Serum levels of advanced glycation end products and their receptors sRAGE and Galectin-3 in chronic pancreatitis.
Adult
Aged
Aged, 80 and over
Aging
Alcoholism
/ complications
Antigens, Neoplasm
/ blood
Blood Proteins
/ genetics
Diabetes Complications
/ blood
Female
Galectins
/ blood
Glycation End Products, Advanced
/ blood
Humans
Inflammation
/ blood
Male
Middle Aged
Mitogen-Activated Protein Kinases
/ blood
Pancreatitis, Chronic
/ blood
Polymorphism, Single Nucleotide
Young Adult
Advanced glycated end products
Alcoholic chronic pancreatitis
Galectin-3
Non-alcoholic chronic pancreatitis
Receptor for advanced glycated end products
SNPs
Journal
Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
ISSN: 1424-3911
Titre abrégé: Pancreatology
Pays: Switzerland
ID NLM: 100966936
Informations de publication
Date de publication:
Mar 2020
Mar 2020
Historique:
received:
16
08
2019
revised:
09
12
2019
accepted:
16
12
2019
pubmed:
25
12
2019
medline:
27
2
2021
entrez:
25
12
2019
Statut:
ppublish
Résumé
/Objectives: AGE and their receptors like RAGE and Galectin-3 can activate inflammatory pathways and have been associated with chronic inflammatory diseases. Several studies investigated the role of AGE, Galectin-3 and sRAGE in pancreatic diseases, whereas no comprehensive data for chronic pancreatitis (CP) are available. Serum samples from CP patients without an active inflammatory process (85 ACP; 26 NACP patients) and 40 healthy controls were collected. Levels of AGE, sRAGE and Galectin-3 were measured by ELISA. To exclude potential influences of previously described RAGE SNPs on detected serum levels, we analyzed variants rs207128, rs207060, rs1800625, and rs1800624 by melting curve technique in 378 CP patients and 338 controls. AGE and Galectin-3 serum levels were significantly elevated in both ACP and NACP patients compared to controls (AGE: 56.61 ± 3.043 vs. 31.71 ± 2.308 ng/mL; p < 0.001; Galectin-3: 16.63 ± 0.6297 vs. 10.81 ± 0.4835 ng/mL; p < 0.001). In contrast, mean serum sRAGE levels were significantly reduced in CP patients compared to controls (sRAGE: 829.7 ± 37.10 vs. 1135 ± 55.74 ng/mL; p < 0.001). All results were consistent after correction for gender, age and diabetes mellitus. No genetic association with CP was found. Our extensive analysis demonstrated the importance of aging related pathways in the pathogenesis of CP. As the results were consistent in ACP and NACP, both entities most likely share common pathomechanisms. Most probably the involved pathways are a general hallmark of an inflammatory state in CP that is even present in symptom-free intervals.
Sections du résumé
BACKGROUND
BACKGROUND
/Objectives: AGE and their receptors like RAGE and Galectin-3 can activate inflammatory pathways and have been associated with chronic inflammatory diseases. Several studies investigated the role of AGE, Galectin-3 and sRAGE in pancreatic diseases, whereas no comprehensive data for chronic pancreatitis (CP) are available.
METHODS
METHODS
Serum samples from CP patients without an active inflammatory process (85 ACP; 26 NACP patients) and 40 healthy controls were collected. Levels of AGE, sRAGE and Galectin-3 were measured by ELISA. To exclude potential influences of previously described RAGE SNPs on detected serum levels, we analyzed variants rs207128, rs207060, rs1800625, and rs1800624 by melting curve technique in 378 CP patients and 338 controls.
RESULTS
RESULTS
AGE and Galectin-3 serum levels were significantly elevated in both ACP and NACP patients compared to controls (AGE: 56.61 ± 3.043 vs. 31.71 ± 2.308 ng/mL; p < 0.001; Galectin-3: 16.63 ± 0.6297 vs. 10.81 ± 0.4835 ng/mL; p < 0.001). In contrast, mean serum sRAGE levels were significantly reduced in CP patients compared to controls (sRAGE: 829.7 ± 37.10 vs. 1135 ± 55.74 ng/mL; p < 0.001). All results were consistent after correction for gender, age and diabetes mellitus. No genetic association with CP was found.
CONCLUSIONS
CONCLUSIONS
Our extensive analysis demonstrated the importance of aging related pathways in the pathogenesis of CP. As the results were consistent in ACP and NACP, both entities most likely share common pathomechanisms. Most probably the involved pathways are a general hallmark of an inflammatory state in CP that is even present in symptom-free intervals.
Identifiants
pubmed: 31870801
pii: S1424-3903(19)30810-5
doi: 10.1016/j.pan.2019.12.013
pii:
doi:
Substances chimiques
Antigens, Neoplasm
0
Blood Proteins
0
Galectins
0
Glycation End Products, Advanced
0
LGALS3 protein, human
0
MOK protein, human
EC 2.7.11.22
Mitogen-Activated Protein Kinases
EC 2.7.11.24
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
187-192Informations de copyright
Copyright © 2019 IAP and EPC. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that there is no conflict of interest.