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Involvement of the gut chemosensory system in the regulation of colonic anion secretion.

Kuwahara A - Biomed Res Int (2015)

Bottom Line: However, study of the regulation of gut function by the gut chemosensory system has become increasingly important, as failure of this system causes dysfunctions in host homeostasis, as well as functional GI disorders.Furthermore, regulation of ion transport in the colon is critical for host defense and for electrolytes balance.This review discusses the role of the gut chemosensory system in epithelial transport, with a particular emphasis on the colon.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Physiology, School of Food and Nutritional Sciences/Graduate Division of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, 422-8526, Japan.

ABSTRACT
The primary function of the gastrointestinal (GI) tract is the extraction of nutrients from the diet. Therefore, the GI tract must possess an efficient surveillance system that continuously monitors the luminal content for beneficial or harmful compounds. Recent studies have shown that specialized cells in the intestinal lining can sense changes in this content. These changes directly influence fundamental GI processes such as secretion, motility, and local blood flow via hormonal and/or neuronal pathways. Until recently, most studies examining the control of ion transport in the colon have focused on neural and hormonal regulation. However, study of the regulation of gut function by the gut chemosensory system has become increasingly important, as failure of this system causes dysfunctions in host homeostasis, as well as functional GI disorders. Furthermore, regulation of ion transport in the colon is critical for host defense and for electrolytes balance. This review discusses the role of the gut chemosensory system in epithelial transport, with a particular emphasis on the colon.

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Schematic diagram of Cl− secretion stimulated by a bitter tastant (6-PTU) in colonic epithelial cells. Activation of apical T2R by luminal bitter tastant results in the synthesis of prostaglandin. This prostaglandin then induces an increase in intracellular cAMP concentration ([cAMP]i). Elevated [cAMP]i activates the CFTR Cl− channels to mediate Cl−/HCO3− secretion. Activation of T2R simultaneously causes an increase in [Ca2+]i. The elevated [Ca2+]i modulates the Ca2+-activated basolateral K+ channels, providing a driving force for the exit of Cl−/HCO3−.
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fig2: Schematic diagram of Cl− secretion stimulated by a bitter tastant (6-PTU) in colonic epithelial cells. Activation of apical T2R by luminal bitter tastant results in the synthesis of prostaglandin. This prostaglandin then induces an increase in intracellular cAMP concentration ([cAMP]i). Elevated [cAMP]i activates the CFTR Cl− channels to mediate Cl−/HCO3− secretion. Activation of T2R simultaneously causes an increase in [Ca2+]i. The elevated [Ca2+]i modulates the Ca2+-activated basolateral K+ channels, providing a driving force for the exit of Cl−/HCO3−.

Mentions: PGE2 is known to increase the concentration of intracellular cAMP in colonic epithelial cells [52]. It has also been reported that STC-1, a mouse enteroendocrine cell line, expresses T2R mRNA and that 10−3 M 6-PTU increases the intracellular Ca2+ concentration ([Ca2+]i) [12]. These results raise the possibility that bitter tastants (including 6-PTU) that induce an increase in [Ca2+]i in colonic epithelia and that elicit Cl−/HCO3− secretion do so via interactions with PGs (Figure 2).


Involvement of the gut chemosensory system in the regulation of colonic anion secretion.

Kuwahara A - Biomed Res Int (2015)

Schematic diagram of Cl− secretion stimulated by a bitter tastant (6-PTU) in colonic epithelial cells. Activation of apical T2R by luminal bitter tastant results in the synthesis of prostaglandin. This prostaglandin then induces an increase in intracellular cAMP concentration ([cAMP]i). Elevated [cAMP]i activates the CFTR Cl− channels to mediate Cl−/HCO3− secretion. Activation of T2R simultaneously causes an increase in [Ca2+]i. The elevated [Ca2+]i modulates the Ca2+-activated basolateral K+ channels, providing a driving force for the exit of Cl−/HCO3−.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4383346&req=5

fig2: Schematic diagram of Cl− secretion stimulated by a bitter tastant (6-PTU) in colonic epithelial cells. Activation of apical T2R by luminal bitter tastant results in the synthesis of prostaglandin. This prostaglandin then induces an increase in intracellular cAMP concentration ([cAMP]i). Elevated [cAMP]i activates the CFTR Cl− channels to mediate Cl−/HCO3− secretion. Activation of T2R simultaneously causes an increase in [Ca2+]i. The elevated [Ca2+]i modulates the Ca2+-activated basolateral K+ channels, providing a driving force for the exit of Cl−/HCO3−.
Mentions: PGE2 is known to increase the concentration of intracellular cAMP in colonic epithelial cells [52]. It has also been reported that STC-1, a mouse enteroendocrine cell line, expresses T2R mRNA and that 10−3 M 6-PTU increases the intracellular Ca2+ concentration ([Ca2+]i) [12]. These results raise the possibility that bitter tastants (including 6-PTU) that induce an increase in [Ca2+]i in colonic epithelia and that elicit Cl−/HCO3− secretion do so via interactions with PGs (Figure 2).

Bottom Line: However, study of the regulation of gut function by the gut chemosensory system has become increasingly important, as failure of this system causes dysfunctions in host homeostasis, as well as functional GI disorders.Furthermore, regulation of ion transport in the colon is critical for host defense and for electrolytes balance.This review discusses the role of the gut chemosensory system in epithelial transport, with a particular emphasis on the colon.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Physiology, School of Food and Nutritional Sciences/Graduate Division of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, 422-8526, Japan.

ABSTRACT
The primary function of the gastrointestinal (GI) tract is the extraction of nutrients from the diet. Therefore, the GI tract must possess an efficient surveillance system that continuously monitors the luminal content for beneficial or harmful compounds. Recent studies have shown that specialized cells in the intestinal lining can sense changes in this content. These changes directly influence fundamental GI processes such as secretion, motility, and local blood flow via hormonal and/or neuronal pathways. Until recently, most studies examining the control of ion transport in the colon have focused on neural and hormonal regulation. However, study of the regulation of gut function by the gut chemosensory system has become increasingly important, as failure of this system causes dysfunctions in host homeostasis, as well as functional GI disorders. Furthermore, regulation of ion transport in the colon is critical for host defense and for electrolytes balance. This review discusses the role of the gut chemosensory system in epithelial transport, with a particular emphasis on the colon.

Show MeSH
Related in: MedlinePlus