Intestinal chemosensitivity.

Mei, N.

doi:10.1152/physrev.1985.65.2.211

Cited by 241 publications

(101 citation statements)

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“…Similar transduction for mucosal chemosensory afferents can range from a few hundred ms for acetate 33 to 10 or 20 s for amino acids 37,38 , long-chain fatty acids 39 or glucose 35 . As responses to JB-1 were about 8 s, it is unlikely that it's inter-kingdom signalling molecule is acetate or low pH but would be consistent with a saccharide, as we have shown for PSA.…”

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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“…Vagal afferents from the gastrointestinal tract project to the hypothalamus (4,31) and are, among others, important for blood glucose regulation (3,38). The gastrointestinal tract features glucoreceptors and osmoreceptors (13,25), as well as sweet-taste receptors (12). Intestinal glucoreceptors take part in glucoregulation by mediating nervous control of insulin release via the vagus nerve (26) and glucoseinduced increases in pancreatic islet blood flow (6).…”

Section: Discussionmentioning

confidence: 99%

Oral glucose intake inhibits hypothalamic neuronal activity more effectively than glucose infusion

Smeets¹,

Vidarsdottir²,

Graaf³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Smeets PA, Vidarsdottir S, de Graaf C, Stafleu A, van Osch MJ, Viergever MA, Pijl H, van der Grond J. Oral glucose intake inhibits hypothalamic neuronal activity more effectively than glucose infusion. Am J Physiol Endocrinol Metab 293: E754-E758, 2007. First published June 12, 2007; doi:10.1152/ajpendo.00231.2007.-We previously showed that hypothalamic neuronal activity, as measured by the blood oxygen level-dependent (BOLD) functional MRI signal, declines in response to oral glucose intake. To further explore the mechanism driving changes in hypothalamic neuronal activity in response to an oral glucose load, we here compare hypothalamic BOLD signal changes subsequent to an oral vs. an intravenous (iv) glucose challenge in healthy humans. Seven healthy, normal-weight men received four interventions in random order after an overnight fast: 1) ingestion of glucose solution (75 g in 300 ml) or 2) water (300 ml), and 3) iv infusion of 40% glucose solution (0.5 g/kg body wt, maximum 35 g) or 4) infusion of saline (0.9% NaCl, equal volume). The BOLD signal was recorded as of 8 min prior to intervention (baseline) until 30 min after. Glucose infusion was associated with a modest and transient signal decline in the hypothalamus. In contrast, glucose ingestion was followed by a profound and persistent signal decrease despite the fact that plasma glucose levels were almost threefold lower than in response to iv administration. Accordingly, glucose ingestion tended to suppress hunger more than iv infusion (P Ͻ 0.1). We infer that neural and endocrine signals emanating from the gastrointestinal tract are critical for the hypothalamic response to nutrient ingestion. functional magnetic resonance imaging; glucose homeostasis; insulin; incretins THE BLOOD OXYGEN LEVEL-DEPENDENT (BOLD) signal, produced by functional magnetic resonance imaging (fMRI), is a noninvasive measure of neuronal activity (19, 30,35). We (36, 37) have recently shown that the BOLD signal in the upper part of the hypothalamus of healthy, normal-weight humans consistently declines in response to an oral glucose load, which strongly suggests that glucose ingestion blunts hypothalamic neuronal activity in these subjects. The hypothalamus plays a critical role in the control of energy balance. Neural circuits in hypothalamic nuclei perceive and integrate endocrine and metabolic cues reflecting bodily energy content to coordinate behavior and fuel flux so as to maintain energy homeostasis (28, 34). Thus, adaptations of hypothalamic neuronal activity driven by nutrient ingestion may serve to guard energy equilibrium in the face of an environmental challenge.The mechanism linking glucose intake and changes in hypothalamic neuronal activity in humans is currently unknown. Various metabolic and endocrine cues are worthwhile to consider. Circulating levels of glucose can be sensed by specialized neurons in the arcuate and ventromedial nuclei of the hypothalamus, and these neurons project to other key nuclei (21). Alternatively, insulin inhibits NPY neuronal activit...

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“…This chemosensory information appears to be important for the regulation of various aspects of gastrointestinal secretion, resorption, and motility (1,2). Classical examples of intestinal chemosensitivity are the dependence of gastric emptying on the chemical nature of the nutrients present in the small intestine and the involvement of chemical preabsorption information in short-term regulation of food intake (2).…”

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confidence: 99%

Taste receptor-like cells in the rat gut identified by expression of alpha-gustducin.

Höfer

Püschel²,

Drenckhahn³

1996

Proc. Natl. Acad. Sci. U.S.A.

358

292

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The a-subunit of the trimeric G-protein complex specific for taste receptor cells of the tongue, a-gustducin, is described here to be also expressed in the stomach and intestine. The a-gustducin-containing cells were identified as brush cells that are scattered throughout the surface epithelium of the gut and share structural features of taste receptor cells of the tongue. These findings provide clues to the long-sought molecular and cellular basis for chemoreception in the gut.It is generally believed that the epithelium lining the inner surface of the gut can sense chemical components of the lumenal contents. This chemosensory information appears to be important for the regulation of various aspects of gastrointestinal secretion, resorption, and motility (1, 2). Classical examples of intestinal chemosensitivity are the dependence of gastric emptying on the chemical nature of the nutrients present in the small intestine and the involvement of chemical preabsorption information in short-term regulation of food intake (2). The cellular and molecular basis for chemoreception in the gut is hitherto unknown. In this study we addressed the question ofwhether the epithelium of the gut might express a-gustducin, the GTP-binding a-subunit of a trimeric Gprotein complex that is specific for taste receptor cells of the tongue (3). Here we show that a-gustducin is also expressed in the epithelium of the gut where it is associated with a specialized cell type long known under the names brush cell, tufted cell, or caveolated cell (4-6). The function of this cell type, which is present in humans, rats, and probably all other mammals, had been enigmatic until now. MATERIALS AND METHODSAntibodies and Immunostaining. A polyclonal antibody specific for a-gustducin was raised in a rabbit immunized with a synthetic peptide comprising amino acid residues 92-113 of the rat a-gustducin sequence (3). This sequence stretch is unique for a-gustducin and is not present in the sequences of any other known G-protein. Antibodies were affinity-purified to the peptide adsorbed to nitrocellulose (7,8). Polyclonal rabbit antibodies specific for chromogranin A and serotonin (9) and mouse monoclonal antibodies to villin (Dianova, Hamburg, Germany) and cytokeratin 18 (Progen, Heidelberg) were also used in this study. Indirect immunofluorescence was applied to 1-,um thick tissue sections of quick-frozen and Epon-embedded tissues as described (8). For doubleimmunofluorescence sections were incubated with a mixture of the rabbit antibody against a-gustducin and mouse monoclonal antibodies either specific for villin or cytokeratin 18. Primary antibodies were diluted with PBS: anti-gustducin (1:200), anti-chromogranin (1:4,000), anti-serotonin (1:10,000), anti-villin (0.1 /Lg/ml-1), anti-cytokeratin 18 (0.5 ,ug/ml-1). As secondary antibodies fluorescein isothiocyanate-labeled goat anti-mouse IgG and tetramethylrhodamine isothiocyanate-labeled goat anti-rabbit IgG (Dianova) were used at concentrations of 0.1 Ag/ml-1.Immunoblotting. Various tissue...

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Intestinal chemosensitivity.

Cited by 241 publications

References 0 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

Oral glucose intake inhibits hypothalamic neuronal activity more effectively than glucose infusion

Taste receptor-like cells in the rat gut identified by expression of alpha-gustducin.

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