Interleukin-32 Contributes to Human Nonalcoholic Fatty Liver Disease and Insulin Resistance.
Journal
Hepatology communications
ISSN: 2471-254X
Titre abrégé: Hepatol Commun
Pays: United States
ID NLM: 101695860
Informations de publication
Date de publication:
Sep 2019
Sep 2019
Historique:
received:
19
12
2018
accepted:
21
05
2019
entrez:
10
9
2019
pubmed:
10
9
2019
medline:
10
9
2019
Statut:
epublish
Résumé
Nonalcoholic fatty liver disease (NAFLD) is a metabolic disorder due to increased accumulation of fat in the liver and in many cases to enhanced inflammation. Although the contribution of inflammation in the pathogenesis of NAFLD is well established, the cytokines that are involved and how they influence liver transformation are still poorly characterized. In addition, with other modifiers, inflammation influences NAFLD progression to liver cirrhosis and hepatocellular carcinoma, demonstrating the need to find new molecular targets with potential future therapeutic applications. We investigated gene signatures in 38 liver biopsies from patients with NAFLD and obesity who had received bariatric surgery and compared these to 10 control patients who had received a cholecystectomy, using DNA microarray technology. A subset of differentially expressed genes was then validated on a larger cohort of 103 patients who had received bariatric surgery for obesity; data were thoroughly analyzed in terms of correlations with NAFLD pathophysiological parameters. Finally, the impact of a specific cytokine, interleukin-32 (
Identifiants
pubmed: 31497742
doi: 10.1002/hep4.1396
pii: HEP41396
pmc: PMC6719754
doi:
Types de publication
Journal Article
Langues
eng
Pagination
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