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Antidiabetic effects of a lipophilic extract obtained from flowers of Wisteria sinensis by activating Akt/GLUT4 and Akt/GSK3?

ABSTRACT: Background Type 2 diabetes mellitus is primarily caused by insulin resistance (IR) in insulin-sensitive tissues, including liver, white adipose tissues (WAT), and skeletal muscles. Discovering nutritious foods with antidiabetic effects is of great significance. Numerous published reports indicated that protein kinase B (Akt) and glucose transporter 4 (GLUT4) play crucial roles in ameliorating IR and diabetic symptoms. Objective In the present study, antidiabetic effects and the potential mechanism of action of WS-PE (a lipophilic extract from edible flowers of Wisteria sinensis) were explored with L6 cells in vitro and in high-fat diet (HFD) + Streptozocin (STZ)-induced diabetic mice in vivo. Design In vivo, HFD + STZ-induced diabetic mice were used as diabetic models to investigate the potential antidiabetic and antidyslipidemic activities. In vitro, a novel GLUT4 translocation assay system was established to evaluate the potential effects of WS-PE on GLUT4 translocation. Western blot analysis was adopted to investigate the molecular mechanisms of WS-PE both in vivo and in vitro. Results vitro, WS-PE increased glucose uptake by stimulating GLUT4 expression and translocation, which were regulated by Akt phosphorylation. In vivo, the WS-PE treatment ameliorated the hyperglycemia, IR, and dyslipidemia and reversed hepatic steatosis and pancreatic damage in diabetic mice. The WS-PE treatment increased GLUT4 expression by Akt activation in WAT and skeletal muscle. Akt activation stimulated GSK3? phosphorylation in liver and skeletal muscles, indicating that WS-PE showed regulatory effects on glycogen synthesis in liver and skeletal muscles. Conclusion These in vitro and in vivo results indicated that the WS-PE treatment exerted antidiabetic effects by activating Akt/GLUT4 and Akt/GSK3?.

SUBMITTER: Lv Y

PROVIDER: S-EPMC7534953 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Project description:PurposeCurrent knowledge of TMEM17, a recently identified protein of the transmembrane (TMEM) family, is limited, especially with respect to its expression and biological functions in malignant tumors. This study analyzed TMEM17 expression in invasive breast cancer tissue and breast cell lines and its relevance to clinicopathological factors, and investigated the mechanisms underlying the biological effects of TMEM17 on breast cancer cells.Patients and methodsTMEM17 protein expression was determined in 20 freshly harvested specimens (tumor and paired normal tissues) by Western blotting. Immunohistochemical analysis was performed to determine the expression and subcellular localization of TMEM17 in samples from 167 patients (mean age, 49 years) diagnosed with invasive ductal carcinoma (38 with triple-negative breast cancer; 129 with non-triple-negative breast cancer) who underwent complete resection in the First Affiliated Hospital of China Medical University between 2011 and 2013. Furthermore, TMEM17 was knocked down by small interfering RNAs in breast cancer cell lines.ResultsTMEM17 was found to be significantly upregulated in breast cancer tissues compared to the corresponding normal breast tissues by Western blotting (p=0.015). Immunohistochemical analysis revealed that TMEM was significantly upregulated in invasive breast cancer cells compared to adjacent normal breast duct glandular epithelial cells (10.78% vs 76.05%, p<0.001), and its expression was closely related to the patient's T-stage (p=0.022), advanced TNM stages (p=0.007), and lymph node metastasis (p=0.012). After TMEM17 knockdown or overexpression in breast cancer cell lines, TMEM17 upregulated p-AKT, p-GSK3β, active β-catenin, and Snail, and downstream target proteins c-myc and cyclin D1, and downregulated E-cadherin, resulting in increased cancer cell proliferation, invasion, and migration. These effects were reversed by the AKT inhibitor LY294002.ConclusionOur results indicate that TMEM17 is upregulated in breast cancer tissues and can promote malignant progression of breast cancer cells by activating the AKT/GSK3β signaling pathway.

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Antidiabetic effects of a lipophilic extract obtained from flowers of Wisteria sinensis by activating Akt/GLUT4 and Akt/GSK3?

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