Glucagon-like peptide-1 (GLP-1) receptor agonism or DPP-4 inhibition does not accelerate neoplasia in carcinogen treated mice

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Standard

Glucagon-like peptide-1 (GLP-1) receptor agonism or DPP-4 inhibition does not accelerate neoplasia in carcinogen treated mice. / Kissow, Hannelouise; Hartmann, Bolette; Holst, Jens Juul; Viby, Niels-Erik; Hansen, Lærke Schmidt; Rosenkilde, Mette Marie; Hare, Kristine Juul; Poulsen, Steen Seier.

I: Regulatory Peptides, Bind 179, Nr. 1-3, 10.11.2012, s. 91-100.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Kissow, H, Hartmann, B, Holst, JJ, Viby, N-E, Hansen, LS, Rosenkilde, MM, Hare, KJ & Poulsen, SS 2012, 'Glucagon-like peptide-1 (GLP-1) receptor agonism or DPP-4 inhibition does not accelerate neoplasia in carcinogen treated mice', Regulatory Peptides, bind 179, nr. 1-3, s. 91-100. https://doi.org/10.1016/j.regpep.2012.08.016

APA

Kissow, H., Hartmann, B., Holst, J. J., Viby, N-E., Hansen, L. S., Rosenkilde, M. M., Hare, K. J., & Poulsen, S. S. (2012). Glucagon-like peptide-1 (GLP-1) receptor agonism or DPP-4 inhibition does not accelerate neoplasia in carcinogen treated mice. Regulatory Peptides, 179(1-3), 91-100. https://doi.org/10.1016/j.regpep.2012.08.016

Vancouver

Kissow H, Hartmann B, Holst JJ, Viby N-E, Hansen LS, Rosenkilde MM o.a. Glucagon-like peptide-1 (GLP-1) receptor agonism or DPP-4 inhibition does not accelerate neoplasia in carcinogen treated mice. Regulatory Peptides. 2012 nov. 10;179(1-3):91-100. https://doi.org/10.1016/j.regpep.2012.08.016

Author

Kissow, Hannelouise ; Hartmann, Bolette ; Holst, Jens Juul ; Viby, Niels-Erik ; Hansen, Lærke Schmidt ; Rosenkilde, Mette Marie ; Hare, Kristine Juul ; Poulsen, Steen Seier. / Glucagon-like peptide-1 (GLP-1) receptor agonism or DPP-4 inhibition does not accelerate neoplasia in carcinogen treated mice. I: Regulatory Peptides. 2012 ; Bind 179, Nr. 1-3. s. 91-100.

Bibtex

@article{434bf085e4054714aef855fc38501d72,
title = "Glucagon-like peptide-1 (GLP-1) receptor agonism or DPP-4 inhibition does not accelerate neoplasia in carcinogen treated mice",
abstract = "Glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) are secreted in parallel from the intestinal endocrine cells after nutrient intake. GLP-1 is an incretin hormone and analogues are available for the treatment of type 2 diabetes mellitus (T2DM). GLP-2 is an intestinal growth hormone and is shown to promote growth of colonic adenomas in carcinogen treated mice. Both peptides are degraded by dipeptidyl peptidase-4 (DPP-4) into inactive metabolites. DPP-4 inhibitors are therefore also in use for treatment of T2DM. It is possible that DPP-4 inhibition by enhancing the exposure of endogenous GLP-2 to the intestinal epithelia also might mediate growth and promote neoplasia. We investigated the intestinal growth effect of the GLP-1 receptor agonists (GLP-1 RAs) (liraglutide and exenatide) and DPP-4 inhibition (sitagliptin) in healthy mice. We also investigated the potential tumour promoting effect of liraglutide and sitaglitin in the colon of carcinogen treated mice. We used GLP-2 as a positive control.",
keywords = "1,2-Dimethylhydrazine, Aberrant Crypt Foci, Adenoma, Anatomy, Cross-Sectional, Animals, COS Cells, Cercopithecus aethiops, Colon, Colonic Neoplasms, Cyclic AMP, Diabetes Mellitus, Type 2, Dipeptidyl Peptidase 4, Dipeptidyl-Peptidase IV Inhibitors, Female, Glucagon-Like Peptide 1, Hypoglycemic Agents, Intestinal Mucosa, Intestine, Small, Mice, Mice, Inbred C57BL, Organ Size, Peptides, Pyrazines, Receptors, Glucagon, Transfection, Triazoles, Venoms",
author = "Hannelouise Kissow and Bolette Hartmann and Holst, {Jens Juul} and Niels-Erik Viby and Hansen, {L{\ae}rke Schmidt} and Rosenkilde, {Mette Marie} and Hare, {Kristine Juul} and Poulsen, {Steen Seier}",
note = "Copyright {\textcopyright} 2012 Elsevier B.V. All rights reserved.",
year = "2012",
month = nov,
day = "10",
doi = "10.1016/j.regpep.2012.08.016",
language = "English",
volume = "179",
pages = "91--100",
journal = "Regulatory Peptides",
issn = "0167-0115",
publisher = "Elsevier",
number = "1-3",

}

RIS

TY - JOUR

T1 - Glucagon-like peptide-1 (GLP-1) receptor agonism or DPP-4 inhibition does not accelerate neoplasia in carcinogen treated mice

AU - Kissow, Hannelouise

AU - Hartmann, Bolette

AU - Holst, Jens Juul

AU - Viby, Niels-Erik

AU - Hansen, Lærke Schmidt

AU - Rosenkilde, Mette Marie

AU - Hare, Kristine Juul

AU - Poulsen, Steen Seier

N1 - Copyright © 2012 Elsevier B.V. All rights reserved.

PY - 2012/11/10

Y1 - 2012/11/10

N2 - Glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) are secreted in parallel from the intestinal endocrine cells after nutrient intake. GLP-1 is an incretin hormone and analogues are available for the treatment of type 2 diabetes mellitus (T2DM). GLP-2 is an intestinal growth hormone and is shown to promote growth of colonic adenomas in carcinogen treated mice. Both peptides are degraded by dipeptidyl peptidase-4 (DPP-4) into inactive metabolites. DPP-4 inhibitors are therefore also in use for treatment of T2DM. It is possible that DPP-4 inhibition by enhancing the exposure of endogenous GLP-2 to the intestinal epithelia also might mediate growth and promote neoplasia. We investigated the intestinal growth effect of the GLP-1 receptor agonists (GLP-1 RAs) (liraglutide and exenatide) and DPP-4 inhibition (sitagliptin) in healthy mice. We also investigated the potential tumour promoting effect of liraglutide and sitaglitin in the colon of carcinogen treated mice. We used GLP-2 as a positive control.

AB - Glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) are secreted in parallel from the intestinal endocrine cells after nutrient intake. GLP-1 is an incretin hormone and analogues are available for the treatment of type 2 diabetes mellitus (T2DM). GLP-2 is an intestinal growth hormone and is shown to promote growth of colonic adenomas in carcinogen treated mice. Both peptides are degraded by dipeptidyl peptidase-4 (DPP-4) into inactive metabolites. DPP-4 inhibitors are therefore also in use for treatment of T2DM. It is possible that DPP-4 inhibition by enhancing the exposure of endogenous GLP-2 to the intestinal epithelia also might mediate growth and promote neoplasia. We investigated the intestinal growth effect of the GLP-1 receptor agonists (GLP-1 RAs) (liraglutide and exenatide) and DPP-4 inhibition (sitagliptin) in healthy mice. We also investigated the potential tumour promoting effect of liraglutide and sitaglitin in the colon of carcinogen treated mice. We used GLP-2 as a positive control.

KW - 1,2-Dimethylhydrazine

KW - Aberrant Crypt Foci

KW - Adenoma

KW - Anatomy, Cross-Sectional

KW - Animals

KW - COS Cells

KW - Cercopithecus aethiops

KW - Colon

KW - Colonic Neoplasms

KW - Cyclic AMP

KW - Diabetes Mellitus, Type 2

KW - Dipeptidyl Peptidase 4

KW - Dipeptidyl-Peptidase IV Inhibitors

KW - Female

KW - Glucagon-Like Peptide 1

KW - Hypoglycemic Agents

KW - Intestinal Mucosa

KW - Intestine, Small

KW - Mice

KW - Mice, Inbred C57BL

KW - Organ Size

KW - Peptides

KW - Pyrazines

KW - Receptors, Glucagon

KW - Transfection

KW - Triazoles

KW - Venoms

U2 - 10.1016/j.regpep.2012.08.016

DO - 10.1016/j.regpep.2012.08.016

M3 - Journal article

C2 - 22989472

VL - 179

SP - 91

EP - 100

JO - Regulatory Peptides

JF - Regulatory Peptides

SN - 0167-0115

IS - 1-3

ER -

ID: 45041252