Sonchus oleraceus Linn extract enhanced glucose homeostasis through the AMPK/Akt/ GSK-3β signaling pathway in diabetic liver and HepG2 cell culture
The extracts of S. oleraceus Linn (SOL) and its main phenolic compounds have shown anti-diabetic effects, but their underlying mechanisms for glucose homeostasis remain unclear. The aim of this study is to evaluate the anti-diabetic mechanism of SOL by using the streptozocin (STZ) induced diabetic r...
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Veröffentlicht in: | Food and chemical toxicology 2020-02, Vol.136, p.111072-111072, Article 111072 |
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Sprache: | eng |
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Zusammenfassung: | The extracts of S. oleraceus Linn (SOL) and its main phenolic compounds have shown anti-diabetic effects, but their underlying mechanisms for glucose homeostasis remain unclear. The aim of this study is to evaluate the anti-diabetic mechanism of SOL by using the streptozocin (STZ) induced diabetic rat model. When diabetic rats were fed with SOL at a dose of 400 mg/kg/day for 6 weeks, the concentrations of triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) were reduced by 43%, 22%, and 16%, respectively. Meanwhile, it was also found that daily feeding of SOL to diabetic rats led to a decrease in plasma glucose level by approximately 23%. Positive effects were observed on glucose homeostasis due to the down-regulation of AMPK/Akt/GSK-3β pathway, as indicated by the suppressions of adenosine 5‘-monophosphate (AMP)-activated protein kinase (AMPK), protein kinase (Akt) phosphorylation, glycogen synthase kinase 3 beta (GSK-3β), and the hepatic insulin resistance. In HepG2 cells, AMPK, Akt and GSK-3β showed a consistent transcript regulation. SOL at dose of 400 mg/kg/day feeding for 6 weeks showed a positive effect comparable to metformin.
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•Major phenolics in S oleraceus Linn (SOL) was found to have intestinal stability.•SOL represented a very effective role in high blood glucose.•SOL regulated AMPK/Akt/GSK-3β signaling pathway in diabetic rat and HepG2. |
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ISSN: | 0278-6915 1873-6351 |
DOI: | 10.1016/j.fct.2019.111072 |