Temporal differentiation and migration of substance P, serotonin, and secretin immunoreactive enteroendocrine cells in the mouse proximal small intestine

1992 ◽  
Vol 194 (4) ◽  
pp. 303-310 ◽  
Author(s):  
Kimberly D. Aiken ◽  
Kevin A. Roth
Keyword(s):  
Small Intestine ◽  
Substance P ◽  
Enteroendocrine Cells ◽  
Proximal Small Intestine ◽  
Temporal Differentiation ◽  
And Migration

Heligmosomoides, polygyrus, (syn. Nematospiroides, dubius), (Nematoda): distribution and net fluxes of glucose, H2O, Na+, K+, and Cl− in the mouse small intestine

1984 ◽  
Vol 62 (1) ◽  
pp. 37-40 ◽  
Author(s):  
M. V. K. Sukhdeo ◽  
D. F. Mettrick
Keyword(s):  
Small Intestine ◽  
Water Flux ◽  
Heligmosomoides Polygyrus ◽  
Glucose Flux ◽  
Proximal Small Intestine ◽  
Normal Transmission ◽  
And Migration ◽  
Duodenal Lumen ◽  
Net Fluxes

Mice were infected with 150 larvae of Heligmosomoides, polygyrus, and the effect of the worms on net fluxes of glucose, H2O, and electrolytes was followed from days 1–21 postinfection (PI) by means of an in vivo, perfusion technique. Maximum recovery of larvae was 77% at 5 days PI, and 64% for adults at 12 days PI following their emergence and migration into the duodenal lumen between days 7 and 9 PI. Inflammation decreased rapidly from day 9 PI onwards. Net glucose flux significantly decreased during the emergence of the adult worms (7–9 days PI). Water flux decreased and Na+ fluxes became negative at 5 days PI; Na+ and Cl− fluxes were negative at 7 days PI. Following the relocation of the adult worms in the proximal small intestine, fluxes returned to their normal levels. The differential changes in the net fluxes of glucose, H2O, and electrolytes suggest the secretion of a toxinlike substance by the parasites. In the normal mouse host, small infections have a temporary pathophysiological effect on the intestinal mucosa, differing significantly from previous studies using the abnormal rat host and large larval infections. As normal transmission of H. polygyrus, is by contamination, small infections, as employed in this study, probably reflect the natural condition.

scholarly journals Pdx1 inactivation restricted to the intestinal epithelium in mice alters duodenal gene expression in enterocytes and enteroendocrine cells

2009 ◽  
Vol 297 (6) ◽  
pp. G1126-G1137 ◽  
Author(s):  
Chin Chen ◽  
Rixun Fang ◽  
Corrine Davis ◽  
Charalambos Maravelias ◽  
Eric Sibley
Keyword(s):  
Gene Expression ◽  
Alkaline Phosphatase ◽  
Small Intestine ◽  
Intestinal Epithelium ◽  
Mouse Strain ◽  
Paneth Cell ◽  
Cell Number ◽  
Enteroendocrine Cells ◽  
Mrna Abundance ◽  
Proximal Small Intestine

Null mutant mice lacking the transcription factor pancreatic and duodenal homeobox 1 (Pdx1) are apancreatic and survive only a few days after birth. The role of Pdx1 in regulating intestinal gene expression has therefore yet to be determined in viable mice with normal pancreatic development. We hypothesized that conditional inactivation of Pdx1 restricted to the intestinal epithelium would alter intestinal gene expression and cell differentiation. Pdx1 flox/flox; VilCre mice with intestine-specific Pdx1 inactivation were generated by crossing a transgenic mouse strain expressing Cre recombinase, driven by a mouse villin 1 gene promoter fragment, with a mutant mouse strain homozygous for loxP site-flanked Pdx1. Pdx1 protein is undetectable in all epithelial cells in the intestinal epithelium of Pdx1 flox/flox; VilCre mice. Goblet cell number and mRNA abundance for mucin 3 and mucin 13 genes in the proximal small intestine are comparable between Pdx1 flox/flox; VilCre and control mice. Similarly, Paneth cell number and expression of Paneth cell-related genes Defa1, Defcr-rs1, and Mmp7 in the proximal small intestine remain statistically unchanged by Pdx1 inactivation. Although the number of enteroendocrine cells expressing chromogranin A/B, gastric inhibitory polypeptide (Gip), or somatostatin (Sst) is unaffected in the Pdx1 flox/flox; VilCre mice, mRNA abundance for Gip and Sst is significantly reduced in the proximal small intestine. Conditional Pdx1 inactivation attenuates intestinal alkaline phosphatase (IAP) activity in the duodenal epithelium, consistent with an average 91% decrease in expression of the mouse enterocyte IAP gene, alkaline phosphatase 3 (a novel Pdx1 target candidate), in the proximal small intestine following Pdx1 inactivation. We conclude that Pdx1 is necessary for patterning appropriate gene expression in enterocytes and enteroendocrine cells of the proximal small intestine.

The Patterns of Simultaneous Intraluminal Pressure Changes in the Human Proximal Small Intestine

1964 ◽  
Vol 47 (3) ◽  
pp. 258-268 ◽  
Author(s):  
Gerald Friedman ◽  
Jerome D. Waye ◽  
Leonard A. Weingarten ◽  
Henry D. Janowitz
Keyword(s):  
Small Intestine ◽  
Intraluminal Pressure ◽  
Proximal Small Intestine ◽  
Pressure Changes

scholarly journals A High Retinol Dietary Intake Increases its Apical Absorption by the Proximal Small Intestine of Juvenile Sunshine Bass (Morone chrysops × M. saxatilis)

2002 ◽  
Vol 132 (9) ◽  
pp. 2713-2716 ◽  
Author(s):  
Randal K. Buddington ◽  
Karyl K. Buddington ◽  
Dong-Fang Deng ◽  
Gro-Ingunn Hemre ◽  
Robert P. Wilson
Keyword(s):  
Small Intestine ◽  
Dietary Intake ◽  
Morone Chrysops ◽  
Sunshine Bass ◽  
Proximal Small Intestine

Tachykinin Activation of Muscarinic Inhibition in Canine Small Intestine is Substance P in Nature

1987 ◽  
pp. 146-148
Author(s):  
J. E. T. Fox ◽  
T. J. McDonald ◽  
L. Alford ◽  
F. Kostolanska
Keyword(s):  
Small Intestine ◽  
Substance P

Splanchnic tissues undergo hypoxic stress during whole body hyperthermia

1999 ◽  
Vol 276 (5) ◽  
pp. G1195-G1203 ◽  
Author(s):  
David M. Hall ◽  
Kirk R. Baumgardner ◽  
Terry D. Oberley ◽  
Carl V. Gisolfi
Keyword(s):  
Small Intestine ◽  
Heat Stress ◽  
Heat Exposure ◽  
Metabolic Stress ◽  
Liver Glycogen ◽  
Whole Body ◽  
Hypoxic Cell ◽  
Hypoxic Stress ◽  
Proximal Small Intestine ◽  
Radical Content

Exposure of conscious animals to environmental heat stress increases portal venous radical content. The nature of the observed heat stress-inducible radical molecules suggests that hyperthermia produces cellular hypoxic stress in liver and intestine. To investigate this hypothesis, conscious rats bearing in-dwelling portal venous and femoral artery catheters were exposed to normothermic or hyperthermic conditions. Blood gas levels were monitored during heat stress and for 24 h following heat exposure. Hyperthermia significantly increased arterial O2saturation, splanchnic arterial-venous O2difference, and venous[Formula: see text], while decreasing venous O2saturation and venous pH. One hour after heat exposure, liver glycogen levels were decreased ∼20%. Two hours after heat exposure, the splanchnic arterial-venous O2difference remained elevated in heat-stressed animals despite normal Tc. A second group of rats was exposed to similar conditions while receiving intra-arterial injections of the hypoxic cell marker [3H]misonidazole. Liver and intestine were biopsied, and [3H]misonidazole content was quantified. Heat stress increased tissue [3H]misonidazole retention 80% in the liver and 29% in the small intestine. Cellular [3H]misonidazole levels were significantly elevated in intestinal epithelial cells and liver zone 2 and 3 hepatocytes and Kupffer cells. This effect was most prominent in the proximal small intestine and small liver lobi. These data provide evidence that hyperthermia produces cellular hypoxia and metabolic stress in splanchnic tissues and suggest that cellular metabolic stress may contribute to radical generation during heat stress.

Transport of butyric acid in vascularly perfused anuran small intestine: importance of pH and anion transport

1986 ◽  
Vol 250 (4) ◽  
pp. G469-G474
Author(s):  
D. Hollander ◽  
E. M. Gerard ◽  
C. A. Boyd
Keyword(s):  
Small Intestine ◽  
Butyric Acid ◽  
Nonlinear Function ◽  
Anion Transport ◽  
Transport Protein ◽  
Disulfonic Acid ◽  
Flux Analysis ◽  
Acid Transport ◽  
Distal Small Intestine ◽  
Proximal Small Intestine

Butyric acid transport was studied in the isolated, vascularly perfused frog small intestine. At luminal butyric acid concentrations of 5-50 mM, absorption was a nonlinear function of the luminal concentration, whereas the relationship of absorption to concentration remained linear at 0-1,000 microM. The most important factor regulating the rate and direction of butyric acid transport was the pH. We used unidirectional flux analysis to determine net transport across the epithelium while the pH of the luminal or vascular compartments was changed. We found a four- to fivefold decrease in butyric acid transport into the portal circulation as the lumen pH was increased from 6.0 to 8.0. The pH of the vascular perfusate influenced the vascular-to-lumen transport of butyric acid in the same proportions. The second important regulatory factor of butyric acid transport was the 4,4'-diisothiocyananostilbene-2,2'-disulfonic acid (DIDS)-sensitive anion transport protein. DIDS added to the lumen at 10(-6) M decreased butyric acid transport by approximately 40% at pH 7.4. DIDS also inhibited butyric acid transport when added to the vascular perfusate or when transport was measured in a vascular-to-lumen direction. We suggest that, at the relatively low pH of the proximal small intestine, butyric acid becomes protonated and lipophilic and is mainly transported directly through the cell membrane. At the more alkaline pH of the distal small intestine butyric acid is in the ionized form and transport by the DIDS-sensitive anion transport protein may predominate.

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