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

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Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome. / Martin, G R; Wallace, L E; Hartmann, B; Holst, Jens Juul; Demchyshyn, L; Toney, K; Sigalet, D L.

In: American Journal of Physiology: Gastrointestinal and Liver Physiology, Vol. 288, No. 3, 03.2005, p. G431-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Martin, GR, Wallace, LE, Hartmann, B, Holst, JJ, Demchyshyn, L, Toney, K & Sigalet, DL 2005, 'Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome', American Journal of Physiology: Gastrointestinal and Liver Physiology, vol. 288, no. 3, pp. G431-8. https://doi.org/10.1152/ajpgi.00242.2004

APA

Martin, G. R., Wallace, L. E., Hartmann, B., Holst, J. J., Demchyshyn, L., Toney, K., & Sigalet, D. L. (2005). Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome. American Journal of Physiology: Gastrointestinal and Liver Physiology, 288(3), G431-8. https://doi.org/10.1152/ajpgi.00242.2004

Vancouver

Martin GR, Wallace LE, Hartmann B, Holst JJ, Demchyshyn L, Toney K et al. Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome. American Journal of Physiology: Gastrointestinal and Liver Physiology. 2005 Mar;288(3):G431-8. https://doi.org/10.1152/ajpgi.00242.2004

Author

Martin, G R ; Wallace, L E ; Hartmann, B ; Holst, Jens Juul ; Demchyshyn, L ; Toney, K ; Sigalet, D L. / Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome. In: American Journal of Physiology: Gastrointestinal and Liver Physiology. 2005 ; Vol. 288, No. 3. pp. G431-8.

Bibtex

@article{031c245d7cb64977a5aae91bd6d0f7bf,
title = "Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome",
abstract = "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.",
keywords = "Adaptation, Physiological, Animals, Antimetabolites, Body Weight, Bromodeoxyuridine, Cell Proliferation, Dietary Fats, Dietary Proteins, Enzyme-Linked Immunosorbent Assay, Food, Glucagon-Like Peptide 2, Glucagon-Like Peptides, Intestinal Absorption, Intestinal Mucosa, Intestines, Male, Peptides, Rats, Rats, Sprague-Dawley, Short Bowel Syndrome",
author = "Martin, {G R} and Wallace, {L E} and B Hartmann and Holst, {Jens Juul} and L Demchyshyn and K Toney and Sigalet, {D L}",
year = "2005",
month = "3",
doi = "10.1152/ajpgi.00242.2004",
language = "English",
volume = "288",
pages = "G431--8",
journal = "American Journal of Physiology: Gastrointestinal and Liver Physiology",
issn = "0193-1857",
publisher = "American Physiological Society",
number = "3",

}

RIS

TY - JOUR

T1 - Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome

AU - Martin, G R

AU - Wallace, L E

AU - Hartmann, B

AU - Holst, Jens Juul

AU - Demchyshyn, L

AU - Toney, K

AU - Sigalet, D L

PY - 2005/3

Y1 - 2005/3

N2 - 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.

AB - 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.

KW - Adaptation, Physiological

KW - Animals

KW - Antimetabolites

KW - Body Weight

KW - Bromodeoxyuridine

KW - Cell Proliferation

KW - Dietary Fats

KW - Dietary Proteins

KW - Enzyme-Linked Immunosorbent Assay

KW - Food

KW - Glucagon-Like Peptide 2

KW - Glucagon-Like Peptides

KW - Intestinal Absorption

KW - Intestinal Mucosa

KW - Intestines

KW - Male

KW - Peptides

KW - Rats

KW - Rats, Sprague-Dawley

KW - Short Bowel Syndrome

U2 - 10.1152/ajpgi.00242.2004

DO - 10.1152/ajpgi.00242.2004

M3 - Journal article

VL - 288

SP - G431-8

JO - American Journal of Physiology: Gastrointestinal and Liver Physiology

JF - American Journal of Physiology: Gastrointestinal and Liver Physiology

SN - 0193-1857

IS - 3

ER -

ID: 132054177