ABSTRACT
Long-term stored oolong tea has recently attracted considerable attention concerning its salutary effect. In this study, the anti-obesity effect of different years' oolong tea on high-fat diet-fed mice was compared. Wuyi rock tea of 2001, 2011, and 2020 were chosen to be the representative samples of oolong tea. The results showed that eight-week administration of 2001 Wuyi rock tea (WRT01), 2011 Wuyi rock tea (WRT11), and 2020 Wuyi rock tea (WRT20) extracts (400 mg per kg per d) significantly decreased the body weight and attenuated the obesity in high-fat diet-fed mice. 2001 and 2011 Wuyi rock teas reduced obesity mainly through regulating lipid metabolism and activating the AMPK/SREBP-1 pathway, downregulating the expression of SREBP-1, FAS, and ACC and upregulating CPT-1a expression; while the 2011 and 2020 Wuyi rock teas by moderating the gut microbiota dysbiosis, reshaping the gut microbiota, and promoting the growth of beneficial bacteria, especially Akkermansia. 2011 Wuyi rock tea was proven to be more effective in reducing body weight gain and liver oxidative stress than the others. Collectively, all three Wuyi rock teas of different years alleviated high-fat diet-induced obesity by regulating lipid metabolism and modulating gut microbiota, whereas the emphasis of their internal mechanism is different with different storage ages.
Subject(s)
Diet, High-Fat , Gastrointestinal Microbiome , Mice , Animals , Diet, High-Fat/adverse effects , Sterol Regulatory Element Binding Protein 1/genetics , Sterol Regulatory Element Binding Protein 1/metabolism , Lipid Metabolism , Tea/metabolism , Obesity/metabolism , Body Weight , Mice, Inbred C57BLABSTRACT
An important puzzle for tea consumers is which type of tea is effective in treating metabolic syndrome (MS). In this study, the effects of six types of tea extracts (TEs) on high-fat diet (HFD)-induced MS, as well as chemical components of six TEs, were investigated and compared. Each TE consisted of representative tea originated from different places in China to avoid one-sidedness of sampling. All six TEs were found to attenuate MS and ameliorate intestinal barrier function in HFD-fed rats. Further, white tea performed better in body weight control, while dark tea had more advantages in protecting intestinal barrier. Moreover, all six TEs alleviated the gut microbiota dysbiosis, which was manifested by decreased Firmicutes/Bacteroidetes ratio and enriched beneficial bacteria, such as Akkermansia, Bacteroides, and Bifidobacterium. Together, all six TEs attenuate HFD-induced MS although their efficiency varies, and this therapeutic effect is related to the modulation of gut microbiota.
Subject(s)
Gastrointestinal Microbiome , Metabolic Syndrome , Animals , Diet, High-Fat/adverse effects , Metabolic Syndrome/drug therapy , Plant Extracts/pharmacology , Plant Extracts/therapeutic use , Rats , TeaABSTRACT
Liquiritigenin (LQ) is a non-toxic dietary flavonoid with chemopreventive and anticancer properties. However, the mechanism of its antiangiogenesis remains unclear. Hypoxia-inducible factor-1α (HIF-1α) and its downstream target, vascular endothelial growth factor (VEGF), play a critical role in tumour angiogenesis and represent an attractive chemotherapeutic target. In this study, we investigated the effect of LQ on the molecular mechanism of angiogenesis. We found that LQ inhibited VEGF expression at both mRNA and protein levels. Liquiritigenin did not affect HIF-1α expression at the mRNA level, but it dramatically inhibited both serum- and mimicked hypoxic-induced HIF-1α protein accumulation in HeLa cells. Furthermore, we showed that LQ inhibited serum-induced expression of HIF-1α by reducing its stability and decreased the synthesis in a dose-dependent manner. Mechanistically, we demonstrated that LQ inhibited HIF-1α and VEGF expression involved in blocking the protein kinase B (PKB/Akt) signalling pathway, and the mechanisms correlated with dephosphorylation of the mammalian target of rapamycin (mTOR) and its effector ribosomal protein S6 kinase (p70S6K). In addition, LQ inhibited VEGF-induced formation of capillary-like structures in human umbilical vein endothelial cells (HUVEC). Taken together, our study provided valuable insights into the mechanism of antiangiogenic effect of LQ.