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Click on the blue to pay attention to the AgRP neurons and POMC neurons of the arcuate nucleus (ARH) of our hypothalamus that control appetite.
Among them, AgRP neurons produce appetite, and POMC neurons inhibit appetite.
Asprosin is a protein hormone released from adipose tissue, which can activate AgRP neurons and inhibit POMC neurons.
Studies have shown that mice have anorexia symptoms after inhibiting AgRP neurons, and after activating this type of neurons, the mice will continue to eat even if they are full.
Although AgRP neurons have a two-way regulatory effect on eating, there is currently no specific target for this loop therapy.
On April 21, 2021, the Roger D.
Cone research team of the University of Michigan Life Sciences Institute published an article in Science Translational Medicine, revealing that the melanocortin receptor 3 has the potential to treat anorexia by regulating the AgRP neuronal circuit.
The distribution of MC3R in the brain The researchers used clear brain technology to detect MC3R (melanocortin receptor 3) mainly distributed in the ventromedial nucleus of the hypothalamus and ARH.
In terms of neuron types, MC3R is more expressed in AgRP neurons that promote diet.
In addition, the distribution of MC3R in hypothalamic ARH is gender-specific: the expression level in male mice is almost twice that of female mice.
This gender-specific distribution of MC3R also exists in humans.
After the researchers performed social isolation models on wild-type mice and MC3R knockout mice, they found that MC3R knockout mice (whether female or male) raised in a single cage showed symptoms of anorexia, weight loss, and anxiety-like symptoms.
.
In the chronic restraint stress model, wild-type mice showed anorexia symptoms.
However, anorexia was aggravated after MC3R was knocked out, but it only appeared in male mice.Even if there is no stress, mice still show anorexia after MC3R is knocked out.
Chemical genetics technology manipulates MC3R neurons to regulate dietary behavior.
In order to further determine the role of MC3R-expressing neurons in the ARH brain area in the diet, the researchers injected AAV-DREADD-hM3Dq or AAV-DREADD-hM3Dq into the ARH brain area of MC3R-cre tool mice.
The AAV-DREADD-hM4Di virus achieves chronic activation or inhibition of MC3R neurons.
The results found that after activating the above-mentioned neurons, it can significantly promote the diet of mice and improve anxiety-like behavior; while inhibiting this type of neurons, it inhibits eating and promotes anxiety-like behavior.
Previous studies have shown that low-dose MC3R agonist d-Trp-8-γ-melanocyte stimulating hormone promotes diet, and high-dose can cause anorexia symptoms.
After the researchers injected the MC3R specific agonist C18 into the brain ventricle, wild-type mice developed severe appetite, which promoted food intake by more than 50% 6 hours after the administration.
However, knocking out the MC3R agonist completely failed.
The chronically inhibiting the activity of AgRP neurons in the ARH brain area after C18 injection into the cerebral ventricle can block the effect of C18 in promoting diet.
However, wild-type mice developed severe anorexia symptoms after injection of the MC3R specific antagonist C11 into the cerebral ventricle, and the dietary intake was reduced by about 4 times 6 hours after the administration.
After injecting AAV-GCAMP6s into the paraventricular nucleus of MC4R-cre mice, the researchers found that C18 can indeed inhibit the activity of MC4R neurons in the paraventricular nucleus after administration of C18 to the cerebral ventricle.
This is consistent with the results of previous studies: MC3R regulates the presynaptic release of the inhibitory transmitter GABA into the paraventricular nucleus MC4R neurons in AgRP neurons.
In general, this article uses a variety of techniques to determine the gender difference in the distribution of MC3R in the hypothalamus, and reveals the great potential of MC3R compounds in solving binge eating or anorexia.
[References] 1.
Sweeney et al.
, Sci.
Transl.
Med.
13, eabd6434 (2021) The pictures in the article are all from the references
Among them, AgRP neurons produce appetite, and POMC neurons inhibit appetite.
Asprosin is a protein hormone released from adipose tissue, which can activate AgRP neurons and inhibit POMC neurons.
Studies have shown that mice have anorexia symptoms after inhibiting AgRP neurons, and after activating this type of neurons, the mice will continue to eat even if they are full.
Although AgRP neurons have a two-way regulatory effect on eating, there is currently no specific target for this loop therapy.
On April 21, 2021, the Roger D.
Cone research team of the University of Michigan Life Sciences Institute published an article in Science Translational Medicine, revealing that the melanocortin receptor 3 has the potential to treat anorexia by regulating the AgRP neuronal circuit.
The distribution of MC3R in the brain The researchers used clear brain technology to detect MC3R (melanocortin receptor 3) mainly distributed in the ventromedial nucleus of the hypothalamus and ARH.
In terms of neuron types, MC3R is more expressed in AgRP neurons that promote diet.
In addition, the distribution of MC3R in hypothalamic ARH is gender-specific: the expression level in male mice is almost twice that of female mice.
This gender-specific distribution of MC3R also exists in humans.
After the researchers performed social isolation models on wild-type mice and MC3R knockout mice, they found that MC3R knockout mice (whether female or male) raised in a single cage showed symptoms of anorexia, weight loss, and anxiety-like symptoms.
.
In the chronic restraint stress model, wild-type mice showed anorexia symptoms.
However, anorexia was aggravated after MC3R was knocked out, but it only appeared in male mice.Even if there is no stress, mice still show anorexia after MC3R is knocked out.
Chemical genetics technology manipulates MC3R neurons to regulate dietary behavior.
In order to further determine the role of MC3R-expressing neurons in the ARH brain area in the diet, the researchers injected AAV-DREADD-hM3Dq or AAV-DREADD-hM3Dq into the ARH brain area of MC3R-cre tool mice.
The AAV-DREADD-hM4Di virus achieves chronic activation or inhibition of MC3R neurons.
The results found that after activating the above-mentioned neurons, it can significantly promote the diet of mice and improve anxiety-like behavior; while inhibiting this type of neurons, it inhibits eating and promotes anxiety-like behavior.
Previous studies have shown that low-dose MC3R agonist d-Trp-8-γ-melanocyte stimulating hormone promotes diet, and high-dose can cause anorexia symptoms.
After the researchers injected the MC3R specific agonist C18 into the brain ventricle, wild-type mice developed severe appetite, which promoted food intake by more than 50% 6 hours after the administration.
However, knocking out the MC3R agonist completely failed.
The chronically inhibiting the activity of AgRP neurons in the ARH brain area after C18 injection into the cerebral ventricle can block the effect of C18 in promoting diet.
However, wild-type mice developed severe anorexia symptoms after injection of the MC3R specific antagonist C11 into the cerebral ventricle, and the dietary intake was reduced by about 4 times 6 hours after the administration.
After injecting AAV-GCAMP6s into the paraventricular nucleus of MC4R-cre mice, the researchers found that C18 can indeed inhibit the activity of MC4R neurons in the paraventricular nucleus after administration of C18 to the cerebral ventricle.
This is consistent with the results of previous studies: MC3R regulates the presynaptic release of the inhibitory transmitter GABA into the paraventricular nucleus MC4R neurons in AgRP neurons.
In general, this article uses a variety of techniques to determine the gender difference in the distribution of MC3R in the hypothalamus, and reveals the great potential of MC3R compounds in solving binge eating or anorexia.
[References] 1.
Sweeney et al.
, Sci.
Transl.
Med.
13, eabd6434 (2021) The pictures in the article are all from the references
