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Click on the blue word to pay attention to that the sensory neurons that innervate our intestines are the main afferent pathways of the gut-brain axis.
After eating, they transmit nutrients and energy signals from the intestine to the brain, causing a feeling of fullness and adjusting glucose
.
Different sensory neurons innervate different organs of the gastrointestinal tract and respond to different intestinal signals
.
Binge eating, weight gain, insulin resistance and many other factors can cause sensory neurons to damage intestinal nutrient delivery signals
.
Single-cell sequencing results showed that there are neurons with multiple molecular characteristics in the vagus nerve nodule and dorsal root ganglion, and these vagus neurons are involved in gastrointestinal reactions
.
Infusion of nutrients or hypertonic solution into the small intestine can activate GRP65-expressing neurons
.
In addition, stimulating neurons expressing GLP1 receptors can reduce feeding, while activating neurons expressing tyrosine hydroxylase in the nucleus tractus solitarius can promote feeding behavior
.
On May 26, 2021, the Henning Fenselau research team of the Max Planck Institute in Germany published an article in Cell Metabolism, revealing that different enteric nerves and vagus nerve afferents form different neural circuits, which control food intake and peripheral glucose respectively.
Metabolism
.
Vagus nerve input of vagus nerve nodule and dorsal root ganglion.
Researchers have constructed specific GLP1R-cre and GRP65-cre tool mice and found that vagus nerve fibers expressing GLP1 are mainly enriched and expressed in the fundus and body of the stomach, while GPR65 is expressed in the vagus nerve.
The incoming gastric nerves are very sparsely innervated and are limited to the mucosal layer of the gastric body and antrum
.
But in the small intestine, GLP1R and GPR65 vagus nerve afferent nerves densely innervate the duodenum and jejunum villi
.
This indicates that GLP1R and GPR65 vagus nerve afferents have different innervation patterns for the stomach and small intestine
.
Inhibition of GLP1R and GPR65 vagus nerve afferent activity.
They further used hM3Dq-ZsGreen tool mice to hybridize with GLP1R-cre and GRP65-cre to achieve specific activation of GLP1R and GRP65 vagus nerves.
They found that GLP1R was activated at night or in fasting for 16 hours The eating behavior of middle mice was significantly reduced, and activating GRP65 did not affect the eating behavior of mice
.
Through PET imaging technology, it is found that after activation of GLP1R, it is projected to the basal hypothalamus (MBH) of the brain, the supraoptic nucleus (SON) of the hypothalamus, the lateral parabrachial nucleus, the nucleus tractus solitarius (NTS), and the ventral tegmental area (VTA) ), paraventricular thalamus (PVT), basolateral amygdala (BLA), insular cortex (IC) and dorsal striatum, and many other brain regions are all activated; and the main downstream brain regions MBH, VTA after activation of GRP65 , PVT and BLA are activated
.
Although inhibiting GLP1R at night or after fasting did not affect the eating behavior of mice
.
However, in anorexia caused by lithium chloride or CCK, inhibiting the GLP1R vagus nerve can promote the eating behavior of mice, and inhibiting GRP65 will not exert the effect of promoting diet
.
After activating the GLP1R vagus nerve of satiety mice, the blood glucose content decreases, which promotes glucose tolerance by enhancing the ability of skeletal muscle glucose uptake; while activating the GRP65 vagus nerve mainly promotes the production of liver glucose and causes the increase of peripheral glucose content
.
In the process of food intake and blood glucose regulation, GLP1 and GRP65 have different mechanisms of action on the vagus nerve
.
In summary, this article uses a variety of tools to systematically dissect the molecular characteristics of intestinal sensory neurons.
The vagus nerve afferent to the glucagon-like peptide 1 receptor (GLP1R) that innervates the intestinal nerve will cause anorexia.
The signal is transmitted to the parabrachial nucleus neurons that inhibit eating, and GRP65 vagus nerve afferents that innervate the intestinal nerves stimulate the peripheral liver to synthesize glucose
.
[References] 1.
https://doi.
org/10.
1016/j.
cmet.
2021.
05.
002, the pictures in the text are all from the reference original download link: https://pan.
baidu.
com/s/1YkugrKFbp_iCQ7KiPIz3Ug Extraction code: qe6k
After eating, they transmit nutrients and energy signals from the intestine to the brain, causing a feeling of fullness and adjusting glucose
.
Different sensory neurons innervate different organs of the gastrointestinal tract and respond to different intestinal signals
.
Binge eating, weight gain, insulin resistance and many other factors can cause sensory neurons to damage intestinal nutrient delivery signals
.
Single-cell sequencing results showed that there are neurons with multiple molecular characteristics in the vagus nerve nodule and dorsal root ganglion, and these vagus neurons are involved in gastrointestinal reactions
.
Infusion of nutrients or hypertonic solution into the small intestine can activate GRP65-expressing neurons
.
In addition, stimulating neurons expressing GLP1 receptors can reduce feeding, while activating neurons expressing tyrosine hydroxylase in the nucleus tractus solitarius can promote feeding behavior
.
On May 26, 2021, the Henning Fenselau research team of the Max Planck Institute in Germany published an article in Cell Metabolism, revealing that different enteric nerves and vagus nerve afferents form different neural circuits, which control food intake and peripheral glucose respectively.
Metabolism
.
Vagus nerve input of vagus nerve nodule and dorsal root ganglion.
Researchers have constructed specific GLP1R-cre and GRP65-cre tool mice and found that vagus nerve fibers expressing GLP1 are mainly enriched and expressed in the fundus and body of the stomach, while GPR65 is expressed in the vagus nerve.
The incoming gastric nerves are very sparsely innervated and are limited to the mucosal layer of the gastric body and antrum
.
But in the small intestine, GLP1R and GPR65 vagus nerve afferent nerves densely innervate the duodenum and jejunum villi
.
This indicates that GLP1R and GPR65 vagus nerve afferents have different innervation patterns for the stomach and small intestine
.
Inhibition of GLP1R and GPR65 vagus nerve afferent activity.
They further used hM3Dq-ZsGreen tool mice to hybridize with GLP1R-cre and GRP65-cre to achieve specific activation of GLP1R and GRP65 vagus nerves.
They found that GLP1R was activated at night or in fasting for 16 hours The eating behavior of middle mice was significantly reduced, and activating GRP65 did not affect the eating behavior of mice
.
Through PET imaging technology, it is found that after activation of GLP1R, it is projected to the basal hypothalamus (MBH) of the brain, the supraoptic nucleus (SON) of the hypothalamus, the lateral parabrachial nucleus, the nucleus tractus solitarius (NTS), and the ventral tegmental area (VTA) ), paraventricular thalamus (PVT), basolateral amygdala (BLA), insular cortex (IC) and dorsal striatum, and many other brain regions are all activated; and the main downstream brain regions MBH, VTA after activation of GRP65 , PVT and BLA are activated
.
Although inhibiting GLP1R at night or after fasting did not affect the eating behavior of mice
.
However, in anorexia caused by lithium chloride or CCK, inhibiting the GLP1R vagus nerve can promote the eating behavior of mice, and inhibiting GRP65 will not exert the effect of promoting diet
.
After activating the GLP1R vagus nerve of satiety mice, the blood glucose content decreases, which promotes glucose tolerance by enhancing the ability of skeletal muscle glucose uptake; while activating the GRP65 vagus nerve mainly promotes the production of liver glucose and causes the increase of peripheral glucose content
.
In the process of food intake and blood glucose regulation, GLP1 and GRP65 have different mechanisms of action on the vagus nerve
.
In summary, this article uses a variety of tools to systematically dissect the molecular characteristics of intestinal sensory neurons.
The vagus nerve afferent to the glucagon-like peptide 1 receptor (GLP1R) that innervates the intestinal nerve will cause anorexia.
The signal is transmitted to the parabrachial nucleus neurons that inhibit eating, and GRP65 vagus nerve afferents that innervate the intestinal nerves stimulate the peripheral liver to synthesize glucose
.
[References] 1.
https://doi.
org/10.
1016/j.
cmet.
2021.
05.
002, the pictures in the text are all from the reference original download link: https://pan.
baidu.
com/s/1YkugrKFbp_iCQ7KiPIz3Ug Extraction code: qe6k
