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Data on the expression of PEPCK in HepG2 hepatocytes transfected with miR-195

Dietary fats rich in saturated fatty acid (SFA) increase the risk of metabolic diseases, and certain microRNAs (miRNAs) dysregulated by SFA are associated with the pathogenesis of insulin resistance and type 2 diabetes. A previous study found that miR-195 is increased by SFA and impairs hepatic insu...

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Detalles Bibliográficos
Autores principales: Yang, Won-Mo, Min, Kyung-Ho, Park, Se-Whan, Lee, Wan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5676084/
https://www.ncbi.nlm.nih.gov/pubmed/29159212
http://dx.doi.org/10.1016/j.dib.2017.10.061
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author Yang, Won-Mo
Min, Kyung-Ho
Park, Se-Whan
Lee, Wan
author_facet Yang, Won-Mo
Min, Kyung-Ho
Park, Se-Whan
Lee, Wan
author_sort Yang, Won-Mo
collection PubMed
description Dietary fats rich in saturated fatty acid (SFA) increase the risk of metabolic diseases, and certain microRNAs (miRNAs) dysregulated by SFA are associated with the pathogenesis of insulin resistance and type 2 diabetes. A previous study found that miR-195 is increased by SFA and impairs hepatic insulin signaling through the suppression of INSR (Yang et al., 2014) [1]. This article reports accompanying data to determine the effect of miR-195 on the expression of PEPCK, a key player in hepatic gluconeogenesis. The transfection of miR-195 in HepG2 hepatocytes was found to increase the mRNA and protein expression of PEPCK. Moreover, the insulin-stimulated reduction of PEPCK expression was attenuated drastically by miR-195. More detailed analysis and understanding of the role of miR-195 in diet-induced hepatic insulin resistance can be found in "Saturated fatty acid-induced miR-195 impairs insulin signaling and glycogen metabolism in HepG2 cells" (Yang et al., 2014) [1].
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spelling pubmed-56760842017-11-20 Data on the expression of PEPCK in HepG2 hepatocytes transfected with miR-195 Yang, Won-Mo Min, Kyung-Ho Park, Se-Whan Lee, Wan Data Brief Cell biology    Dietary fats rich in saturated fatty acid (SFA) increase the risk of metabolic diseases, and certain microRNAs (miRNAs) dysregulated by SFA are associated with the pathogenesis of insulin resistance and type 2 diabetes. A previous study found that miR-195 is increased by SFA and impairs hepatic insulin signaling through the suppression of INSR (Yang et al., 2014) [1]. This article reports accompanying data to determine the effect of miR-195 on the expression of PEPCK, a key player in hepatic gluconeogenesis. The transfection of miR-195 in HepG2 hepatocytes was found to increase the mRNA and protein expression of PEPCK. Moreover, the insulin-stimulated reduction of PEPCK expression was attenuated drastically by miR-195. More detailed analysis and understanding of the role of miR-195 in diet-induced hepatic insulin resistance can be found in "Saturated fatty acid-induced miR-195 impairs insulin signaling and glycogen metabolism in HepG2 cells" (Yang et al., 2014) [1]. Elsevier 2017-10-28 /pmc/articles/PMC5676084/ /pubmed/29159212 http://dx.doi.org/10.1016/j.dib.2017.10.061 Text en © 2017 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Cell biology   
Yang, Won-Mo
Min, Kyung-Ho
Park, Se-Whan
Lee, Wan
Data on the expression of PEPCK in HepG2 hepatocytes transfected with miR-195
title Data on the expression of PEPCK in HepG2 hepatocytes transfected with miR-195
title_full Data on the expression of PEPCK in HepG2 hepatocytes transfected with miR-195
title_fullStr Data on the expression of PEPCK in HepG2 hepatocytes transfected with miR-195
title_full_unstemmed Data on the expression of PEPCK in HepG2 hepatocytes transfected with miR-195
title_short Data on the expression of PEPCK in HepG2 hepatocytes transfected with miR-195
title_sort data on the expression of pepck in hepg2 hepatocytes transfected with mir-195
topic Cell biology   
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5676084/
https://www.ncbi.nlm.nih.gov/pubmed/29159212
http://dx.doi.org/10.1016/j.dib.2017.10.061
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