Glucagon-like peptide-1 and glucagon-like peptide-2 regulation during human liver regeneration

Glucagon-like peptide-1 and glucagon-like peptide-2 regulation during human liver regeneration

Accumulating evidence suggests that metabolic demands of the regenerating liver are met via lipid metabolism and critical regulators of this process. As such, glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) critically affect hepatic regeneration in rodent models. The present stud...

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Published in:Scientific reports Vol. 13; no. 1; p. 15980
Main Authors: Ammann, Markus, Santol, Jonas, Pereyra, David, Kalchbrenner, Tamara, Wuerger, Tanja, Laengle, Johannes, Smoot, Rory L., Hulla, Wolfgang, Laengle, Friedrich, Starlinger, Patrick
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 25-09-2023
Nature Publishing Group
Nature Portfolio
Subjects:
692/308
692/308/575
692/4020/4021
Animal models
Glucagon
Glucagon-like peptide 1
Glucagon-like peptide 2
Hepatectomy
Humanities and Social Sciences
Inflammation
Interleukin 6
Lipid metabolism
Lipids
Liver
Liver diseases
Metabolism
multidisciplinary
Peptides
Science
Science (multidisciplinary)
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Summary:Accumulating evidence suggests that metabolic demands of the regenerating liver are met via lipid metabolism and critical regulators of this process. As such, glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) critically affect hepatic regeneration in rodent models. The present study aimed to evaluate potential alterations and dynamics of circulating GLP-1 and GLP-2 in patients undergoing liver resections, focusing on post-hepatectomy liver failure (PHLF). GLP-1, GLP-2, Interleukin-6 (IL-6) and parameters of lipid metabolism were determined perioperatively in fasting plasma of 46 patients, who underwent liver resection. GLP-1 and GLP-2 demonstrated a rapid and consistently inverse time course during hepatic regeneration with a significant decrease of GLP-1 and increase of GLP-2 on POD1. Importantly, these postoperative dynamics were significantly more pronounced when PHLF occurred. Of note, the extent of resection or development of complications were not associated with these alterations. IL-6 mirrored the time course of GLP-2. Assessing the main degradation protein dipeptidyl peptidase 4 (DPP4) no significant association with either GLP-1 or -2 could be found. Additionally, in PHLF distinct postoperative declines in plasma lipid parameters were present and correlated with GLP-2 dynamics. Our data suggest dynamic inverse regulation of GLP-1 and GLP-2 during liver regeneration, rather caused by an increase in expression/release than by changes in degradation capacity and might be associated with inflammatory responses. Their close association with circulating markers of lipid metabolism and insufficient hepatic regeneration after liver surgery suggest a critical involvement during these processes in humans.
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ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-023-43283-8