic metabolism and survival for the human body system to maintain energy balance through eating in order to keep us alive
.
The AgRP neurons in the arcuate nucleus region of the hypothalamus are responsible for this important event.
After being activated by the hunger signal, they urge us to eat quickly [2]
.
If you want to eat, you have to mention dopamine, the source of happiness, which is the reward mechanism
.
Like a high-fat and high-sugar food, the dopaminergic neurons (VTA-DA) of the striatum will be induced to release dopamine quickly and in large quantities as soon as it is ingested, and enjoy the ultimate happiness [2]
.
But having said that, the two neural circuits "want to eat" and "want to eat" are of course not completely independent of each other [2]
.
Since the motivation for cooking is so sufficient, who is going to suppress appetite? After all, everything cannot be addictive, and eating all the time is not a problem.
For example, patients with Prader Wiley syndrome (PWS) have constant hunger from childhood, and often overeating leads to obesity and type 2 diabetes [3]
.
Studies have found that the hindbrain and hypothalamus are related to the desire to dry meals, but the weight loss treatment for these two areas is not effective [4]
.
So this time, Betley and her colleagues conducted further research and found that the cerebellum turned out to be helping us gauge how much we should eat
.
They first used functional magnetic resonance imaging (fMRI) to track the brain responses of PWS patients and normal people to different signals (food vs.
non-food pictures) under different feelings of fullness (fasting vs.
after eating)
.
The results show that between the PWS group and the control group, the deep cerebellar nucleus (DCN) is the only brain area with significant differences in neural activity, and the lack of response to food signals in the deep cerebellum may be related to the increased food intake of PWS patients
.
Later, the researchers also found in the mouse model that the deep nucleus (aDCN-Lat) region of the lateral cerebellum (aDCN-Lat) of the mouse was activated after eating and the nutrition of the food was digested
.
According to fMRI results, the deep cerebellar nuclei are related to appetite control (dogs and cakes look like real ones) To determine the role of DCN in regulating food intake, Betley and her colleagues performed DCN neuronal activity in mice And eating conditions were tested
.
The results showed that compared with other areas of DCN (aDCN-Int, pDCN-Int, pDCN-Med), only the neurons that activate the aDCN-Lat area can affect the eating of mice
.
And when the aDCN-Lat neurons were activated, the eating frequency and eating speed of the mice were not affected, but the amount and duration of eating were reduced
.
This reduction in food intake has nothing to do with the hunger or fullness of the mice, and whether it makes the mood happy or not (even if you don't eat happy high-fat and high-sugar foods, it is)
.
Conversely, once the aDCN-Lat neurons are inhibited, the mice's food intake will increase
.
Further use of calcium imaging and other technologies found that it is a type of glutamatergic neurons (all expressing Spp1) located in the aDCN-Lat region that are activated after eating, which inhibits appetite and reduces subsequent food intake
.
Compared with other areas of DCN, activation of aDCN-Lat will reduce the eating time and amount of food in mice, but it does not affect the frequency of eating and has nothing to do with satiety
.
(Ad: mice fast for 24 hours; eh: mice eat casually) Regarding how eating makes the neurons in the aDCN-Lat area "energetic", researchers believe that this is related to the vagus nerve
.
After eating, the intestine ventilates to the hindbrain through the vagus nerve and projects the signal to aDCN-Lat[5], which activates the neuron and tells you "No, I will not eat"
.
So, how does activated aDCN-Lat neurons cause a reduction in food intake? This is to mention the two kinds of dry food desires mentioned at the beginning of "want to eat" and "want to eat"
.
Betley and her colleagues found that when neurons in the aDCN-Lat area and AgRP neurons were activated at the same time, the increase in food intake that should have been caused by the activation of AgRP neurons did not occur, only the activation of aDCN-Lat neurons The resulting reduction in food intake
.
This seems to be in line with the previous observations.
As long as the neurons in the aDCN-Lat area give an order, even when the AgRP neurons are activated in the starvation state, it is "I am starving to death.
If I jump from here, I won’t Eat something"
.
The activation of aDCN-Lat neurons can cover the activation of AgRP neurons.
On the other hand, the activation of aDCN-Lat neurons actually makes us not feel the joy of dry food! A series of research results show that the activation of aDCN-Lat neurons can enhance the activity of VTA-DA neurons, increase the basal release level of dopamine, reduce the strong and short-term stimulation peaks caused by eating, and thus weaken the reward value of eating
.
For mice with activated aDCN-Lat neurons, once the activity of VTA-DA neurons is inhibited, dopamine levels and food intake will return to normal levels
.
In this regard, the researchers proposed that aDCN-Lat can affect food intake by regulating dopamine levels, which provides a new strategy for the drug treatment of binge eating and deep brain stimulation
.
The activation of aDCN-Lat neurons makes us eat more and less want to eat [6] In general, Betley and her colleagues discovered for the first time that in addition to the hypothalamus that we are familiar with, the cerebellum actually plays a key role in suppressing appetite.
effect
.
After eating, signals from the intestine will activate the glutamatergic neurons of the deep cerebellar nucleus (aDCN-Lat), thereby increasing the basal release level of dopamine, thereby reducing the value of rewards from extra food and reducing food intake
.
This is quite in line with the "personality" of the cerebellum-responsible for our sense of balance
.
"When we mention the cerebellum, we think of its role in coordinating and calibrating sports behavior," commented Dr.
Ralph J.
DiLeone from Yale University School of Medicine.
"This research teaches us that the cerebellum can not only maintain sports balance.
It even maintains a sense of balance in appetite” [6]
.
References: [1]Low AYT, Goldstein N, Gaunt JR, et al.
Reverse-translational identification of a cerebellar satiation network.
Nature.
2021 Nov 17.
doi: 10.
1038/s41586-021-04143-5.
Epub ahead of print PMID: 34789878.
[2]Rossi MA, Stuber GD.
Overlapping Brain Circuits for Homeostatic and Hedonic Feeding.
Cell Metab.
2018 Jan 9;27(1):42-56.
doi: 10.
1016/j.
cmet.
2017.
09.
021 .
Epub 2017 Nov 5.
PMID: 29107504; PMCID: PMC5762260.
[3]Angulo, MA, Butler, MG & Cataletto, ME Prader–Willi syndrome: a review of clinical, genetic, and endocrine findings.
J.
Endocrinol.
Invest.
38, 1249–1263 (2015).
[4]Gautron, L.
, Elmquist, JK & Williams, KW Neural control of energy balance: translatingcircuits to therapies.
Cell 161, 133–145 (2015).
[5]Somana, R .
& Walberg, F.
Cerebellar afferents from the nucleus of the solitary tract.
Neurosci.
Lett.
11,41–47 (1979).
[6]Simerly R, DiLeone R.
Cerebellar neurons that curb food consumption.
Nature.
2021 Nov 17.
doi: 10.
1038/d41586-021-03383-9.
Epub ahead of print.
PMID: 34789886.
Author of this article | Zhang Aidi
.
A friend of Singularity Cake finally determined to lose weight, from "mouth" to "legs"
.
As his strong backing and leading by example, this cake also followed the control of food intake, mainly based on light diets such as round lettuce and broccoli, and refused high-fat food (legs are really immobile)
.
However, the good times are not long
.
Singularity Cake only lasted for three days.
On the fourth day, it broke the defense directly at 9 o'clock in the evening, and dragged him to eat kebabs, grilled small waist, grilled chicken crispy bones, grilled leeks, grilled plate tendons, and grilled steamed buns.
That's right.
, Add a portion of roasted trotters and roasted brain flower
.
The scene was a joy~ After the storm was inhaled, Singularity Cake couldn't help but patted his belly and roared-Is there any way to control this appetite? Recently, J.
Nicholas Betley and her colleagues from the University of Pennsylvania in the United States published an article in the journal “Nature” to clarify the singularity
.
Our cerebellum is the key to suppressing appetite! They found that after eating, signals from the intestine activate the glutamatergic neurons in the deep cerebellar nucleus (aDCN-Lat).
The activation of these neurons will increase the basal release level of dopamine and reduce the intensity caused by eating.
The short-term stimulation peak weakens the reward value brought about by extra food and reduces the food intake [1]
.
Screenshot of the paper's homepage It is often said that we must be the masters of desire! However, one of the strongest desires in nature-dry rice, is really hard to control
.
(Tired, tears) To elaborate on the desire for dry rice, it can be divided into "want to eat" and "want to eat"[2]
.
"To eat" is a "life event" necessary for basic metabolism and survival for the human body system to maintain energy balance through eating in order to keep us alive
.
The AgRP neurons in the arcuate nucleus region of the hypothalamus are responsible for this important event.
After being activated by the hunger signal, they urge us to eat quickly [2]
.
If you want to eat, you have to mention dopamine, the source of happiness, which is the reward mechanism
.
Like a high-fat and high-sugar food, the dopaminergic neurons (VTA-DA) of the striatum will be induced to release dopamine quickly and in large quantities as soon as it is ingested, and enjoy the ultimate happiness [2]
.
But having said that, the two neural circuits "want to eat" and "want to eat" are of course not completely independent of each other [2]
.
Since the motivation for cooking is so sufficient, who is going to suppress appetite? After all, everything cannot be addictive, and eating all the time is not a problem.
For example, patients with Prader Wiley syndrome (PWS) have constant hunger from childhood, and often overeating leads to obesity and type 2 diabetes [3]
.
Studies have found that the hindbrain and hypothalamus are related to the desire to dry meals, but the weight loss treatment for these two areas is not effective [4]
.
So this time, Betley and her colleagues conducted further research and found that the cerebellum turned out to be helping us gauge how much we should eat
.
They first used functional magnetic resonance imaging (fMRI) to track the brain responses of PWS patients and normal people to different signals (food vs.
non-food pictures) under different feelings of fullness (fasting vs.
after eating)
.
The results show that between the PWS group and the control group, the deep cerebellar nucleus (DCN) is the only brain area with significant differences in neural activity, and the lack of response to food signals in the deep cerebellum may be related to the increased food intake of PWS patients
.
Later, the researchers also found in the mouse model that the deep nucleus (aDCN-Lat) region of the lateral cerebellum (aDCN-Lat) of the mouse was activated after eating and the nutrition of the food was digested
.
According to fMRI results, the deep cerebellar nuclei are related to appetite control (dogs and cakes look like real ones) To determine the role of DCN in regulating food intake, Betley and her colleagues performed DCN neuronal activity in mice And eating conditions were tested
.
The results showed that compared with other areas of DCN (aDCN-Int, pDCN-Int, pDCN-Med), only the neurons that activate the aDCN-Lat area can affect the eating of mice
.
And when the aDCN-Lat neurons were activated, the eating frequency and eating speed of the mice were not affected, but the amount and duration of eating were reduced
.
This reduction in food intake has nothing to do with the hunger or fullness of the mice, and whether it makes the mood happy or not (even if you don't eat happy high-fat and high-sugar foods, it is)
.
Conversely, once the aDCN-Lat neurons are inhibited, the mice's food intake will increase
.
Further use of calcium imaging and other technologies found that it is a type of glutamatergic neurons (all expressing Spp1) located in the aDCN-Lat region that are activated after eating, which inhibits appetite and reduces subsequent food intake
.
Compared with other areas of DCN, activation of aDCN-Lat will reduce the eating time and amount of food in mice, but it does not affect the frequency of eating and has nothing to do with satiety
.
(Ad: mice fast for 24 hours; eh: mice eat casually) Regarding how eating makes the neurons in the aDCN-Lat area "energetic", researchers believe that this is related to the vagus nerve
.
After eating, the intestine ventilates to the hindbrain through the vagus nerve and projects the signal to aDCN-Lat[5], which activates the neuron and tells you "No, I will not eat"
.
So, how does activated aDCN-Lat neurons cause a reduction in food intake? This is to mention the two kinds of dry food desires mentioned at the beginning of "want to eat" and "want to eat"
.
Betley and her colleagues found that when neurons in the aDCN-Lat area and AgRP neurons were activated at the same time, the increase in food intake that should have been caused by the activation of AgRP neurons did not occur, only the activation of aDCN-Lat neurons The resulting reduction in food intake
.
This seems to be in line with the previous observations.
As long as the neurons in the aDCN-Lat area give an order, even when the AgRP neurons are activated in the starvation state, it is "I am starving to death.
If I jump from here, I won’t Eat something"
.
The activation of aDCN-Lat neurons can cover the activation of AgRP neurons.
On the other hand, the activation of aDCN-Lat neurons actually makes us not feel the joy of dry food! A series of research results show that the activation of aDCN-Lat neurons can enhance the activity of VTA-DA neurons, increase the basal release level of dopamine, reduce the strong and short-term stimulation peaks caused by eating, and thus weaken the reward value of eating
.
For mice with activated aDCN-Lat neurons, once the activity of VTA-DA neurons is inhibited, dopamine levels and food intake will return to normal levels
.
In this regard, the researchers proposed that aDCN-Lat can affect food intake by regulating dopamine levels, which provides a new strategy for the drug treatment of binge eating and deep brain stimulation
.
The activation of aDCN-Lat neurons makes us eat more and less want to eat [6] In general, Betley and her colleagues discovered for the first time that in addition to the hypothalamus that we are familiar with, the cerebellum actually plays a key role in suppressing appetite.
effect
.
After eating, signals from the intestine will activate the glutamatergic neurons of the deep cerebellar nucleus (aDCN-Lat), thereby increasing the basal release level of dopamine, thereby reducing the value of rewards from extra food and reducing food intake
.
This is quite in line with the "personality" of the cerebellum-responsible for our sense of balance
.
"When we mention the cerebellum, we think of its role in coordinating and calibrating sports behavior," commented Dr.
Ralph J.
DiLeone from Yale University School of Medicine.
"This research teaches us that the cerebellum can not only maintain sports balance.
It even maintains a sense of balance in appetite” [6]
.
References: [1]Low AYT, Goldstein N, Gaunt JR, et al.
Reverse-translational identification of a cerebellar satiation network.
Nature.
2021 Nov 17.
doi: 10.
1038/s41586-021-04143-5.
Epub ahead of print PMID: 34789878.
[2]Rossi MA, Stuber GD.
Overlapping Brain Circuits for Homeostatic and Hedonic Feeding.
Cell Metab.
2018 Jan 9;27(1):42-56.
doi: 10.
1016/j.
cmet.
2017.
09.
021 .
Epub 2017 Nov 5.
PMID: 29107504; PMCID: PMC5762260.
[3]Angulo, MA, Butler, MG & Cataletto, ME Prader–Willi syndrome: a review of clinical, genetic, and endocrine findings.
J.
Endocrinol.
Invest.
38, 1249–1263 (2015).
[4]Gautron, L.
, Elmquist, JK & Williams, KW Neural control of energy balance: translatingcircuits to therapies.
Cell 161, 133–145 (2015).
[5]Somana, R .
& Walberg, F.
Cerebellar afferents from the nucleus of the solitary tract.
Neurosci.
Lett.
11,41–47 (1979).
[6]Simerly R, DiLeone R.
Cerebellar neurons that curb food consumption.
Nature.
2021 Nov 17.
doi: 10.
1038/d41586-021-03383-9.
Epub ahead of print.
PMID: 34789886.
Author of this article | Zhang Aidi
