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Visfatin exacerbates hepatic inflammation and fibrosis in a methionine-choline-deficient diet mouse model

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dc.contributor.authorHeo, YJ-
dc.contributor.authorChoi, SE-
dc.contributor.authorLee, N-
dc.contributor.authorJeon, JY-
dc.contributor.authorHan, SJ-
dc.contributor.authorKim, DJ-
dc.contributor.authorKang, Y-
dc.contributor.authorLee, KW-
dc.contributor.authorKim, HJ-
dc.date.accessioned2023-01-05T03:03:28Z-
dc.date.available2023-01-05T03:03:28Z-
dc.date.issued2021-
dc.identifier.issn0815-9319-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/23705-
dc.description.abstractBackground and Aim: Non-alcoholic fatty liver disease (NAFLD) ranges from simple steatosis to non-alcoholic steatohepatitis, which is characterized by hepatic inflammation that can progress to fibrosis, cirrhosis, and hepatocellular carcinoma. Visfatin, an adipocytokine, was reported to induce pro-inflammatory cytokines and can be associated with liver fibrosis. We investigated the role of visfatin on hepatic inflammation and fibrosis in a methionine-choline-deficient (MCD)-diet-induced steatohepatitis mouse model. Methods: Eight-week-old male C57BL/6 J mice were randomly assigned into one of three groups: (1) saline-injected control diet group; (2) saline-injected MCD diet group; and (3) visfatin-injected MCD diet group (n = 8 per group). Mice were administered intravenous saline or 10 μg/kg of recombinant murine visfatin for 2 weeks. Histologic assessment of liver and biochemical and molecular measurements of endoplasmic reticulum (ER) stress, reactive oxidative stress (ROS), inflammation, and fibrosis were performed in livers from these animals. Results: Visfatin injection aggravated hepatic steatosis and increased plasma alanine aminotransferase and aspartate aminotransferase concentrations. Visfatin increased inflammatory cell infiltration (as indicated by F4/80, CD68, ly6G, and CD3 mRNA expression) and expression of chemokines in the liver. Visfatin also increased the expression of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) and activated fibrosis markers (CTGF, TIMP1, collagen 1α2, collagen 3α2, αSMA, fibronectin, and vimentin) in liver. Livers of visfatin-injected mice showed upregulation of ER stress and ROS and activation of JNK signaling. Conclusions: These results suggest that visfatin aggravates hepatic inflammation together with induction of ER and oxidative stress and exacerbates fibrosis in an MCD-diet-fed mouse model of NAFLD.-
dc.language.isoen-
dc.subject.MESHAdipokines-
dc.subject.MESHAnimals-
dc.subject.MESHChemical and Drug Induced Liver Injury-
dc.subject.MESHCholine Deficiency-
dc.subject.MESHDiet-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHInflammation-
dc.subject.MESHLiver-
dc.subject.MESHLiver Cirrhosis-
dc.subject.MESHMale-
dc.subject.MESHMethionine-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHNicotinamide Phosphoribosyltransferase-
dc.subject.MESHNon-alcoholic Fatty Liver Disease-
dc.titleVisfatin exacerbates hepatic inflammation and fibrosis in a methionine-choline-deficient diet mouse model-
dc.typeArticle-
dc.identifier.pmid33600604-
dc.subject.keywordhepatic fibrosis-
dc.subject.keywordhepatic inflammation-
dc.subject.keywordmethionine-choline-deficient diet-
dc.subject.keywordvisfatin-
dc.contributor.affiliatedAuthorHeo, YJ-
dc.contributor.affiliatedAuthorChoi, SE-
dc.contributor.affiliatedAuthorLee, N-
dc.contributor.affiliatedAuthorJeon, JY-
dc.contributor.affiliatedAuthorHan, SJ-
dc.contributor.affiliatedAuthorKim, DJ-
dc.contributor.affiliatedAuthorKang, Y-
dc.contributor.affiliatedAuthorLee, KW-
dc.contributor.affiliatedAuthorKim, HJ-
dc.type.localJournal Papers-
dc.identifier.doi10.1111/jgh.15465-
dc.citation.titleJournal of gastroenterology and hepatology-
dc.citation.volume36-
dc.citation.number9-
dc.citation.date2021-
dc.citation.startPage2592-
dc.citation.endPage2600-
dc.identifier.bibliographicCitationJournal of gastroenterology and hepatology, 36(9). : 2592-2600, 2021-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
dc.identifier.eissn1440-1746-
dc.relation.journalidJ008159319-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Endocrinology & Metabolism
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
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