galanin/dijareja

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Rotavirus infection of murine small intestine causes colonic secretion via age restricted galanin-1 receptor expression.

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OBJECTIVE Mechanisms for age restriction of rotavirus diarrhea are unclear. Because rotavirus primarily infects small intestine, colonic contribution has not been widely studied. Recent data suggest that colonic secretion postbacterial infection is mediated by galanin-1 receptors (Gal1-R). We

Dextran sulfate sodium-induced murine colitis activates NF-kappaB and increases galanin-1 receptor expression.

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Galanin is widely distributed in enteric nerve terminals and acts to modulate intestinal motility by altering smooth muscle contraction. This ligand causes Cl(-) secretion when colonic epithelial cells express the galanin-1 receptor (Gal1-R) subtype. Because Gal1-R expression by colonic epithelia is

Pathogenic Escherichia coli increase Cl- secretion from intestinal epithelia by upregulating galanin-1 receptor expression.

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Galanin is widely distributed in enteric nerve terminals lining the human gastrointestinal (GI) tract. We have shown previously that galanin-1 receptors (Gal1-R) are expressed by epithelial cells lining the human GI tract, and upon activation cause Cl- secretion. Because expression of this receptor

Galanin causes Cl- secretion in the human colon. Potential significance of inflammation-associated NF-kappa B activation on galanin-1 receptor expression and function.

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Galanin is widely distributed in enteric nerves and nerve terminals throughout the gastrointestinal (GI) tract. Within the GI tract galanin is best known for its ability to alter smooth muscle contractility and regulate intestinal motility. However, recent studies also indicate that galanin can

Galanin-1 receptor up-regulation mediates the excess colonic fluid production caused by infection with enteric pathogens.

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Galanin is widely distributed in enteric nerve terminals lining the gastrointestinal tract. We previously showed that pathogenic Escherichia coli, but not normal commensal organisms, increase galanin-1 receptor expression by epithelial cells lining the colon (i.e., colonocytes). When present,

Gastric emptying in animal models of human diabetes: correlation to blood glucose level and gut neuroendocrine peptide content.

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Gastric emptying was measured in non-obese diabetic (NOD) and in obese diabetic mice. The feces were collected and the water content was determined. The neuroendocrine peptides known to regulate gastrointestinal motility, namely secretin, gastric inhibitory peptide (GIP), motilin, somatostatin,

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