Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome. / Okawada, Manabu; Holst, Jens Juul; Teitelbaum, Daniel H.

In: Surgery, Vol. 150, No. 2, 08.2011, p. 217-223.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Okawada, M, Holst, JJ & Teitelbaum, DH 2011, 'Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome', Surgery, vol. 150, no. 2, pp. 217-223. https://doi.org/10.1016/j.surg.2011.05.013

APA

Okawada, M., Holst, J. J., & Teitelbaum, D. H. (2011). Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome. Surgery, 150(2), 217-223. https://doi.org/10.1016/j.surg.2011.05.013

Vancouver

Okawada M, Holst JJ, Teitelbaum DH. Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome. Surgery. 2011 Aug;150(2):217-223. https://doi.org/10.1016/j.surg.2011.05.013

Author

Okawada, Manabu ; Holst, Jens Juul ; Teitelbaum, Daniel H. / Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome. In: Surgery. 2011 ; Vol. 150, No. 2. pp. 217-223.

Bibtex

@article{ee4280854cb94794ba486f49f4f6d0a4,
title = "Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome",
abstract = "Glucagon-like peptide-2 induces small intestine mucosal epithelial cell proliferation and may have benefit for patients who suffer from short bowel syndrome. However, glucagon-like peptide-2 is inactivated rapidly in vivo by dipeptidyl peptidase IV. Therefore, we hypothesized that selectively inhibiting dipeptidyl peptidase IV would prolong the circulating life of glucagon-like peptide-2 and lead to increased intestinal adaptation after development of short bowel syndrome.",
keywords = "Adaptation, Physiological, Animals, Dipeptidyl-Peptidase IV Inhibitors, Disease Models, Animal, Glucagon-Like Peptide 2, Intestine, Small, Mice, Mice, Inbred C57BL, Short Bowel Syndrome",
author = "Manabu Okawada and Holst, {Jens Juul} and Teitelbaum, {Daniel H}",
note = "Copyright {\textcopyright} 2011 Mosby, Inc. All rights reserved.",
year = "2011",
month = aug,
doi = "10.1016/j.surg.2011.05.013",
language = "English",
volume = "150",
pages = "217--223",
journal = "Surgery",
issn = "0263-9319",
publisher = "TheMedicine Publishing Company",
number = "2",

}

RIS

TY - JOUR

T1 - Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome

AU - Okawada, Manabu

AU - Holst, Jens Juul

AU - Teitelbaum, Daniel H

N1 - Copyright © 2011 Mosby, Inc. All rights reserved.

PY - 2011/8

Y1 - 2011/8

N2 - Glucagon-like peptide-2 induces small intestine mucosal epithelial cell proliferation and may have benefit for patients who suffer from short bowel syndrome. However, glucagon-like peptide-2 is inactivated rapidly in vivo by dipeptidyl peptidase IV. Therefore, we hypothesized that selectively inhibiting dipeptidyl peptidase IV would prolong the circulating life of glucagon-like peptide-2 and lead to increased intestinal adaptation after development of short bowel syndrome.

AB - Glucagon-like peptide-2 induces small intestine mucosal epithelial cell proliferation and may have benefit for patients who suffer from short bowel syndrome. However, glucagon-like peptide-2 is inactivated rapidly in vivo by dipeptidyl peptidase IV. Therefore, we hypothesized that selectively inhibiting dipeptidyl peptidase IV would prolong the circulating life of glucagon-like peptide-2 and lead to increased intestinal adaptation after development of short bowel syndrome.

KW - Adaptation, Physiological

KW - Animals

KW - Dipeptidyl-Peptidase IV Inhibitors

KW - Disease Models, Animal

KW - Glucagon-Like Peptide 2

KW - Intestine, Small

KW - Mice

KW - Mice, Inbred C57BL

KW - Short Bowel Syndrome

U2 - 10.1016/j.surg.2011.05.013

DO - 10.1016/j.surg.2011.05.013

M3 - Journal article

C2 - 21719060

VL - 150

SP - 217

EP - 223

JO - Surgery

JF - Surgery

SN - 0263-9319

IS - 2

ER -

ID: 38433225