1 40 1 Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.molmet.2021.101244</a> Pages 3-11 ISSN 2212-8778 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.molmet.2021.101244</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number May 2021 List NEOMED College NEOMED College of Medicine NEOMED Department Department of Integrative Medical Sciences NEOMED Postdoc Publications NEOMED Student Publications Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease. Publisher An entity responsible for making the resource available Molecular Metabolism Date A point or period of time associated with an event in the lifecycle of the resource 2021 2021-04-27 Subject The topic of the resource miR-34a; NAFLD; Lipogenesis; bile acids; Bile acids; lipid absorption; lipogenesis; Lipid absorption Creator An entity primarily responsible for making the resource Xu Y; Zhu Y; Hu S; Pan X; Bawa FC; Wang HH; Wang DQ; Yin L; Zhang Y Description An account of the resource Objectives: Hepatic miR-34a expression is elevated in diet-induced or genetically obese mice, and patients with non-alcoholic steatohepatitis (NASH), yet the role of hepatocyte miR-34a in the progression of non-alcoholic fatty liver disease (NAFLD) from non-alcoholic fatty liver (NAFL) to NASH remains to be elucidated.; Methods: Mice over-expressing or deficient in hepatocyte miR-34a and their control mice were fed a diet enriched in fats, cholesterol and fructose (HFCF) to induce NASH. C57BL/6 mice with NASH were treated with an miR-34a inhibitor or a scramble control oligo. The effect of miR-34a on the development, progression or reversal of NAFLD was determined.; Results: Hepatocyte-specific expression of miR-34a aggravated HFCF diet-induced NAFLD. In contrast, germline or adult-onset loss of hepatocyte miR-34a attenuated the development and progression of NAFLD. In addition, pharmacological inhibition of miR-34a reversed HFCF diet-induced steatohepatitis. Mechanistically, hepatocyte miR-34a regulated the development and progression of NAFLD by inducing lipid absorption, lipogenesis, inflammation and apoptosis, and inhibiting fatty acid oxidation.; Conclusions: Hepatocyte miR-34a is an important regulator in the development and progression of NAFLD. MiR-34a may be a useful target for treating NAFLD. (Copyright © 2021 The Author(s). Published by Elsevier GmbH.. All rights reserved.) Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">10.1016/j.molmet.2021.101244</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Format The file format, physical medium, or dimensions of the resource journalArticle 2021 Bawa FC BILE acids Department of Integrative Medical Sciences Hu S journalArticle lipid absorption Lipogenesis May 2021 List miR-34a Molecular metabolism NAFLD NEOMED College of Medicine NEOMED Postdoc Publications NEOMED Student Publications Pan X Wang DQ Wang HH Xu Y Yin L Zhang Y Zhu Y