Cargando…
Syringaresinol-4-O-β-d-glucoside alters lipid and glucose metabolism in HepG2 cells and C2C12 myotubes
Syringaresinol-4-O-β-d-glucoside (SSG), a furofuran-type lignan, was found to modulate lipid and glucose metabolism through an activity screen of lipid accumulation and glucose consumption, and was therefore considered as a promising candidate for the prevention and treatment of metabolic disorder,...
Autores principales: | , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5518665/ https://www.ncbi.nlm.nih.gov/pubmed/28752030 http://dx.doi.org/10.1016/j.apsb.2017.04.008 |
_version_ | 1783251526814269440 |
---|---|
author | Wang, Shuai Wu, Chongming Li, Xin Zhou, Yue Zhang, Quanyang Ma, Fuchao Wei, Jianhe Zhang, Xiaopo Guo, Peng |
author_facet | Wang, Shuai Wu, Chongming Li, Xin Zhou, Yue Zhang, Quanyang Ma, Fuchao Wei, Jianhe Zhang, Xiaopo Guo, Peng |
author_sort | Wang, Shuai |
collection | PubMed |
description | Syringaresinol-4-O-β-d-glucoside (SSG), a furofuran-type lignan, was found to modulate lipid and glucose metabolism through an activity screen of lipid accumulation and glucose consumption, and was therefore considered as a promising candidate for the prevention and treatment of metabolic disorder, especially in lipid and glucose metabolic homeostasis. In this study, the effects of SSG on lipogenesis and glucose consumption in HepG2 cells and C2C12 myotubes were further investigated. Treatment with SSG significantly inhibited lipid accumulation by oil red O staining and reduced the intracellular contents of total lipid, cholesterol and triglyceride in HepG2 cells. No effect was observed on cell viability in the MTT assay at concentrations of 0.1–10 μmol/L. SSG also increased glucose consumption by HepG2 cells and glucose uptake by C2C12 myotubes. Furthermore, real-time quantitative PCR revealed that the beneficial effects were associated with the down-regulation of sterol regulatory element-binding proteins-1c, -2 (SREBP-1c, -2), fatty acid synthase (FAS), acetyl CoA carboxylase (ACC) and hydroxyl methylglutaryl CoA reductase (HMGR), and up-regulation of peroxisome proliferator-activated receptors alpha and gamma (PPARα and PPARγ). SSG also significantly elevated transcription activity of PPARγ tested by luciferase assay. These results suggest that SSG is an effective regulator of lipogenesis and glucose consumption and might be a candidate for further research in the prevention and treatment of lipid and glucose metabolic diseases. |
format | Online Article Text |
id | pubmed-5518665 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-55186652017-07-27 Syringaresinol-4-O-β-d-glucoside alters lipid and glucose metabolism in HepG2 cells and C2C12 myotubes Wang, Shuai Wu, Chongming Li, Xin Zhou, Yue Zhang, Quanyang Ma, Fuchao Wei, Jianhe Zhang, Xiaopo Guo, Peng Acta Pharm Sin B Original Article Syringaresinol-4-O-β-d-glucoside (SSG), a furofuran-type lignan, was found to modulate lipid and glucose metabolism through an activity screen of lipid accumulation and glucose consumption, and was therefore considered as a promising candidate for the prevention and treatment of metabolic disorder, especially in lipid and glucose metabolic homeostasis. In this study, the effects of SSG on lipogenesis and glucose consumption in HepG2 cells and C2C12 myotubes were further investigated. Treatment with SSG significantly inhibited lipid accumulation by oil red O staining and reduced the intracellular contents of total lipid, cholesterol and triglyceride in HepG2 cells. No effect was observed on cell viability in the MTT assay at concentrations of 0.1–10 μmol/L. SSG also increased glucose consumption by HepG2 cells and glucose uptake by C2C12 myotubes. Furthermore, real-time quantitative PCR revealed that the beneficial effects were associated with the down-regulation of sterol regulatory element-binding proteins-1c, -2 (SREBP-1c, -2), fatty acid synthase (FAS), acetyl CoA carboxylase (ACC) and hydroxyl methylglutaryl CoA reductase (HMGR), and up-regulation of peroxisome proliferator-activated receptors alpha and gamma (PPARα and PPARγ). SSG also significantly elevated transcription activity of PPARγ tested by luciferase assay. These results suggest that SSG is an effective regulator of lipogenesis and glucose consumption and might be a candidate for further research in the prevention and treatment of lipid and glucose metabolic diseases. Elsevier 2017-07 2017-05-09 /pmc/articles/PMC5518665/ /pubmed/28752030 http://dx.doi.org/10.1016/j.apsb.2017.04.008 Text en © 2017 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Article Wang, Shuai Wu, Chongming Li, Xin Zhou, Yue Zhang, Quanyang Ma, Fuchao Wei, Jianhe Zhang, Xiaopo Guo, Peng Syringaresinol-4-O-β-d-glucoside alters lipid and glucose metabolism in HepG2 cells and C2C12 myotubes |
title | Syringaresinol-4-O-β-d-glucoside alters lipid and glucose metabolism in HepG2 cells and C2C12 myotubes |
title_full | Syringaresinol-4-O-β-d-glucoside alters lipid and glucose metabolism in HepG2 cells and C2C12 myotubes |
title_fullStr | Syringaresinol-4-O-β-d-glucoside alters lipid and glucose metabolism in HepG2 cells and C2C12 myotubes |
title_full_unstemmed | Syringaresinol-4-O-β-d-glucoside alters lipid and glucose metabolism in HepG2 cells and C2C12 myotubes |
title_short | Syringaresinol-4-O-β-d-glucoside alters lipid and glucose metabolism in HepG2 cells and C2C12 myotubes |
title_sort | syringaresinol-4-o-β-d-glucoside alters lipid and glucose metabolism in hepg2 cells and c2c12 myotubes |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5518665/ https://www.ncbi.nlm.nih.gov/pubmed/28752030 http://dx.doi.org/10.1016/j.apsb.2017.04.008 |
work_keys_str_mv | AT wangshuai syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes AT wuchongming syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes AT lixin syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes AT zhouyue syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes AT zhangquanyang syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes AT mafuchao syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes AT weijianhe syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes AT zhangxiaopo syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes AT guopeng syringaresinol4obdglucosidealterslipidandglucosemetabolisminhepg2cellsandc2c12myotubes |