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Click on the blue word to follow us Both sucrose and artificial sweeteners can induce sweetness sensations, but animals and humans prefer sucrose
.
Even mice lacking taste receptors were able to distinguish between sucrose and sweeteners
.
While perception of sweetness depends on the tongue, the duodenum plays an important role in distinguishing between sucrose and sweeteners
.
Sweet, bitter or umami taste receptor cells of the tongue form purinergic synapses with afferent nerve fibers to differentiate taste
.
In the nose, olfactory receptor cells transmit odor stimuli to mitral cells through glutamatergic synapses to help animals identify odors
.
In the gut, this function depends on Neuropod cells
.
Neuropod cells are a type of intestinal sensory epithelial cells that can form synapses and release hormones such as CCK (cholecystokinin)
.
CCK-positive Neuropod cells form glutamatergic synapses with vagal nodose neurons to rapidly transmit sensory signals from the duodenum to the brain
.
January 13, 2022 Diego V.
Bohórquez's research team at Duke University explains the biological mechanism by which mice prefer to consume sucrose: through glutamatergic signaling in Neuropod cells
.
The researchers anesthetized the mice and infused them with sucrose, D-glucose, D-fructose, D-galactose, sweeteners, and α-methylglucopyranoside (α-MGP, a sucrose analog), almost all of which were described above.
All stimuli could induce vagal firing, but D-fructose did not
.
Figure 1: Identification of cell populations specifically responsive to sucrose and sweeteners CCK-positive Neuropod cells were found to be partially sucrose and partially responsive to sweeteners by a calcium indicator (Figure 1)
.
To further differentiate cell populations that specifically respond to sucrose or sweeteners, they screened both sweet receptor (T1R3) and sodium-glucose transporter 1 (SGLT1)-positive cells by single-cell sequencing of CCK-positive Neuropod cells.
group
.
After blocking T1R3, sweeteners could not induce vagal firing; while sucrose could not induce vagal firing after SGLT1 inhibition
.
In vitro tissue culture experiments found that sucrose, but not sweeteners, could induce intestinal epithelial secretion of glutamate.
After blocking ionotropic and metabotropic glutamate receptors, sucrose could not induce vagal firing activity, but sweeteners still could.
evoked vagal firing activity, suggesting that the neurotransmitter glutamate is involved in the vagus nerve's perception of sucrose information
.
Previous studies have shown that taste receptor cells in the tongue release ATP, which activates purinergic receptors on sensory neurons in response to sweet stimuli
.
The researchers found that inhibiting purinergic receptors blocked the vagus nerve's response to sweeteners, suggesting that ATP is involved in the vagus nerve's perception of sweeteners
.
Figure 2: Components of the gut optogenetics system To enable further manipulation of gut epithelial cells, researchers developed gut optogenetics tools (Figure 2)
.
After photoinhibition of CCK-positive Neuropod cells in duodenal epithelial cells, perfusion of sucrose and sweeteners did not induce the firing activity of vagus nerve
.
Under normal circumstances, mice prefer sucrose to sweeteners, but after light-specific inhibition of intestinal Neuropod cells, mice ingested less sucrose and more sweeteners
.
Activating this type of cells prompted the mice to eat more sweeteners, a boosting effect that was blocked by inhibiting glutamate receptors
.
Collectively, our findings using gut genetics techniques demonstrate that duodenal Neuropod cells transmit sucrose and sweetener stimulatory signals to distinct vagal ganglion neurons via distinct neurotransmitters (glutamate and ATP) populations (T1R3-positive cells and SGLT1-positive cell populations)
.
[Reference] 1 https://doi.
org/10.
1038/s41593-021-00982-72.
https://doi.
org/10.
1038/s41593-021-00998-z The pictures in the text are from the reference
.
Even mice lacking taste receptors were able to distinguish between sucrose and sweeteners
.
While perception of sweetness depends on the tongue, the duodenum plays an important role in distinguishing between sucrose and sweeteners
.
Sweet, bitter or umami taste receptor cells of the tongue form purinergic synapses with afferent nerve fibers to differentiate taste
.
In the nose, olfactory receptor cells transmit odor stimuli to mitral cells through glutamatergic synapses to help animals identify odors
.
In the gut, this function depends on Neuropod cells
.
Neuropod cells are a type of intestinal sensory epithelial cells that can form synapses and release hormones such as CCK (cholecystokinin)
.
CCK-positive Neuropod cells form glutamatergic synapses with vagal nodose neurons to rapidly transmit sensory signals from the duodenum to the brain
.
January 13, 2022 Diego V.
Bohórquez's research team at Duke University explains the biological mechanism by which mice prefer to consume sucrose: through glutamatergic signaling in Neuropod cells
.
The researchers anesthetized the mice and infused them with sucrose, D-glucose, D-fructose, D-galactose, sweeteners, and α-methylglucopyranoside (α-MGP, a sucrose analog), almost all of which were described above.
All stimuli could induce vagal firing, but D-fructose did not
.
Figure 1: Identification of cell populations specifically responsive to sucrose and sweeteners CCK-positive Neuropod cells were found to be partially sucrose and partially responsive to sweeteners by a calcium indicator (Figure 1)
.
To further differentiate cell populations that specifically respond to sucrose or sweeteners, they screened both sweet receptor (T1R3) and sodium-glucose transporter 1 (SGLT1)-positive cells by single-cell sequencing of CCK-positive Neuropod cells.
group
.
After blocking T1R3, sweeteners could not induce vagal firing; while sucrose could not induce vagal firing after SGLT1 inhibition
.
In vitro tissue culture experiments found that sucrose, but not sweeteners, could induce intestinal epithelial secretion of glutamate.
After blocking ionotropic and metabotropic glutamate receptors, sucrose could not induce vagal firing activity, but sweeteners still could.
evoked vagal firing activity, suggesting that the neurotransmitter glutamate is involved in the vagus nerve's perception of sucrose information
.
Previous studies have shown that taste receptor cells in the tongue release ATP, which activates purinergic receptors on sensory neurons in response to sweet stimuli
.
The researchers found that inhibiting purinergic receptors blocked the vagus nerve's response to sweeteners, suggesting that ATP is involved in the vagus nerve's perception of sweeteners
.
Figure 2: Components of the gut optogenetics system To enable further manipulation of gut epithelial cells, researchers developed gut optogenetics tools (Figure 2)
.
After photoinhibition of CCK-positive Neuropod cells in duodenal epithelial cells, perfusion of sucrose and sweeteners did not induce the firing activity of vagus nerve
.
Under normal circumstances, mice prefer sucrose to sweeteners, but after light-specific inhibition of intestinal Neuropod cells, mice ingested less sucrose and more sweeteners
.
Activating this type of cells prompted the mice to eat more sweeteners, a boosting effect that was blocked by inhibiting glutamate receptors
.
Collectively, our findings using gut genetics techniques demonstrate that duodenal Neuropod cells transmit sucrose and sweetener stimulatory signals to distinct vagal ganglion neurons via distinct neurotransmitters (glutamate and ATP) populations (T1R3-positive cells and SGLT1-positive cell populations)
.
[Reference] 1 https://doi.
org/10.
1038/s41593-021-00982-72.
https://doi.
org/10.
1038/s41593-021-00998-z The pictures in the text are from the reference
