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Aim To explore the effects of corilagin on non-alcoholic fatty liver disease induced by high-fat and high-sugar diet in mice via regulating AMPK-autophagy signaling. Methods Healthy 8-week-old male C57BL/6J mice were randomly divided into control group, model group and corilagin group. The mice of model group and corilagin group were fed with a high-fat and high-sugar diet for four weeks at the age of eight weeks. The corilagin group mice were also intraperitoneally injected with corilagin (20 mg • k g
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Aim To investigate the effect of orientin on proliferation and differentiation of 3T3-L1 pre-adipocytes and on insulin resistance(IR) in 3T3-L1 adipocytes and the possible mechanisms.Methods MTT assay and oil red O staining were applied to investigate the proliferation and the differentiation of 3T3-L1 pre-adipocytes, respectively.The intracellular triglyceride(TG) contents were detected by enzymatic analysis.IR model was induced with dexamethasone.A fluorescent glucose analogue, 2-NBDG, was used to measure the rate of glucose uptake.Western blot was used to detect the protein level of GLUT4 and phosphorylation of AMPK and ACC.The GLUT4 translocation was measured by fluorescent-immunohistochemistry.Results Orientin decreased the formation of lipid droplets and intracellular TG contents(P<0.01) in a concentration-dependent manner(P<0.05), but it had no obvious effects on the cell vitality.Under the IR state, orientin significantly increased 3T3-L1 adipocytes glucose uptake(P<0.05).Meanwhile, orientin up-regulated the protein expression of p-AMPK, p-ACC, and enhanced GLUT4 translocation and its expression.Conclusion Orientin can effectively inhibit the differentiation of 3T3-L1 pre-adipocytes and increase insulin sensitivity due to the activation of AMPK/GLUT4 signal pathway.