Effect of a Feeding Schedule on Crypt Cell Proliferation in the Small Intestine of the Rat

Digestion ◽  
1979 ◽  
Vol 19 (2) ◽  
pp. 140-143 ◽  
Author(s):  
B. Callaghan
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Crypt Cell ◽  
Feeding Schedule ◽  
Crypt Cell Proliferation

scholarly journals The Effect of Ischemic Villus Cell Damage on Crypt Cell Proliferation in the Small Intestine

1976 ◽  
Vol 71 (5) ◽  
pp. 786-792 ◽  
Author(s):  
R.P.C. Rijke ◽  
W.R. Hanson ◽  
H.M. Plaisier ◽  
J.W. Osborne
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Cell Damage ◽  
Crypt Cell ◽  
Crypt Cell Proliferation ◽  
Villus Cell

scholarly journals Spdef deletion rescues the crypt cell proliferation defect in conditional Gata6 null mouse small intestine

2014 ◽  
Vol 15 (1) ◽  
pp. 3 ◽  
Author(s):  
Boaz E Aronson ◽  
Kelly A Stapleton ◽  
Laurens ATM Vissers ◽  
Eva Stokhuijzen ◽  
Hanneke Bruijnzeel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Crypt Cell ◽  
Null Mouse ◽  
Crypt Cell Proliferation ◽  
Mouse Small Intestine

A growth-stimulating activity derived from the proximal small intestine is associated with an adaptive response

1990 ◽  
Vol 68 (5) ◽  
pp. 646-649 ◽  
Author(s):  
V. L. Grey ◽  
C. L. Morin
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Thymidine Kinase ◽  
Kinase Activity ◽  
Crypt Cell ◽  
General Mechanism ◽  
Cell Renewal ◽  
Thymidine Kinase Activity ◽  
Crypt Cell Proliferation ◽  
Proximal Intestine

Luminal nutrition is important for the maintenance of small intestinal structure and function. The equilibrium between crypt cell production and villous cell loss in the mucosal epithelium of the small intestine is altered under certain conditions such as after a small bowel resection. Immediately after resection, there is a marked increase in crypt cell proliferation giving rise to an adaptive hyperplasia in the remnant intestine and for this response luminal nutrition is a critical factor. We have previously demonstrated the presence of a growth-stimulating (GS) activity in a heat-stable acidic extract of the rat proximal intestine 24, 48, and 96 h after resection, which is coincidental with an increase in crypt cell proliferation as measured by thymidine kinase activity. Eight days after resection when the GS activity is no longer detectable, the thymidine kinase activity returns to control values. The molecular weights of the peptides associated with this GS activity are 4500 and 1500, as determined by Sephadex gel filtration. Of note is that the oral intake of food is necessary for the appearance of the GS activity postoperatively. The presence of the GS activity has also been demonstrated upon refeeding after a fast, as well as at weaning in the rat, two physiological situations known to be associated with increased proliferation in the small intestine. This GS activity in the proximal intestine first detected in the resection model may represent a general mechanism by which food controls the cell renewal pattern of the small intestine.Key words: stimulating activity, proximal intestine, adaptation.

Reduction of mucosal crypt cell proliferation in patients with colorectal adenomatous polyps by dietary calcium supplementation

1992 ◽  
Vol 79 (6) ◽  
pp. 581-583 ◽  
Author(s):  
G. H. Barsoum ◽  
C. Hendrickse ◽  
M. C. Winslet ◽  
D. Youngs ◽  
I. A. Donovan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Calcium Supplementation ◽  
Dietary Calcium ◽  
Crypt Cell ◽  
Adenomatous Polyps ◽  
Crypt Cell Proliferation

scholarly journals Glucagon-Like Peptide-2 Activates β-Catenin Signaling in the Mouse Intestinal Crypt: Role of Insulin-Like Growth Factor-I

Endocrinology ◽  
2007 ◽  
Vol 149 (1) ◽  
pp. 291-301 ◽  
Author(s):  
Philip E. Dubé ◽  
Katherine J. Rowland ◽  
Patricia L. Brubaker
Keyword(s):  
Cell Proliferation ◽  
Nuclear Translocation ◽  
Glycogen Synthase ◽  
Crypt Cell ◽  
Acute Administration ◽  
Intestinal Crypt ◽  
Crypt Cell Proliferation ◽  
Igf I ◽  
Glucagon Like Peptide ◽  
Crypt Cells

Chronic administration of glucagon-like peptide-2 (GLP-2) induces intestinal growth and crypt cell proliferation through an indirect mechanism requiring IGF-I. However, the intracellular pathways through which IGF-I mediates GLP-2-induced epithelial tropic signaling remain undefined. Because β-catenin and Akt are important regulators of crypt cell proliferation, we hypothesized that GLP-2 activates these signaling pathways through an IGF-I-dependent mechanism. In this study, fasted mice were administered Gly2-GLP-2 or LR3-IGF-I (positive control) for 0.5–4 h. Nuclear translocation of β-catenin in non-Paneth crypt cells was assessed by immunohistochemistry and expression of its downstream proliferative markers, c-myc and Sox9, by quantitative RT-PCR. Akt phosphorylation and activation of its targets, glycogen synthase kinase-3β and caspase-3, were determined by Western blot. IGF-I receptor (IGF-IR) and IGF-I signaling were blocked by preadministration of NVP-AEW541 and through the use of IGF-I knockout mice, respectively. We found that GLP-2 increased β-catenin nuclear translocation in non-Paneth crypt cells by 72 ± 17% (P < 0.05) and increased mucosal c-myc and Sox9 mRNA expression by 90 ± 20 and 376 ± 170%, respectively (P < 0.05–0.01), with similar results observed with IGF-I. This effect of GLP-2 was prevented by blocking the IGF-IR as well as ablation of IGF-I signaling. GLP-2 also produced a time- and dose-dependent activation of Akt in the intestinal mucosa (P < 0.01), most notably in the epithelium. This action was reduced by IGF-IR inhibition but not IGF-I knockout. We concluded that acute administration of GLP-2 activates β-catenin and proliferative signaling in non-Paneth murine intestinal crypt cells as well as Akt signaling in the mucosa. However, IGF-I is required only for the GLP-2-induced alterations in β-catenin.

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