Ileal mucosal growth during intraluminal infusion of ethylamine or putrescine

Seidel, Edward R.; Haddox, Mari K.; Johnson, L. R.

doi:10.1152/ajpgi.1985.249.4.g434

Cited by 25 publications

(25 citation statements)

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“…In control rats, an effect of DFMO on the small intestine has been reported in weaning but not adult rats (Alarcon et al, 1987). Administration of putrescine in vivo (Seidel et al, 1985) and in vitro (Ginty et al, 1989) increase intestinal epithelial cell proliferation. Similarly when endogenous putrescine concentrations are increased by using aminoguanidine to block diamine oxidase, enhanced ileal proliferation after MSBR results (Erdman et al, 1989).…”

Section: Discussionmentioning

confidence: 95%

Expression of ileal glucagon and peptide tyrosine-tyrosine genes. Response to inhibition of polyamine synthesis in the presence of massive small-bowel resection

Taylor

Beveridge

Fuller

1992

Biochemical Journal

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Massive small-bowel resection results in a marked adaptive response in the residual terminal ileum. Increased polyamine synthesis is a necessary component of this response. The ileal L-cell-derived peptides enteroglucagon and peptide tyrosine tyrosine (PYY) have been implicated as humoral mediators of this response. We have previously reported a rapid and sustained increase in glucagon mRNA concentrations after massive small-bowel resection. In this study using an inhibitor of the rate-limiting enzyme in polyamine biosynthesis, ornithine decarboxylase, we have demonstrated that the response of the glucagon and PYY genes to massive small-bowel resection is dependent on polyamine biosynthesis. In addition, we have examined the response of both the ornithine decarboxylase and c-jun genes in this model of intestinal adaptation.

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Section: Discussionmentioning

confidence: 95%

Expression of ileal glucagon and peptide tyrosine-tyrosine genes. Response to inhibition of polyamine synthesis in the presence of massive small-bowel resection

Taylor

Beveridge

Fuller

1992

Biochemical Journal

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“…As with other physiological stimuli and mucosal growth factors [6][7][8], the PHA-induced small intestinal growth in vivo also coincided with increased poly amine concentrations [3], Moreover, on PHA stimulation, the growth was actually…”

Section: Dietary Kidney Bean (Phaseolus Vulgaris)mentioning

confidence: 97%

Polyamine Metabolism and Uptake during Phaseolus vulgaris Lectin, PHA-Induced Growth of Rat Small Intestine

Bardócz¹,

Grant²,

Brown³

et al. 1990

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Kidney bean lectin, PHA, stimulated the hyperplastic and hypertrophic growth of rat small intestine. This growth was preceded by a rapid accumulation of polyamines in the small intestine. However, since the lectin had little effect on in situ polyamine biosynthesis, most of the polyamines must have been of extracellular origin. To investigate the source of polyamines, both the luminal uptake and basolateral transport of polyamines by the rat small intestine were measured in vivo. Luminal polyamine uptake was apparently by passive diffusion, non-saturable, linearly dependent on concentration and its extent was not stimulated by PHA. In contrast, ¹⁴C-polyamines injected intraperitoneally were probably taken up by a transport system(s). Moreover, basolateral polyamine transport was stimulated in a time-dependent manner when small intestinal growth was stimulated by PHA. However, in keeping with the finding of polyamine accumulation prior to demonstrable growth of the tissue, stimulation by PHA of the polyamine transport system also preceded small intestinal growth. Stimulation of polyamine transport by luminal factors is possibly a general mechanism involved in intestinal adaptation.

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“…Similar effects can be demonstrated in whole animals. Increasing extracellular putrescine levels in vivo, by providing an exogenous source of putrescine or by increasing the con centration of endogenous putrescine, in duces proliferation of the ileal mucosa of the rat [1,2].…”

Section: Discussionmentioning

confidence: 99%

“…Three sets of experiments lend support to the latter of these two possibilities. First, the direct infu sion of putrescine into the lumen of the rat ileum induces mucosal growth [1], Second, increasing ileal putrescine content by inhibi tion of diamine oxidase, the enzyme respon sible for the removal of putrescine from the polyamine biosynthetic pathway, also stimu lates growth of the ileal mucosa [2]. The results of these experiments indicate that putrescine is indeed able to induce growth of the gastrointestinal mucosa in vivo.…”

mentioning

confidence: 90%

Apparent Post-Transcriptional Modification of Ornithine Decarboxylase Accounts for its Induction in IEC-6 Cells in Culture

Seidel¹,

Ginty²

1990

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Putrescine, the product of the ornithine decarboxylase (ODC)-catalyzed reaction, stimulates macromolecular synthesis in a duodenal crypt cell line, IEC-6 cells, grown in culture. In addition, supplementation of medium with putrescine alone reverses the inhibition of proliferation produced by inhibition of ODC with difiuoromethylornithine (DFMO). A series of experiments was initiated in the IEC-6 cell line to study the regulation of induction of ODC, as this enzyme is rate-limiting in putrescine synthesis. Five percent fetal bovine serum (FBS) and 10 nM IGF-II stimulated a 21-fold and 6-fold induction of ODC activity, respectively. Kinetic analysis indicated that the effect was on the V_max of the reaction and not on the K_m, suggesting an increase in total ODC protein. This was verified by measuring [³H]DFMO binding; serum-stimulated induction of activity was accompanied by a corresponding 20-fold increase in the specific binding of DFMO to ODC. In contrast, Northern analysis demonstrated only a two-fold change in ODC mRNA level during induction. Measurement of enzyme stability showed that the half-life of the ODC protein was increased three-fold above basal level in the induced state. Inhibition of induction was produced by pretreatment with either the calmodulin antagonist, W-7, or the product of the ODC-catalyzed reaction, putrescine. Further analysis illustrated that the inhibition produced by these agents was partly the result of destabilization of the enzyme and not a decrease in message level. These results demonstrate that the induction of ODC by trophic agents is the result of post-transcriptional events rather than at the level of RNA synthesis.

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Ileal mucosal growth during intraluminal infusion of ethylamine or putrescine

Cited by 25 publications

References 0 publications

Expression of ileal glucagon and peptide tyrosine-tyrosine genes. Response to inhibition of polyamine synthesis in the presence of massive small-bowel resection

Expression of ileal glucagon and peptide tyrosine-tyrosine genes. Response to inhibition of polyamine synthesis in the presence of massive small-bowel resection

Polyamine Metabolism and Uptake during Phaseolus vulgaris Lectin, PHA-Induced Growth of Rat Small Intestine

Apparent Post-Transcriptional Modification of Ornithine Decarboxylase Accounts for its Induction in IEC-6 Cells in Culture

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