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Plasma levels of glucagon but not GLP-1 are elevated in response to inflammation in humans

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Modrzynska, Justyna ; Klein, Christine F ; Iversen, Kasper ; Bundgaard, Henning ; Hartmann, Bolette ; Moss, Maike ; Rittig, Nikolaj ; Moeller, Niels ; Holst, Jens J ; Wewer Albrechtsen, Nicolai J. / Plasma levels of glucagon but not GLP-1 are elevated in response to inflammation in humans. I: Endocrine Connections. 2021 ; Bind 10, Nr. 2. s. 205-213.

Bibtex

@article{ab5f5665bf5141e082aa7256aac3ddb1,
title = "Plasma levels of glucagon but not GLP-1 are elevated in response to inflammation in humans",
abstract = "OBJECTIVE: Glucagon and glucagon-like peptide-1 (GLP-1) originate from the common precursor, proglucagon, and their plasma concentrations have been reported to be increased during inflammatory conditions. Increased blood glucose levels are frequently observed in septic patients, and therefore we hypothesized that glucagon, but not GLP-1, is increased in individuals with inflammation.DESIGN: Prospective longitudinal cohort study.MATERIALS AND METHODS: We measured glucagon and GLP-1 in plasma sampled consecutively in three cohorts consisting of patients with infective endocarditis (n=16), urosepsis (n=28) and post-operative inflammation following percutaneous aortic valve implantation or thoracic endovascular aortic repair (n=5). Correlations between C-Reactive Protein (CRP), a marker of systemic inflammation, and glucagon and GLP-1 concentrations were investigated. Additionally, glucagon and GLP-1 concentrations were measured after a bolus infusion of lipopolysaccharide (LPS, 1ng/kg) in nine healthy young males.RESULTS: Glucagon and CRP were positively and significantly correlated (r=0.27; P=0.0003), whereas no significant association between GLP-1 and CRP was found (r=0.08, P=0.30). LPS infusion resulted in acute systemic inflammation reflected by increased temperature, pulse, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and concomitantly increased concentrations of glucagon (P<0.05) but not GLP-1.CONCLUSIONS: Systemic inflammation caused by bacterial infections or developed as a non-infected condition is associated with increased plasma concentration of glucagon, but not GLP-1. Hyperglucagonemia may contribute to the impaired glucose control in patients with systemic inflammatory diseases.",
keywords = "Bacteremia, ELISA, Glucose, Hyperglycemia, Immunoassay, Infection, Inflammation",
author = "Justyna Modrzynska and Klein, {Christine F} and Kasper Iversen and Henning Bundgaard and Bolette Hartmann and Maike Moss and Nikolaj Rittig and Niels Moeller and Holst, {Jens J} and {Wewer Albrechtsen}, {Nicolai J}",
year = "2021",
month = feb,
doi = "10.1530/EC-20-0590",
language = "English",
volume = "10",
pages = "205--213",
journal = "Endocrine Connections",
issn = "2049-3614",
publisher = "BioScientifica Ltd",
number = "2",

}

RIS

TY - JOUR

T1 - Plasma levels of glucagon but not GLP-1 are elevated in response to inflammation in humans

AU - Modrzynska, Justyna

AU - Klein, Christine F

AU - Iversen, Kasper

AU - Bundgaard, Henning

AU - Hartmann, Bolette

AU - Moss, Maike

AU - Rittig, Nikolaj

AU - Moeller, Niels

AU - Holst, Jens J

AU - Wewer Albrechtsen, Nicolai J

PY - 2021/2

Y1 - 2021/2

N2 - OBJECTIVE: Glucagon and glucagon-like peptide-1 (GLP-1) originate from the common precursor, proglucagon, and their plasma concentrations have been reported to be increased during inflammatory conditions. Increased blood glucose levels are frequently observed in septic patients, and therefore we hypothesized that glucagon, but not GLP-1, is increased in individuals with inflammation.DESIGN: Prospective longitudinal cohort study.MATERIALS AND METHODS: We measured glucagon and GLP-1 in plasma sampled consecutively in three cohorts consisting of patients with infective endocarditis (n=16), urosepsis (n=28) and post-operative inflammation following percutaneous aortic valve implantation or thoracic endovascular aortic repair (n=5). Correlations between C-Reactive Protein (CRP), a marker of systemic inflammation, and glucagon and GLP-1 concentrations were investigated. Additionally, glucagon and GLP-1 concentrations were measured after a bolus infusion of lipopolysaccharide (LPS, 1ng/kg) in nine healthy young males.RESULTS: Glucagon and CRP were positively and significantly correlated (r=0.27; P=0.0003), whereas no significant association between GLP-1 and CRP was found (r=0.08, P=0.30). LPS infusion resulted in acute systemic inflammation reflected by increased temperature, pulse, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and concomitantly increased concentrations of glucagon (P<0.05) but not GLP-1.CONCLUSIONS: Systemic inflammation caused by bacterial infections or developed as a non-infected condition is associated with increased plasma concentration of glucagon, but not GLP-1. Hyperglucagonemia may contribute to the impaired glucose control in patients with systemic inflammatory diseases.

AB - OBJECTIVE: Glucagon and glucagon-like peptide-1 (GLP-1) originate from the common precursor, proglucagon, and their plasma concentrations have been reported to be increased during inflammatory conditions. Increased blood glucose levels are frequently observed in septic patients, and therefore we hypothesized that glucagon, but not GLP-1, is increased in individuals with inflammation.DESIGN: Prospective longitudinal cohort study.MATERIALS AND METHODS: We measured glucagon and GLP-1 in plasma sampled consecutively in three cohorts consisting of patients with infective endocarditis (n=16), urosepsis (n=28) and post-operative inflammation following percutaneous aortic valve implantation or thoracic endovascular aortic repair (n=5). Correlations between C-Reactive Protein (CRP), a marker of systemic inflammation, and glucagon and GLP-1 concentrations were investigated. Additionally, glucagon and GLP-1 concentrations were measured after a bolus infusion of lipopolysaccharide (LPS, 1ng/kg) in nine healthy young males.RESULTS: Glucagon and CRP were positively and significantly correlated (r=0.27; P=0.0003), whereas no significant association between GLP-1 and CRP was found (r=0.08, P=0.30). LPS infusion resulted in acute systemic inflammation reflected by increased temperature, pulse, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and concomitantly increased concentrations of glucagon (P<0.05) but not GLP-1.CONCLUSIONS: Systemic inflammation caused by bacterial infections or developed as a non-infected condition is associated with increased plasma concentration of glucagon, but not GLP-1. Hyperglucagonemia may contribute to the impaired glucose control in patients with systemic inflammatory diseases.

KW - Bacteremia

KW - ELISA

KW - Glucose

KW - Hyperglycemia

KW - Immunoassay

KW - Infection

KW - Inflammation

UR - http://www.scopus.com/inward/record.url?scp=85103038115&partnerID=8YFLogxK

U2 - 10.1530/EC-20-0590

DO - 10.1530/EC-20-0590

M3 - Journal article

C2 - 33480865

VL - 10

SP - 205

EP - 213

JO - Endocrine Connections

JF - Endocrine Connections

SN - 2049-3614

IS - 2

ER -

ID: 62374897