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The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury

BACKGROUND: The gut incretin hormones GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic peptide) are secreted by enteroendocrine cells following food intake leading to insulin secretion and glucose lowering. Beyond its metabolic function GIP has been found to exhibit direct c...

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Autores principales: Kahles, Florian, Rau, Matthias, Reugels, Martin, Foldenauer, Ann C., Mertens, Robert W., Arrivas, Maria C., Schröder, Jörg, Idel, Paul, Moellmann, Julia, van der Vorst, Emiel P. C., Marx, Nikolaus, Lehrke, Michael
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8817614/
https://www.ncbi.nlm.nih.gov/pubmed/35123462
http://dx.doi.org/10.1186/s12933-022-01454-3
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author Kahles, Florian
Rau, Matthias
Reugels, Martin
Foldenauer, Ann C.
Mertens, Robert W.
Arrivas, Maria C.
Schröder, Jörg
Idel, Paul
Moellmann, Julia
van der Vorst, Emiel P. C.
Marx, Nikolaus
Lehrke, Michael
author_facet Kahles, Florian
Rau, Matthias
Reugels, Martin
Foldenauer, Ann C.
Mertens, Robert W.
Arrivas, Maria C.
Schröder, Jörg
Idel, Paul
Moellmann, Julia
van der Vorst, Emiel P. C.
Marx, Nikolaus
Lehrke, Michael
author_sort Kahles, Florian
collection PubMed
description BACKGROUND: The gut incretin hormones GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic peptide) are secreted by enteroendocrine cells following food intake leading to insulin secretion and glucose lowering. Beyond its metabolic function GIP has been found to exhibit direct cardio- and atheroprotective effects in mice and to be associated with cardiovascular prognosis in patients with myocardial infarction. The aim of this study was to characterize endogenous GIP levels in patients with acute myocardial infarction. METHODS AND RESULTS: Serum concentrations of GIP were assessed in 731 patients who presented with clinical indication of coronary angiography. Circulating GIP levels were significantly lower in patients with STEMI (ST-elevation myocardial infarction; n=100) compared to clinically stable patients without myocardial infarction (n=631) (216.82 pg/mL [Q1–Q3: 52.37–443.07] vs. 271.54 pg/mL [Q1–Q3: 70.12–542.41], p = 0.0266). To characterize endogenous GIP levels in patients with acute myocardial injury we enrolled 18 patients scheduled for cardiac surgery with cardiopulmonary bypass and requirement of extracorporeal circulation as a reproducible condition of myocardial injury. Blood samples were drawn directly before surgery (baseline), upon arrival at the intensive care unit (ICU), 6 h post arrival to the ICU and at the morning of the first and second postoperative days. Mean circulating GIP concentrations decreased in response to surgery from 45.3 ± 22.6 pg/mL at baseline to a minimum of 31.9 ± 19.8 pg/mL at the first postoperative day (p = 0.0384) and rose again at the second postoperative day (52.1 ± 28.0 pg/mL). CONCLUSIONS: Circulating GIP levels are downregulated in patients with myocardial infarction and following cardiac surgery. These results might suggest nutrition-independent regulation of GIP secretion following myocardial injury in humans.
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spelling pubmed-88176142022-02-07 The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury Kahles, Florian Rau, Matthias Reugels, Martin Foldenauer, Ann C. Mertens, Robert W. Arrivas, Maria C. Schröder, Jörg Idel, Paul Moellmann, Julia van der Vorst, Emiel P. C. Marx, Nikolaus Lehrke, Michael Cardiovasc Diabetol Original Investigation BACKGROUND: The gut incretin hormones GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic peptide) are secreted by enteroendocrine cells following food intake leading to insulin secretion and glucose lowering. Beyond its metabolic function GIP has been found to exhibit direct cardio- and atheroprotective effects in mice and to be associated with cardiovascular prognosis in patients with myocardial infarction. The aim of this study was to characterize endogenous GIP levels in patients with acute myocardial infarction. METHODS AND RESULTS: Serum concentrations of GIP were assessed in 731 patients who presented with clinical indication of coronary angiography. Circulating GIP levels were significantly lower in patients with STEMI (ST-elevation myocardial infarction; n=100) compared to clinically stable patients without myocardial infarction (n=631) (216.82 pg/mL [Q1–Q3: 52.37–443.07] vs. 271.54 pg/mL [Q1–Q3: 70.12–542.41], p = 0.0266). To characterize endogenous GIP levels in patients with acute myocardial injury we enrolled 18 patients scheduled for cardiac surgery with cardiopulmonary bypass and requirement of extracorporeal circulation as a reproducible condition of myocardial injury. Blood samples were drawn directly before surgery (baseline), upon arrival at the intensive care unit (ICU), 6 h post arrival to the ICU and at the morning of the first and second postoperative days. Mean circulating GIP concentrations decreased in response to surgery from 45.3 ± 22.6 pg/mL at baseline to a minimum of 31.9 ± 19.8 pg/mL at the first postoperative day (p = 0.0384) and rose again at the second postoperative day (52.1 ± 28.0 pg/mL). CONCLUSIONS: Circulating GIP levels are downregulated in patients with myocardial infarction and following cardiac surgery. These results might suggest nutrition-independent regulation of GIP secretion following myocardial injury in humans. BioMed Central 2022-02-05 /pmc/articles/PMC8817614/ /pubmed/35123462 http://dx.doi.org/10.1186/s12933-022-01454-3 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Original Investigation
Kahles, Florian
Rau, Matthias
Reugels, Martin
Foldenauer, Ann C.
Mertens, Robert W.
Arrivas, Maria C.
Schröder, Jörg
Idel, Paul
Moellmann, Julia
van der Vorst, Emiel P. C.
Marx, Nikolaus
Lehrke, Michael
The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury
title The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury
title_full The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury
title_fullStr The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury
title_full_unstemmed The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury
title_short The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury
title_sort gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury
topic Original Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8817614/
https://www.ncbi.nlm.nih.gov/pubmed/35123462
http://dx.doi.org/10.1186/s12933-022-01454-3
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