Treating fatty liver disease by modulating mitochondrial pyruvate metabolism

Modifying the entry of pyruvate into mitochondria may provide a unique approach to treat metabolic disease. The pharmacology of a new class of insulin sensitizers directed against a newly identified mitochondrial target may treat many aspects of nonalcoholic steatohepatitis, including fibrosis. This...

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Detalles Bibliográficos
Autores principales: Colca, Jerry R., McDonald, William G., McCommis, Kyle S., Finck, Brian N.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Brief Report
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721453/
https://www.ncbi.nlm.nih.gov/pubmed/29404453
http://dx.doi.org/10.1002/hep4.1036
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author Colca, Jerry R.
McDonald, William G.
McCommis, Kyle S.
Finck, Brian N.
author_facet Colca, Jerry R.
McDonald, William G.
McCommis, Kyle S.
Finck, Brian N.
author_sort Colca, Jerry R.
collection PubMed
description Modifying the entry of pyruvate into mitochondria may provide a unique approach to treat metabolic disease. The pharmacology of a new class of insulin sensitizers directed against a newly identified mitochondrial target may treat many aspects of nonalcoholic steatohepatitis, including fibrosis. This commentary suggests treating nonalcoholic steatohepatitis through a newly identified mechanism consistent with pathophysiology. (Hepatology Communications 2017;1:193‐197)
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spelling pubmed-57214532018-02-05 Treating fatty liver disease by modulating mitochondrial pyruvate metabolism Colca, Jerry R. McDonald, William G. McCommis, Kyle S. Finck, Brian N. Hepatol Commun Brief Report Modifying the entry of pyruvate into mitochondria may provide a unique approach to treat metabolic disease. The pharmacology of a new class of insulin sensitizers directed against a newly identified mitochondrial target may treat many aspects of nonalcoholic steatohepatitis, including fibrosis. This commentary suggests treating nonalcoholic steatohepatitis through a newly identified mechanism consistent with pathophysiology. (Hepatology Communications 2017;1:193‐197) John Wiley and Sons Inc. 2017-04-18 /pmc/articles/PMC5721453/ /pubmed/29404453 http://dx.doi.org/10.1002/hep4.1036 Text en © 2017 The Authors. Hepatology Communications published by Wiley Periodicals, Inc., on behalf of the American Association for the Study of Liver Diseases. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Brief Report
Colca, Jerry R.
McDonald, William G.
McCommis, Kyle S.
Finck, Brian N.
Treating fatty liver disease by modulating mitochondrial pyruvate metabolism
title Treating fatty liver disease by modulating mitochondrial pyruvate metabolism
title_full Treating fatty liver disease by modulating mitochondrial pyruvate metabolism
title_fullStr Treating fatty liver disease by modulating mitochondrial pyruvate metabolism
title_full_unstemmed Treating fatty liver disease by modulating mitochondrial pyruvate metabolism
title_short Treating fatty liver disease by modulating mitochondrial pyruvate metabolism
title_sort treating fatty liver disease by modulating mitochondrial pyruvate metabolism
topic Brief Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721453/
https://www.ncbi.nlm.nih.gov/pubmed/29404453
http://dx.doi.org/10.1002/hep4.1036
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