Glucose is an Enterosyne with deleterious impact of insulin sensitivity

Targeting the enteric nervous system that controls gut motility is now considered as an innovative therapeutic approach in T2D. Indeed, it may limit intestinal glucose absorption and restore the gut‐brain axis to improve insulin sensitivity

So far, little is known about the role of glucose on duodenal contraction in fasted and fed states in normal and diabetic conditions.

Type 2 diabetes (T2D) is associated with a duodenal hypermotility in postprandial conditions that favors hyperglycemia and insulin resistance via the gut-brain axis

Enterosynes, molecules produced within the gut with effects on the enteric nervous system, have been recently discovered and pointed to as potential key modulators of the glycemia. Indeed, targeting the enteric nervous system that controls gut motility is now considered as an innovative therapeutic approach in T2D to limit intestinal glucose absorption and restore the gut-brain axis to improve insulin sensitivity.

Thus, the aim of the present study was to investigate these effects in adult mice. (2)

Methods :

Gene-expression level of glucose transporters (SGLT-1 and GLUT2) were quantified in the duodenum and jejunum of normal and diabetic mice fed with an HFD. The effect of glucose at different concentrations on duodenal and jejunal motility was studied ex vivo using an isotonic sensor in fasted and fed conditions in both normal chow and HFD mice. (3)

Results :

Both SGLT1 and GLUT2 expressions were increased in the duodenum (47 and 300%, respectively) and jejunum (75% for GLUT2) of T2D mice. We observed that glucose stimulates intestinal motility in fasted (200%) and fed (400%) control mice via GLUT2 by decreasing enteric nitric oxide release (by 600%), a neurotransmitter that inhibits gut contractions.

This effect was not observed in diabetic mice, suggesting that glucose sensing and mechanosensing are altered during T2D. (4)

Conclusions :

Glucose acts as an enterosyne to control intestinal motility and glucose absorption through the enteric nervous system. Our data demonstrate that GLUT2 and a reduction of NO production could both be involved in this stimulatory contracting effect.

Source : Wemelle E, Carneiro L, Abot A, Lesage J, Cani PD, Knauf C. Glucose Stimulates Gut Motility in Fasted and Fed Conditions: Potential Involvement of a Nitric Oxide Pathway. Nutrients. 2022 May 23;14(10):2176. doi: 10.3390/nu14102176. PMID: 35631317; PMCID: PMC9143273.




Salon BioFIT 2023

Join us for Salon BioFIT2023 where we'll come together to foster a sens of community, collaboration and success. Let's meet !Booking plateform link Maybe you can also like : Foodtech innovative research boosted with gut and gut-brain axis

Enteric neurons for functional applications in health care

Pharmaceuticals Studying the role of the Enteric Nervous System (ENS) in the development of gut-brain pathologies (e.g., Alzheimer’s, Parkinson’s, diabetes, aging, stress, visceral pain) is an ever-expanding research topic. Researchers are starting to propose numerous...

Enteric neurons and glycemia control

The gut-brain axis:You have a message from your gut In the intestine, gut distension and nutrients are detected by mechanoreceptors and chemoreceptors, respectively. The activation of these receptors sends an afferent nervous message to the hypothalamus in the brain....

The enteric nervous system is our second brain

  The enteric nervous system (ENS), referred to as the “second brain,” is an extensive network of different cell types located along the digestive tract. It consists in enteric neurons, enteric glial cells and interstitial cells of Cajal. This network of cells is...