High‐fat diets on the enteric nervous system: Possible interactions and mechanisms underlying dysmotility

Abstract

Summary Obesity is a chronic disease that affects various physiological systems. Among them, the gastrointestinal tract appears to be a main target of this disease. High‐fat diet (HFD) animal models can help recapitulate the classic signs of obesity and present a series of gastrointestinal alterations, mainly dysmotility. Because intestinal motility is governed by the enteric nervous system (ENS), enteric neurons, and glial cells have been studied in HFD models. Given the importance of the ENS in general gut physiology, this review aims to discuss the relationship between HFD‐induced neuroplasticity and gut dysmotility observed in experimental models. Furthermore, we highlight components of the gut environment that might influence enteric neuroplasticity, including gut microbiota, enteric glio‐epithelial unit, serotonin release, immune cells, and disturbances such as inflammation and oxidative stress.

Neurohormonal Changes in the Gut–Brain Axis and Underlying Neuroendocrine Mechanisms following Bariatric Surgery

“…Lastly, one of the main divisions of the ANS is the enteric nervous system (ENS), which is derived from neural crest cells and governs the motility of the GI tract [ 80 ]. The ENS is found in two forms: the myenteric plexus located between the longitudinal and circular muscle layers in the GI tract and the submucosal plexus located in the submucosa layer [ 80 ].…”

“…Lastly, one of the main divisions of the ANS is the enteric nervous system (ENS), which is derived from neural crest cells and governs the motility of the GI tract [ 80 ]. The ENS is found in two forms: the myenteric plexus located between the longitudinal and circular muscle layers in the GI tract and the submucosal plexus located in the submucosa layer [ 80 ]. The ENS is characterized as the “second brain”, as it can operate independently from the SNS and PNS through neurotransmitters similar to those that used by the CNS (serotonin, GABA, NPY and endocannabinoids) that are involved in appetite regulation and energy metabolism [ 81 , 82 ].…”

“…The ENS is significantly influenced by changes in gut microbiota that lead to alterations in appetite-regulatory neurotransmitters. These alterations may affect aspects of gut motility related to gastric emptying and intestinal transit [ 80 ]. Bravo et al observed that modifications to the animal gut microbiome after treatment with Lactobacillus rhamnosis led to changes in the mRNA expression of GABA in CNS regions [ 83 ].…”

Antihypertensives and Antibiotics: Impact on Intestinal Dysfunction and Hypertension

“…10 Mechanistically, studies in obese animal models link dysbiosis and low-grade inflammation to altered nerve function and dysmotility. 9,11…”

The role of the gastrointestinal barrier in obesity‐associated systemic inflammation

“…Various morphological alterations have also been reported in the myenteric plexus following exposure to Western and high fat diet including axonal swelling, cytoskeletal filament disruption, and shrinkage of both ganglia and neuronal soma 119,120 . Changes in enteric neuron density, morphology, and neurochemical coding have previously been correlated with GI dysfunction in several conditions including IBD, IBS, and Hirschsprung's disease, and achalasia only recently has an emerging relationship between the ENS and GI symptoms in obesity been reported 122 …”