Neurotensin up-regulation is associated with advanced fibrosis and hepatocellular carcinoma in patients with MAFLD.


Journal

Biochimica et biophysica acta. Molecular and cell biology of lipids
ISSN: 1879-2618
Titre abrégé: Biochim Biophys Acta Mol Cell Biol Lipids
Pays: Netherlands
ID NLM: 101731727

Informations de publication

Date de publication:
10 2020
Historique:
received: 15 04 2020
revised: 24 06 2020
accepted: 07 07 2020
pubmed: 15 7 2020
medline: 9 1 2021
entrez: 15 7 2020
Statut: ppublish

Résumé

Neurotensin (NTS), a 13-aminoacid peptide localized in central nervous system and gastrointestinal tract, is involved in lipid metabolism and promotes various cancers onset mainly by binding to neurotensin receptor 1 (NTSR1). Increased plasma levels of pro-NTS, the stable NTS precursor, have been associated with type 2 diabetes (T2D), cardiovascular diseases and metabolic associated fatty liver disease (MAFLD). We aimed to evaluate 1) the impact of NTS rs1800832 and NTSR1 rs6090453 genetic variants on liver damage in 1166 MAFLD European individuals, 2) the relation between NTS variant and circulating pro-NTS and 3) the hepatic NTS expression by RNAseq transcriptomic analysis in 125 bariatric patients. The NTS rs1800832 G allele was associated with hepatic fibrosis (OR 1.27, 95% confidence interval (CI). 1.02-1.58; p = 0.03), even more in carriers of both NTS and NTSR1 G risk alleles (OR 1.17, 95% CI. 1.03-1.34; p = 0.01), with cirrhosis (OR 1.58, 95% CI. 1.07-2.34; p = 0.02) and HCC (OR 1.98, 95% CI. 1.24-3.2; p = 0.004). Pro-NTS circulating levels were correlated with T2D (p = 0.005), BMI, (p = 0.04), age (p = 0.0016), lobular inflammation (p = 0.0025), fibrosis>2 (p < 0.0001), cirrhosis (p = 0.0009) and HCC (p < 0.0001) and more so after stratification for the NTS G allele. Transcriptomic data showed that hepatic NTS expression correlated with that of fibrogenic genes (p < 0.05). NTS rs1800832 variant is associated with advanced fibrosis and HCC in MAFLD patients likely affecting NTS protein activity. The rs6090453 NTSR1 gene variant synergizes with NTS rs1800832 mutation to promote liver damage. Prospective studies are necessary to confirm NTS role in liver disease progression.

Sections du résumé

BACKGROUND & AIMS
Neurotensin (NTS), a 13-aminoacid peptide localized in central nervous system and gastrointestinal tract, is involved in lipid metabolism and promotes various cancers onset mainly by binding to neurotensin receptor 1 (NTSR1). Increased plasma levels of pro-NTS, the stable NTS precursor, have been associated with type 2 diabetes (T2D), cardiovascular diseases and metabolic associated fatty liver disease (MAFLD). We aimed to evaluate 1) the impact of NTS rs1800832 and NTSR1 rs6090453 genetic variants on liver damage in 1166 MAFLD European individuals, 2) the relation between NTS variant and circulating pro-NTS and 3) the hepatic NTS expression by RNAseq transcriptomic analysis in 125 bariatric patients.
RESULTS
The NTS rs1800832 G allele was associated with hepatic fibrosis (OR 1.27, 95% confidence interval (CI). 1.02-1.58; p = 0.03), even more in carriers of both NTS and NTSR1 G risk alleles (OR 1.17, 95% CI. 1.03-1.34; p = 0.01), with cirrhosis (OR 1.58, 95% CI. 1.07-2.34; p = 0.02) and HCC (OR 1.98, 95% CI. 1.24-3.2; p = 0.004). Pro-NTS circulating levels were correlated with T2D (p = 0.005), BMI, (p = 0.04), age (p = 0.0016), lobular inflammation (p = 0.0025), fibrosis>2 (p < 0.0001), cirrhosis (p = 0.0009) and HCC (p < 0.0001) and more so after stratification for the NTS G allele. Transcriptomic data showed that hepatic NTS expression correlated with that of fibrogenic genes (p < 0.05).
CONCLUSIONS
NTS rs1800832 variant is associated with advanced fibrosis and HCC in MAFLD patients likely affecting NTS protein activity. The rs6090453 NTSR1 gene variant synergizes with NTS rs1800832 mutation to promote liver damage. Prospective studies are necessary to confirm NTS role in liver disease progression.

Identifiants

pubmed: 32663609
pii: S1388-1981(20)30157-8
doi: 10.1016/j.bbalip.2020.158765
pii:
doi:

Substances chimiques

Receptors, Neurotensin 0
neurotensin type 1 receptor 0
Neurotensin 39379-15-2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

158765

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest None.

Auteurs

Paola Dongiovanni (P)

General Medicine and Metabolic Diseases, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy.

Marica Meroni (M)

General Medicine and Metabolic Diseases, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy; Departments of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy.

Salvatore Petta (S)

Sezione di Gastroenterologia e Epatologia, PROMISE, University of Palermo, Italy.

Miriam Longo (M)

General Medicine and Metabolic Diseases, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy; Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy.

Anna Alisi (A)

Research Unit of Molecular Genetics of Complex Phenotypes, "Bambino Gesù" Children's Hospital IRCCS, Rome, Italy.

Giorgio Soardo (G)

Department of Medical Area (DAME), University of Udine and Italian Liver Foundation, Bldg Q AREA Science Park - Basovizza Campus, Trieste, Italy.

Luca Valenti (L)

Translational Medicine, University of Milan, Fondazione IRCCS Cà Granda Pad Marangoni, Milan, Italy.

Luca Miele (L)

Area Medicina Interna, Gastroenterologia e Oncologia Medica, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

Stefania Grimaudo (S)

Sezione di Gastroenterologia e Epatologia, PROMISE, University of Palermo, Italy.

Grazia Pennisi (G)

Sezione di Gastroenterologia e Epatologia, PROMISE, University of Palermo, Italy.

Grieco Antonio (G)

Area Medicina Interna, Gastroenterologia e Oncologia Medica, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

Dario Consonni (D)

Epidemiology Unit, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy.

Silvia Fargion (S)

General Medicine and Metabolic Diseases, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy.

Anna Ludovica Fracanzani (AL)

General Medicine and Metabolic Diseases, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy; Departments of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy. Electronic address: anna.fracanzani@unimi.it.

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