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. 2019 Jun 21;9:9055. doi: 10.1038/s41598-019-45099-x

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Impacts of SCH on glucose uptake and GLUT2 protein in FFA-induced steatotic HepG2 cells. (A) Relative fluorescence intensity (2-NBDG) of HepG2 cells implying glucose uptake rate. (B) Representative fluorescence images of steatotic HepG2 showing relative glucose uptake rate. Cells were untreated (a), FFA-treated (b), exposed to FFA with 10 μg/ml of SCH (c), exposed to 50 μg/ml of SCH (d). (C) Representative blot of GLUT2 protein is depicted. (D) Band intensity was measured with densitometric analysis and normalized to the intensity of β-actin. (E) Immunofluorescence images showing the impact of SCH on localization of Glut 2 protein in insulin-stimulated FFA-induced HepG2 cells. Images were taken at magnification of 400×. Data are expressed as mean ± SD.