The cornucopia of intestinal chemosensory transduction

Bertrand, Paul

doi:10.3389/neuro.21.003.2009

Cited by 39 publications

(36 citation statements)

References 111 publications

(135 reference statements)

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“…S1), axonal conduction between mucosa and the MP was required for the increased IPAN excitability elicited. APs would conduct the sensory signals orthodromically (that is, in the usual direction) from the region of sensory transduction towards the somata within the MP 46 . We devised experiments to record such orthodromic responses from IPANs in real-time 21 .…”

Section: Discussionmentioning

confidence: 99%

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

et al. 2013

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Symbionts or probiotics are known to affect the nervous system. To understand the mechanisms involved, it is important to measure sensory neuron responses and identify molecules responsible for this interaction. Here we test the effects of adding Lactobacillus rhamnosus (JB-1) and Bacteroides fragilis to the epithelium while making voltage recordings from intestinal primary afferent neurons. Sensory responses are recorded within 8 s of applying JB-1 and excitability facilitated within 15 min. Bacteroides fragilis produces similar results, as does its isolated, capsular exopolysaccharide, polysaccharide A. Lipopolysaccharide-free polysaccharide A completely mimics the neuronal effects of the parent organism. Experiments with a mutant Bacteroides fragilis devoid of polysaccharide A shows that polysaccharide A is necessary and sufficient for the neuronal effects. Complex carbohydrates have not been reported before as candidates for such signalling between symbionts and the host. These observations indicate new neuronal targets and invite further study of bacterial carbohydrates as inter-kingdom signalling molecules between beneficial bacteria and sensory neurons.

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Section: Discussionmentioning

confidence: 99%

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

et al. 2013

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“…Although originally located in enteric neurons (64), it may also exist in intestinal cells where it could detect luminal glucose (80,258). There are many comprehensive reviews of this fast-developing field (25,30,71,79,183,221,224,228,247,279), and the present paper focuses instead on the postoral sugar-sensing processes that may mediate carbohydrate-conditioned flavor preferences.…”

Section: Oral and Postoral Carbohydrate Sensing And Preferencementioning

confidence: 97%

Role of gut nutrient sensing in stimulating appetite and conditioning food preferences

Sclafani

Ackroff

2012

American Journal of Physiology-Regulatory, Integrative and Comp

166

186

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The discovery of taste and nutrient receptors (chemosensors) in the gut has led to intensive research on their functions. Whereas oral sugar, fat, and umami taste receptors stimulate nutrient appetite, these and other chemosensors in the gut have been linked to digestive, metabolic, and satiating effects that influence nutrient utilization and inhibit appetite. Gut chemosensors may have an additional function as well: to provide positive feedback signals that condition food preferences and stimulate appetite. The postoral stimulatory actions of nutrients are documented by flavor preference conditioning and appetite stimulation produced by gastric and intestinal infusions of carbohydrate, fat, and protein. Recent findings suggest an upper intestinal site of action, although postabsorptive nutrient actions may contribute to flavor preference learning. The gut chemosensors that generate nutrient conditioning signals remain to be identified; some have been excluded, including sweet (T1R3) and fatty acid (CD36) sensors. The gut-brain signaling pathways (neural, hormonal) are incompletely understood, although vagal afferents are implicated in glutamate conditioning but not carbohydrate or fat conditioning. Brain dopamine reward systems are involved in postoral carbohydrate and fat conditioning but less is known about the reward systems mediating protein/glutamate conditioning. Continued research on the postoral stimulatory actions of nutrients may enhance our understanding of human food preference learning.

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“… Model of intestinal sensing by sweet taste cells and mucosal vagal afferents (adapted, with permission, from Bertrand, 2009) . (A) Intestinal wall showing villus–crypt and location of sweet taste cells.…”

Section: Parallels Between Tongue and Small Intestinal Taste Mechanismsmentioning

confidence: 99%

Sensing Via Intestinal Sweet Taste Pathways

Young¹

2011

Front. Neurosci.

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The detection of nutrients in the gastrointestinal (GI) tract is of fundamental significance to the control of motility, glycemia and energy intake, and yet we barely know the most fundamental aspects of this process. This is in stark contrast to the mechanisms underlying the detection of lingual taste, which have been increasingly well characterized in recent years, and which provide an excellent starting point for characterizing nutrient detection in the intestine. This review focuses on the form and function of sweet taste transduction mechanisms identified in the intestinal tract; it does not focus on sensors for fatty acids or proteins. It examines the intestinal cell types equipped with sweet taste transduction molecules in animals and humans, their location, and potential signals that transduce the presence of nutrients to neural pathways involved in reflex control of GI motility.

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The cornucopia of intestinal chemosensory transduction

Cited by 39 publications

References 111 publications

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

Role of gut nutrient sensing in stimulating appetite and conditioning food preferences

Sensing Via Intestinal Sweet Taste Pathways

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