Stimulation of intestinal growth and function with DPP-IV inhibition in a mouse short bowel syndrome model

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Stimulation of intestinal growth and function with DPP-IV inhibition in a mouse short bowel syndrome model. / Sueyoshi, Ryo; Ignatoski, Kathleen M Woods; Okawada, Manabu; Hartmann, Bolette; Holst, Jens Juul; Teitelbaum, Daniel H.

In: American Journal of Physiology: Gastrointestinal and Liver Physiology, Vol. 307, No. 4, 26.06.2014, p. G410-19.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Sueyoshi, R, Ignatoski, KMW, Okawada, M, Hartmann, B, Holst, JJ & Teitelbaum, DH 2014, 'Stimulation of intestinal growth and function with DPP-IV inhibition in a mouse short bowel syndrome model', American Journal of Physiology: Gastrointestinal and Liver Physiology, vol. 307, no. 4, pp. G410-19. https://doi.org/10.1152/ajpgi.00363.2013

APA

Sueyoshi, R., Ignatoski, K. M. W., Okawada, M., Hartmann, B., Holst, J. J., & Teitelbaum, D. H. (2014). Stimulation of intestinal growth and function with DPP-IV inhibition in a mouse short bowel syndrome model. American Journal of Physiology: Gastrointestinal and Liver Physiology, 307(4), G410-19. https://doi.org/10.1152/ajpgi.00363.2013

Vancouver

Sueyoshi R, Ignatoski KMW, Okawada M, Hartmann B, Holst JJ, Teitelbaum DH. Stimulation of intestinal growth and function with DPP-IV inhibition in a mouse short bowel syndrome model. American Journal of Physiology: Gastrointestinal and Liver Physiology. 2014 Jun 26;307(4):G410-19. https://doi.org/10.1152/ajpgi.00363.2013

Author

Sueyoshi, Ryo ; Ignatoski, Kathleen M Woods ; Okawada, Manabu ; Hartmann, Bolette ; Holst, Jens Juul ; Teitelbaum, Daniel H. / Stimulation of intestinal growth and function with DPP-IV inhibition in a mouse short bowel syndrome model. In: American Journal of Physiology: Gastrointestinal and Liver Physiology. 2014 ; Vol. 307, No. 4. pp. G410-19.

Bibtex

@article{108489453263458b80bcba6c0c49a0a4,
title = "Stimulation of intestinal growth and function with DPP-IV inhibition in a mouse short bowel syndrome model",
abstract = "Glucagon-like peptide-2 (GLP-2) has been shown to be effective in patients with short bowel syndrome (SBS), but is rapidly inactivated by dipeptidyl peptidase-IV (DPP4). We used an orally-active DPP4 inhibitor (DPP4-I), MK-0626, to determine the efficacy of this approach to promote adaptation after SBS, determined optimal dosing, and identified further functional actions in a SBS mouse model. Ten week old mice underwent a 50{\%} proximal small bowel resection (SBR). Dose optimization was determined over a 3-day post-SBS period. The established optimal dose was given for 7 days, 30 days, 90 days, and 7 days followed by 23 days washout period. Adaptive response was assessed by morphology, intestinal epithelial cell (IEC) proliferation (PCNA), epithelial barrier function (transepithelial resistance), RT-PCR for intestinal transport proteins, GLP-2R, and IGF-1R, and GLP-2 plasma levels. Glucose-stimulated sodium transport was assessed for intestinal absorptive function. Seven days of DPP4-I treatment facilitated an increase in GLP-2R levels, intestinal growth, and IEC proliferation. Treatment led to differential effects over time with greater absorptive function early, and enhanced proliferation at later time points. Interestingly, 7 day treatment followed by 23 days of non-treatment showed continued adaptation. DPP-IV-I enhanced IEC proliferative action up to 90-days post-resection, but this action seemed to peak by 30 days, as did GLP-2 plasma levels. Thus, use of DPP4-I treatment may prove to be a viable treatment for accelerating intestinal adaptation with SBS.",
author = "Ryo Sueyoshi and Ignatoski, {Kathleen M Woods} and Manabu Okawada and Bolette Hartmann and Holst, {Jens Juul} and Teitelbaum, {Daniel H}",
note = "Copyright {\circledC} 2013, American Journal of Physiology- Gastrointestinal and Liver Physiology.",
year = "2014",
month = "6",
day = "26",
doi = "10.1152/ajpgi.00363.2013",
language = "English",
volume = "307",
pages = "G410--19",
journal = "American Journal of Physiology: Gastrointestinal and Liver Physiology",
issn = "0193-1857",
publisher = "American Physiological Society",
number = "4",

}

RIS

TY - JOUR

T1 - Stimulation of intestinal growth and function with DPP-IV inhibition in a mouse short bowel syndrome model

AU - Sueyoshi, Ryo

AU - Ignatoski, Kathleen M Woods

AU - Okawada, Manabu

AU - Hartmann, Bolette

AU - Holst, Jens Juul

AU - Teitelbaum, Daniel H

N1 - Copyright © 2013, American Journal of Physiology- Gastrointestinal and Liver Physiology.

PY - 2014/6/26

Y1 - 2014/6/26

N2 - Glucagon-like peptide-2 (GLP-2) has been shown to be effective in patients with short bowel syndrome (SBS), but is rapidly inactivated by dipeptidyl peptidase-IV (DPP4). We used an orally-active DPP4 inhibitor (DPP4-I), MK-0626, to determine the efficacy of this approach to promote adaptation after SBS, determined optimal dosing, and identified further functional actions in a SBS mouse model. Ten week old mice underwent a 50% proximal small bowel resection (SBR). Dose optimization was determined over a 3-day post-SBS period. The established optimal dose was given for 7 days, 30 days, 90 days, and 7 days followed by 23 days washout period. Adaptive response was assessed by morphology, intestinal epithelial cell (IEC) proliferation (PCNA), epithelial barrier function (transepithelial resistance), RT-PCR for intestinal transport proteins, GLP-2R, and IGF-1R, and GLP-2 plasma levels. Glucose-stimulated sodium transport was assessed for intestinal absorptive function. Seven days of DPP4-I treatment facilitated an increase in GLP-2R levels, intestinal growth, and IEC proliferation. Treatment led to differential effects over time with greater absorptive function early, and enhanced proliferation at later time points. Interestingly, 7 day treatment followed by 23 days of non-treatment showed continued adaptation. DPP-IV-I enhanced IEC proliferative action up to 90-days post-resection, but this action seemed to peak by 30 days, as did GLP-2 plasma levels. Thus, use of DPP4-I treatment may prove to be a viable treatment for accelerating intestinal adaptation with SBS.

AB - Glucagon-like peptide-2 (GLP-2) has been shown to be effective in patients with short bowel syndrome (SBS), but is rapidly inactivated by dipeptidyl peptidase-IV (DPP4). We used an orally-active DPP4 inhibitor (DPP4-I), MK-0626, to determine the efficacy of this approach to promote adaptation after SBS, determined optimal dosing, and identified further functional actions in a SBS mouse model. Ten week old mice underwent a 50% proximal small bowel resection (SBR). Dose optimization was determined over a 3-day post-SBS period. The established optimal dose was given for 7 days, 30 days, 90 days, and 7 days followed by 23 days washout period. Adaptive response was assessed by morphology, intestinal epithelial cell (IEC) proliferation (PCNA), epithelial barrier function (transepithelial resistance), RT-PCR for intestinal transport proteins, GLP-2R, and IGF-1R, and GLP-2 plasma levels. Glucose-stimulated sodium transport was assessed for intestinal absorptive function. Seven days of DPP4-I treatment facilitated an increase in GLP-2R levels, intestinal growth, and IEC proliferation. Treatment led to differential effects over time with greater absorptive function early, and enhanced proliferation at later time points. Interestingly, 7 day treatment followed by 23 days of non-treatment showed continued adaptation. DPP-IV-I enhanced IEC proliferative action up to 90-days post-resection, but this action seemed to peak by 30 days, as did GLP-2 plasma levels. Thus, use of DPP4-I treatment may prove to be a viable treatment for accelerating intestinal adaptation with SBS.

U2 - 10.1152/ajpgi.00363.2013

DO - 10.1152/ajpgi.00363.2013

M3 - Journal article

C2 - 24970775

VL - 307

SP - G410-19

JO - American Journal of Physiology: Gastrointestinal and Liver Physiology

JF - American Journal of Physiology: Gastrointestinal and Liver Physiology

SN - 0193-1857

IS - 4

ER -

ID: 117850667