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Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice

  • Authors:
    • Zhongkun Ren
    • Zhiyong Yang
    • Yi Lu
    • Rongping Zhang
    • Hui Yang
  • View Affiliations / Copyright

    Affiliations: Department of Medical Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, P.R. China, Department of Medical Imaging, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, P.R. China, School of Pharmaceutical Sciences and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, Yunnan 650500, P.R. China, Biomedical Engineering Center, Kunming Medical University, Kunming, Yunnan 650500, P.R. China
    Copyright: © Ren et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2475-2483
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    Published online on: March 26, 2020
       https://doi.org/10.3892/mmr.2020.11041
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Abstract

Epigallocatechin-3-gallate (EGCG) is beneficial for inhibiting dyslipidemia and reducing hyperlipidemic risk. The purpose of the present study was to investigate the glycolipid regulatory effects and potential mechanisms of EGCG in a high‑fat diet and streptozotocin‑induced type 2 diabetes mellitus (T2DM) mouse model. The results demonstrated that EGCG can decrease blood glucose levels and increase insulin resistance in T2DM mice. In addition, EGCG can regulate serum lipid levels, including those of total cholesterol, triglyceride and low‑density lipoprotein receptor (LDL‑r), and reduce lipid deposition in vascular endothelial cells in a dose‑dependent manner. In addition, the gene and protein expression of related scavenger receptors, including cluster of differentiation 36, sterol regulatory element binding protein 2 (SREBP), SREBP cleavage‑activating protein and LDL‑r, were downregulated in a dose‑dependent manner. The present study noted that EGCG possesses potential as a natural product for preventing and treating metabolic hyperlipidemia syndrome, probably by reducing the blood lipid levels, alleviating vascular endothelial cell damage, maintaining normal lipid metabolism in blood vessels and ameliorating glycolipid disorders.
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Spandidos Publications style
Ren Z, Yang Z, Lu Y, Zhang R and Yang H: Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice. Mol Med Rep 21: 2475-2483, 2020.
APA
Ren, Z., Yang, Z., Lu, Y., Zhang, R., & Yang, H. (2020). Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice. Molecular Medicine Reports, 21, 2475-2483. https://doi.org/10.3892/mmr.2020.11041
MLA
Ren, Z., Yang, Z., Lu, Y., Zhang, R., Yang, H."Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice". Molecular Medicine Reports 21.6 (2020): 2475-2483.
Chicago
Ren, Z., Yang, Z., Lu, Y., Zhang, R., Yang, H."Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice". Molecular Medicine Reports 21, no. 6 (2020): 2475-2483. https://doi.org/10.3892/mmr.2020.11041
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Spandidos Publications style
Ren Z, Yang Z, Lu Y, Zhang R and Yang H: Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice. Mol Med Rep 21: 2475-2483, 2020.
APA
Ren, Z., Yang, Z., Lu, Y., Zhang, R., & Yang, H. (2020). Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice. Molecular Medicine Reports, 21, 2475-2483. https://doi.org/10.3892/mmr.2020.11041
MLA
Ren, Z., Yang, Z., Lu, Y., Zhang, R., Yang, H."Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice". Molecular Medicine Reports 21.6 (2020): 2475-2483.
Chicago
Ren, Z., Yang, Z., Lu, Y., Zhang, R., Yang, H."Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice". Molecular Medicine Reports 21, no. 6 (2020): 2475-2483. https://doi.org/10.3892/mmr.2020.11041
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