[…] the microbiome and its products directly influence differentiation and function of EECs…
[…] prebiotics change the gut microbiota composition […] and thereby increase the integrity of the gut barrier and prevent bacterial metabolites from crossing the barrier, entering the circulation, and promoting systemic inflammation…
[…] changing the quality of nutritional intake is accompanied by a modulation of the gut microbiota, which in turn probably affects EECs…
Learning about gut peptides or hormones can lead to surprises. For instance, taste receptors (bitter, sweet, etc.) exist not only in the mouth, but also in the intestinal tract, and exert influence over what the neurotransmitters and neuromodulators do throughout the body.
Why does the stomach have taste receptors? For Gizmodo.com, Esther Inglis-Arkell writes:
Bitter-flavored compounds have an effect on us as they are digested. The effect takes about a half hour, and it kicks in only after a decent meal, but eventually the bitter flavor causes the stomach to stop emptying, making us feel fuller longer.
Researchers have developed a theory about this. Since bitterness could be a sign of toxicity, which might overwhelm the body’s defenses if released all at once, the stomach retains these contents longer so the other organs have a chance to handle the possible threat in an orderly manner.
The taste receptors in the mouth are connected with the conscious mind, for the pleasure of eating, of course, but also to warn us about things that we should make the decision immediately to spit out. As the other half of an elegant two-part expulsion system, there are also taste receptors deep in the colon, over which we have no conscious control. But if it detects too much bitterness, the colon “triggers a release of ions, which in turn causes water to pour into the gut via osmosis, and the body experiences diarrhea.”
The main thing to know about the interior taste receptors is that in obese people, they are somehow out of whack. For example:
Altered expression of taste molecules, including increased expression of gustatory signaling elements and a decrease in T1R3, the sweet-umami receptor, has also been reported in the gastric mucosa of morbidly obese patients compared to controls.
The point here is, chances are good that members of the gut microbiome are capable of either enhancing or impeding the efforts of EECs to do the right thing. If the bugs can help prevent or reverse obesity, their help needs to be enlisted.
As these study authors express it:
The identification of sensory receptors detecting changes in luminal contents in diet-induced weight increase represents an important step toward the elucidation of the molecular events underlying intraluminal chemosensing and ultimately the discovery of new therapeutic approaches for obesity.
The other point is, when faced with the challenge to rewire eating habits, there is no better tool than W8Loss2Go.
Your responses and feedback are welcome!
Source: “Regulation of Appetite, Satiation, and Body Weight by Enteroendocrine Cell,” Karger.com, February 2015
Source: “You Have Taste Receptors in Your Colon. Here’s Why,” Gizmodo.com, 08/18/15
Source: “Expression of the Bitter Taste Receptor, T2R38, in Enteroendocrine Cells of the Colonic Mucosa of Overweight/Obese vs. Lean Subjects,” Plos.org, 02/11/16
Photo credit: Pierre Vignau via Visualhunt.com/CC BY