Stimulation of Mucosal Growth in the Rat Ileum by Bile and Pancreatic Secretions After Jejunal Resection

Weser, Elliot; Heller, Randy; Tawil, Tippy

doi:10.1016/s0016-5085(19)32134-1

Cited by 120 publications

(25 citation statements)

References 33 publications

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“…This may be augmented by the presence of pancreaticobiliary secretions not normally present in the distal bowel. Previous studies (3,18,45) have shown that bile and pancreatic secretions diverted into the ileal lumen can stimulate mucosal growth and ileal adaptation. As noted in the era before the discovery of GLP-2, bile and pancreatic secretions may stimulate the intestinal segment containing the "enteroglucagon" containing cells to release peptide (3).…”

Section: Discussionmentioning

confidence: 98%

“…After surgery, we monitored the subsequent meal-stimulated GLP-2 release, as well as the adaptive response of the remnant bowel. Effects of massive resection on GLP-2 release were first investigated in an early time-course study in which the control (transected and reanastomosed) or 90% proximal small intestinal resected animals (n ϭ 12) were assessed after 4 days for their fasting and postprandial GLP-2 levels (15,30,45,60, 90 min postprandial).…”

Section: Methodsmentioning

confidence: 99%

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Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome

Martin¹,

Wallace²,

Hartmann³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

121

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Glucagon-like peptide-2 (GLP-2) is an enteroendocrine peptide that is released in response to luminal nutrients and has unique trophic actions in the gastrointestinal tract. These features suggest GLP-2 may be important in controlling intestinal adaptation. We examined the relationship over time of GLP-2 production and adaptation to intestinal resection, the effects of resection-induced malabsorption on GLP-2 production, and the correlation of endogenous serum GLP-2 levels with adaptation as measured by crypt-cell proliferation (CCP). We initially examined the effect of nutrient malabsorption, induced by a 90% resection of the proximal intestine studied on day 4, on the time course and levels of GLP-2 release. Secondly, the degree of malabsorption was varied by performing intestinal transection or 50, 75, or 90% resection of proximal small intestine. Finally, the relationship of GLP-2 levels over time with adaptation to a 90% resection was examined by determining GLP-2 levels on days 7, 14, and 28, and correlating this with intestinal adaptation, as assessed by morphology and CCP rate. A 90% resection significantly increased basal and postprandial GLP-2 levels, with a net increase in nutrient-stimulated exposure over 90 min; GLP-2 exposure (integrated levels vs. time) increased 12.7-fold in resected animals (P< 0.001). Basal and postprandial GLP-2 levels significantly correlated with the magnitude of intestinal resection (r(2) = 0.71; P < 0.001), CCP (r(2) = 0.48; P < 0.005), and nutrient malabsorption (protein, P < 0.001; fat, P < 0.005). The increase in CCP was maintained to 28 days after small bowel resection and was associated with an ongoing elevation in GLP-2 release. These findings suggest that GLP-2 is important in initiating and maintaining the small intestinal adaptive response to resection.

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Section: Discussionmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome

Martin¹,

Wallace²,

Hartmann³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

121

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“…It has been suggested that certain "preferred substrates" may have a direct positive effect on the growth of the epithelial cells. Nutrients may also stimulate bile and pancreatic secretions that could have a direct effect on the mucosa [34][35][36][37][38], or the action could be indirect through stimulation of the release of enteric hormones with interrelated effects on intestinal secretion, motility, or growth. Regardless of the mechanism, the role of enteral nutrition in the process of bowel adaptation is supported by the finding that the absence of luminal nutrients inhibits the intestinal adaptive hyperplasia, even when the necessary amount of calories is administered via total parenteral nutrition [39][40][41].…”

Section: Luminal Nutrients and Pancreatobiliary Secretionsmentioning

confidence: 99%

Enhancing bowel adaptation in short bowel syndrome

Jeppesen

Mortensen

2002

Curr Gastroenterol Rep

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Malabsorption of both nonessential and essential nutrients, fluid, and electrolytes will, if not compensated for by increased intake, lead to diminished body stores and to subclinical and eventually clinical deficiencies. By definition, intestinal failure prevails when parenteral support is necessary to maintain nutritional equilibrium. After intestinal resection, adaptation, a progressive recovery from the malabsorptive disorder, may be seen. Research has focused on optimizing remnant intestinal function through dietary or pharmacologic interventions. In this review, factors responsible for the morphologic and functional changes in the adaptive processes are described. Results of clinical trials employing either growth hormone and glutamine or glucagon-like peptide-2 in short bowel patients are presented.

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“…The mechanism that triggers intestinal adaptation is not fully understood. The main factors recognized are luminal nutrients, pancreaticobiliary secretions, various peptide growth factors, and hormones [9][10][11][12][13]. Intraluminal nutrients may be most essential in promoting intestinal adaptation.…”

Section: What Is Intestinal Adaptation?mentioning

confidence: 99%

Nutritional support for the patient with short-bowel syndrome

Ukleja¹,

Tammela²,

Lankisch³

et al. 1999

Curr Gastroenterol Rep

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Short-bowel syndrome refers to the clinical consequences that follow extensive resection of the small bowel. As a result of resection, malabsorption of macro- and micronutrients occurs. The prognosis after resection depends on the extent and location of resection, the presence of a colon, the function of the residual intestinal mucosa, and the extent of intestinal adaptation. Intestinal adaptation is influenced by the presence of intraluminal nutrients and various trophic peptides and hormones. This article discusses the dietary management of the patient with short-bowel syndrome and the recent literature on growth factors (ie, growth hormone and glutamine) and small-bowel transplantation.

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Stimulation of Mucosal Growth in the Rat Ileum by Bile and Pancreatic Secretions After Jejunal Resection

Cited by 120 publications

References 33 publications

Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome

Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome

Enhancing bowel adaptation in short bowel syndrome

Nutritional support for the patient with short-bowel syndrome

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