You know when you’re eating and you feel your stomach getting full and you start to slow down? The reason we are able to do that is because our stomach has innervations from both the sympathetic and parasympathetic nervous system.
Our stomach sends and receives information via the vagus nerve (Dr. Campisi’s favorite), dorsal root ganglion (DRG), and enteric neurons (Umans, 2018). Enteric neurons come from our enteric nervous system, which is the nervous system that works independently from our central nervous system and helps control gastrointestinal functions. The vagus nerve plays an important role in detecting the stretch of our stomach. These sensors can activate neural responses that decrease appetite and control our digestion. The sensory transduction at the molecular level is not yet well understood, but with further research it is possible that it could provide some therapeutic targets to help curb appetite (Umans, 2018).
Some of the gut hormones that communicate with our brain when we are full include cholecystokinin (CCK) and peptide YY (PYY) and are considered satiety hormones (Umans, 2018). The nutrients that our intestines absorb are what triggers CCK release but surprisingly do not activate gastric mechanoreceptors that would detect the stretch. It turns out that the gastric mechanoreceptors and the intestinal chemoreceptors are different populations of cells (Umans, 2018). It is hypothesized that the mechanoreceptors have a certain threshold to activate the satiety signals during a meal before the intestines can register the intake of nutrients (Umans, 2018).
It’s interesting to see how our body works together but also independently of other systems in order to tell us what exactly we need to know.
Umans, B. D., & Liberles, S. D. (2018). Neural Sensing of Organ Volume. Trends in neurosciences, 41(12), 911–924. https://doi.org/10.1016/j.tins.2018.07.008
The above description clearly illustrates the importance of enteric and central nervous system communication. What happens if this communication is disrupted? Are satiety signals still a valuable control mechanism?
ReplyDeleteAs an attempt to answer these questions I found a few animal studies that lesioned specific brain regions believed to be involved in the regulation of eating. Interesting results were found; however, there has not been success in illustrating similar results in humans. Obvious ethical concerns prevent the exact experiment from being performed on humans, but I did find a study by Farr et al., (2016) who creatively utilized brain imaging techniques to test the regulation of the central nervous system in individuals who overeat. Interestingly, they did not indicate any physical disruption or abnormalities in neural tissue. The results actually indicated altered activity in the reward pathway that sends a reward signal through the release of neurotransmitters, like dopamine (Farr et al., 2016).
I can personally relate to this rewarding sensation when eating my favorite meal or treat, but it seems to occur prior to the sensation of satiety. Although, the transition from enjoyably full to uncomfortably full can happen extremely quick, I personally feel the sensation of satiety inhibits my reward response. Individuals who overeat are believed to either have a hyperactive or hypoactive reward response to eating (Farr et al., 2016). This indicates that an individual may continue to eat pass the level of satiety because they are still receiving enjoyment that overrides the sensation of being full or that an individual will continue to overeat until they receive the delayed reward (Farr et al., 2016).
I believe incorporating the reward response into the mechanisms of satiety could offer some valuable information to help better understand sensory transduction at the molecular level. Understanding, this complicated interaction between the enteric system and reward pathway may also allow for pharmaceutical control that is often seen for addictive substances.
Farr OM, Li CR, Mantzoros CS. Central nervous system regulation of eating: Insights from human brain imaging. Metabolism. 2016 May;65(5):699-713. doi: 10.1016/j.metabol.2016.02.002. Epub 2016 Feb 6. PMID: 27085777; PMCID: PMC4834455.