1,2,3,4,6 penta-O-galloyl-?-D-glucose ameliorates high-fat diet-induced nonalcoholic fatty liver disease and maintains the expression of genes involved in lipid homeostasis in mice - 28/08/20
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Graphical abstract |
Highlights |
• | HFD consumption alteres the expression of genes involved in lipid metabolism. |
• | PGG reduces HFD-mediated body weight gain and hepatic steatosis. |
• | PGG reverses HDF-induced alterations in hepatic lipid metabolic gene expression. |
• | PGG, a well tolerated natural product, holds the potential for NAFLD treatment. |
Abstract |
Non-alcoholic fatty liver disease (NAFLD) is currently the most frequently occurring liver disorder in the world. However, a specific drug for the treatment of patients with NAFLD is not available. Therefore, the discovery of novel compounds for the treatment of NAFLD and elucidation of the underlying mechanisms of therapeutic drugs that can be used to treat this disease are urgently needed. 1,2,3,4,6 penta-O-galloyl-β-d-glucose (PGG) is known to exert anti-inflammatory, antidiabetic, and hepatoprotective effects. However, little is known about the therapeutic potential of PGG in NAFLD. In this study, we investigated the effects of PGG on a high-fat diet (HFD)-induced mouse model of NAFLD. PGG was co-administered along with an HFD to C57BL/6 mice. After eight weeks of treatment, serum biochemistry, liver steatosis, and lipid metabolism-related genes were examined. The results showed that PGG treatment significantly reduced HFD-induced gain in body weight, liver steatosis, and leukocyte infiltration in a dose-dependent manner. Furthermore, PGG treatment markedly reduced serum triglyceride and glucose levels in HFD mice. Moreover, alterations in the mRNA expression of genes involved in lipid metabolism, including Hmgcr, Acc1, Abca1, Mttp, and Cd36, observed in the livers of HFD-treated mice were significantly reversed by PGG treatment. PGG significantly reduced HFD-induced protein expression of CD36, which is associated with fatty acid uptake, insulin resistance, hyperinsulinemia, and increased hepatic steatosis, in the liver of HFD mice. These results suggest that PGG inhibits HFD-induced hepatic steatosis and reverses HFD-induced alterations of gene expression in lipid metabolism. PGG has been shown to be well tolerated; therefore, it has potential uses in NAFLD treatment.
El texto completo de este artículo está disponible en PDF.Abbreviations : PGG, HFD, ND, HFD + PGG 25mpk, HFD + PGG 300mpk, Glu, TC, TG, HDLC, ALT, Cd36, Abca1, Acc1, Cd11c, Hmgcr, Cyp7a1, Mttp
Keywords : PGG, High-Fat diet, NAFLD, Hepatic lipid metabolism, Cd36
Esquema
Vol 129
Artículo 110348- septembre 2020 Regresar al númeroBienvenido a EM-consulte, la referencia de los profesionales de la salud.
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