scholarly journals Esophageal Angiolipoma: A Tongue-Like Mucosal Mass

2020 ◽  
Author(s):  
Jun Yi ◽  
Xiaowei Liu ◽  
Fujun Li
Keyword(s):  
Mucosal Mass

scholarly journals Insulin signal transduction in rat small intestine: role of MAP kinases in expression of mucosal hydrolases

2001 ◽  
Vol 280 (2) ◽  
pp. G229-G240 ◽  
Author(s):  
Soheila Marandi ◽  
Nadine De Keyser ◽  
Alain Saliez ◽  
Anne-Sophie Maernoudt ◽  
Etienne Marc Sokal ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Map Kinase ◽  
Insulin Receptor ◽  
Map Kinases ◽  
Kinase Inhibitor ◽  
Protein Kinase B ◽  
Insulin Signal Transduction ◽  
Mitogen Activated Protein ◽  
Src Homology ◽  
Mucosal Mass

The postreceptor events regulating the signal of insulin downstream in rat intestinal cells have not yet been analyzed. Our objectives were to identify the nature of receptor substrates and phosphorylated proteins involved in the signaling of insulin and to investigate the mechanism(s) by which insulin enhances intestinal hydrolases. In response to insulin, the following proteins were rapidly phosphorylated on tyrosine residues: 1) insulin receptor substrates-1 (IRS-1), -2, and -4; 2) phospholipase C-isoenzyme-γ; 3) the Ras-GTPase-activating protein (GAP) associated with Rho GAP and p62Src; 4) the insulin receptor β-subunit; 5) the p85 subunits of phosphatidylinositol 3-kinase (PI 3-kinase); 6) the Src homology 2 α-collagen protein; 7) protein kinase B; 8) mitogen-activated protein (MAP) kinase-1 and -2; and 9) growth receptor-bound protein-2. Compared with controls, insulin enhanced the intestinal activity of MAP kinase-2 and protein kinase B by two- and fivefold, respectively, but did not enhance p70/S6 ribosomal kinase. Administration of an antireceptor antibody or MAP-kinase inhibitor PD-98059 but not a PI 3-kinase inhibitor (wortmannin) to sucklings inhibited the effects of insulin on mucosal mass and enzyme expression. We conclude that normal rat enterocytes express all of the receptor substrates and mediators involved in different insulin signaling pathways and that receptor binding initiates a signal enhancing brush-border membrane hydrolase, which appears to be regulated by the cascade of MAP kinases but not by PI 3-kinase.

scholarly journals Early but not late administration of glucagon-like peptide-2 following ileo-cecal resection augments putative intestinal stem cell expansion

2009 ◽  
Vol 296 (3) ◽  
pp. G643-G650 ◽  
Author(s):  
Aaron P. Garrison ◽  
Christopher M. Dekaney ◽  
Douglas C. von Allmen ◽  
P. Kay Lund ◽  
Susan J. Henning ◽  
...  
Keyword(s):  
Side Population ◽  
Intestinal Failure ◽  
Serum Levels ◽  
Optimal Timing ◽  
Side Population Cells ◽  
Stem Cell Expansion ◽  
Crypt Fission ◽  
Igf I ◽  
Glucagon Like Peptide ◽  
Mucosal Mass

Expansion of intestinal progenitors and putative stem cells (pISC) occurs early and transiently following ileo-cecal resection (ICR). The mechanism controlling this process is not defined. We hypothesized that glucagon-like peptide-2 (GLP-2) would augment jejunal pISC expansion only when administered to mice immediately after ICR. Since recent reports demonstrated increases in intestinal insulin-like growth factor (IGF)-I following GLP-2 administration, we further hypothesized that increased intestinal IGF-I expression would correlate with pISC expansion following ICR. To assess this, GLP-2 or vehicle was administered to mice either immediately after resection (early) or before tissue harvest 6 wk following ICR (late). Histological analysis quantified proliferation and intestinal morphometrics. Serum levels of GLP-2 were measured by ELISA and jejunal IGF-I mRNA by qRT-PCR. Expansion of jejunal pISC was assessed by fluorescent-activated cell sorting of side population cells, immunohistochemistry for phosphorylated β-catenin at serine 552 (a pISC marker), percent of crypt fission, and total numbers of crypts per jejunal circumference. We found that early but not late GLP-2 treatment after ICR significantly augmented pISC expansion. Increases in jejunal IGF-I mRNA correlated temporally with early pISC expansion and effects of GLP-2. Early GLP-2 increased crypt fission and accelerated adaptive increases in crypt number and intestinal caliber. GLP-2 increased proliferation and intestinal morphometrics in all groups. This study shows that, in mice, GLP-2 promotes jejunal pISC expansion only in the period immediately following ICR. This is associated with increased IGF-I and accelerated adaptive increases in mucosal mass. These data provide clinical rationale relevant to the optimal timing of GLP-2 in patients with intestinal failure.

Trophic action of local intraileal infusion of insulin-like growth factor I: polyamine dependence

1992 ◽  
Vol 263 (2) ◽  
pp. E282-E286 ◽  
Author(s):  
H. Olanrewaju ◽  
L. Patel ◽  
E. R. Seidel
Keyword(s):  
Growth Factor ◽  
Animal Experiments ◽  
Insulin Like Growth Factor ◽  
Potential Growth ◽  
Factor I ◽  
Igf I ◽  
Half Maximal Effective Concentration ◽  
Related Enzyme ◽  
Growth Factor I ◽  
Mucosal Mass

Experiments were performed to determine potential growth-promoting effects of human recombinant insulin-like growth factor I (hrIGF-I) in the gastrointestinal tract. IGF-I and IGF-II, but not insulin, were potent (half-maximal effective concentration 0.3 nM) and efficacious inducers of the growth-related enzyme ornithine decarboxylase (ODC) in the gut-derived cell line IEC-6. Maximal ODC induction was observed after treatment of cells with 10 nM IGF-I. In whole animal experiments, bolus intraileal injection of 10 nM hrIGF-I in anesthetized rats induced a 300% increase in ileal mucosal ODC activity, which was sensitive to inhibition with difluoromethylornithine (DFMO). Rats were implanted intraperitoneally with osmotic minipumps filled with 0.9% NaCl or 10 nM IGF-I that was delivered to the ileal lumen by a short Silastic catheter. Sixty-six hours of 1 microliter/h intraluminal IGF-I infusion produced an approximate doubling of mucosal wet weight (NaCl 50 mg vs. IGF-I 102 micrograms/2 cm mucosa) and total mucosal RNA, DNA, and protein content over that in rats that were infused with NaCl. Intraperitoneal treatment with 200 mg/kg DFMO three times per day had little effect on ileal mucosal mass, but completely inhibited the trophic response to IGF-I infusion. IGF-I infusion had no effect on body weight.

Postnatal Proximodistal Development of the Small Bowel Mucosal Mass in Growing Rats

Neonatology ◽  
1981 ◽  
Vol 40 (1-2) ◽  
pp. 62-69 ◽  
Author(s):  
Jean-Paul Buts ◽  
Roger de Meyer
Keyword(s):  
Small Bowel ◽  
Growing Rats ◽  
Mucosal Mass

GH elevates serum IGF-I levels but does not alter mucosal atrophy in parenterally fed rats

1997 ◽  
Vol 272 (5) ◽  
pp. G1100-G1108 ◽  
Author(s):  
C. A. Peterson ◽  
H. V. Carey ◽  
P. L. Hinton ◽  
H. C. Lo ◽  
D. M. Ney
Keyword(s):  
Specific Activity ◽  
Growth Parameters ◽  
Villus Height ◽  
Intestinal Growth ◽  
Factor I ◽  
Ion Secretion ◽  
Igf I ◽  
Mucosal Mass ◽  
And Function ◽  
Induced Changes

Growth hormone (GH) action is primarily mediated by insulin-like growth factor I (IGF-I), although both growth factors show tissue-selective effects. We investigated the effects of GH, IGF-I, and GH plus IGF-I on jejunal growth and function in rats maintained with total parenteral nutrition (TPN) and given recombinant human GH (rhGH) (400 micrograms/day sc, twice daily) and/or rhIGF-I (800 micrograms/day in TPN solution) for 5 days. Administration of GH or IGF-I alone produced similar increases in serum IGF-I levels and body weight; GH plus IGF-I further increased these parameters. TPN reduced mucosal mass, protein and DNA content, villus height, crypt depth, and enterocyte migration rate. IGF-I or GH plus IGF-I produced equivalent increases in all intestinal growth parameters; GH alone had no effect. GH, IGF-I, or GH plus IGF-I reduced TPN-induced increases in sucrase-specific activity. IGF-I, but not GH, attenuated TPN-induced increases in tissue conductance and carbachol-stimulated ion secretion. In contrast to IGF-I, GH does not stimulate intestinal growth during TPN and has less effect on normalizing TPN-induced changes in epithelial function.

Redistribution of blood flow after thermal injury and hemorrhagic shock

1988 ◽  
Vol 65 (4) ◽  
pp. 1782-1788 ◽  
Author(s):  
E. A. Carter ◽  
R. G. Tompkins ◽  
M. L. Yarmush ◽  
W. A. Walker ◽  
J. F. Burke
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Intestinal Mucosa ◽  
Thermal Injury ◽  
Burn Injury ◽  
Flow Distribution ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Mucosal Mass ◽  
Small And Large Intestine

Diminished mucosal mass and a diminished rate of DNA synthesis by the intestinal mucosa have been identified in the rat after thermal injury. Because these changes may be associated with ischemia, the distribution of intestinal blood flow was studied after a thermal injury and compared with the blood flow distribution after hemorrhagic shock. For the thermal injury, anesthetized animals received a standardized 20% body surface area, full-thickness injury and were given intraperitoneal saline resuscitation. By the use of 46Sc- or 141Ce-labeled microspheres, no changes in intestinal and hepatic blood flow occurred after thermal injury. In contrast, a marked redistribution of blood flow was identified after hemorrhagic shock in which a decrease in arterial blood flow was identified to the stomach and to the small and large intestine. Although clinical shock was not present, the cardiac output decreased to a comparable degree in the hemorrhagic shock and the thermal injury. These studies indicate that although physiological changes in intestinal mucosa can be demonstrated after burn injury, these changes are not due to decreases in mesenteric arterial blood flow.

scholarly journals Cell-specific effects of insulin receptor substrate-1 deficiency on normal and IGF-I-mediated colon growth

2007 ◽  
Vol 293 (5) ◽  
pp. G995-G1003 ◽  
Author(s):  
J. G. Simmons ◽  
Y. Ling ◽  
H. Wilkins ◽  
C. R. Fuller ◽  
A. J. D'Ercole ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Insulin Receptor ◽  
Intestinal Epithelial Cells ◽  
Insulin Receptor Substrate ◽  
Intestinal Epithelial ◽  
Insulin Receptor Substrate 1 ◽  
Specific Effects ◽  
Igf I ◽  
Mucosal Mass

Insulin-like growth factor I (IGF-I) potently stimulates intestinal growth. Insulin receptor substrate-1 (IRS-1) mediates proliferative and antiapoptotic actions of IGF-I in cell lines, but its in vivo relevance in intestine is not defined. This study tested the hypothesis that there is cell type-specific dependence on IRS-1 as a mediator of IGF-I action. Length, mass, crypt cell proliferation, and apoptosis were measured in small intestine and colon of IRS-1-null mice and wild-type (WT) littermates and in colon of IRS-1-null or WT mice expressing IGF-I transgenes. Expression of IGF-I receptor and signaling intermediates was examined in intestine of WT and IRS-1-null mice, cultured intestinal epithelial cells, and myofibroblasts. Absolute IRS-1 deficiency reduced mucosal mass in jejunum and colon, but effects were more pronounced in colon. Muscularis mass was decreased in both segments. In IGF-I transgenics, IRS-1 deficiency significantly attenuated IGF-I-stimulated growth of colonic mucosa and abolished antiapoptotic but not mitogenic effects of IGF-I transgene on crypt cells. IGF-I-induced muscularis growth was unaffected by IRS-1 deficiency. In intestinal epithelial cells, IRS-1 was expressed at higher levels than IRS-2 and was preferentially activated by IGF-I. In contrast, IGF-I activated both IRS-1 and IRS-2 in intestinal myofibroblasts and IRS-2 activation was upregulated in IRS-1-null myofibroblasts. We conclude that the intestinal epithelium but not the muscularis requires IRS-1 for normal trophic actions of IGF-I and that IRS-1 is required for antiapoptotic but not mitogenic effects of IGF-I in the intestinal crypts in vivo.

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