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Xanthohumol Restores Hepatic Glucolipid Metabolism Balance in Type 1 Diabetic Wistar Rats.
Journal of Agricultural and Food Chemistry 2017 August 31
Diabetes exhibits increased inflammation, angiogenesis, and apoptosis, three processes attenuated by xanthohumol (XN). Herein, we evaluate the effect of XN-enriched stout beer consumption in hepatic glucolipid metabolism imbalance seen in type 1 diabetes (T1D). Five groups of Wistar rats were established: streptozotocin-induced diabetic rats drinking water, treated with 5% ethanol, stout beer, and stout beer supplemented with 10 mg of XN/L and healthy rats drinking water. Hepatic periodic acid-Schiff, reticulin, sirius red, and oil red O histological staining was performed. Lipogenic enzymes and glucose transporter 2 (GLUT2) expression was evaluated by western blotting. Increased fibrosis in T1D animals was significantly decreased to control levels by XN (3.85 ± 0.38 in T1D-beer versus 1.78 ± 0.27 in controls, p < 0.05; 2.27 ± 0.69 in T1D-beer + XN versus 1.78 ± 0.27 in controls, p > 0.05). XN reduced T1D hepatic reticulin staining (9.74 ± 3.78 in T1D-beer, p < 0.05 versus control) to healthy levels (4.45 ± 1.05 in T1D-beer + XN versus 4.60 ± 0.20 in healthy controls, p > 0.05). XN consumption interfered with the T1D liver catabolic state, reversing glycogen depletion (22.09 ± 7.70 in T1D-beer + XN versus 4.68 ± 4.84 in T1D-beer, p < 0.05) and GLUT2 upregulation (1.71 ± 0.46 in T1D-beer + XN versus 2.13 ± 0.34 in T1D-beer, p < 0.05) and enhancing lipogenesis (1.19 ± 0.11 in T1D-beer + XN versus 1.96 ± 0.36 in T1D, p < 0.05 for acetyl-CoA carboxylase; 1.10 ± 0.04 in T1D-beer + XN versus 0.44 ± 0.31 in T1D, p < 0.05 for fatty acid synthase). These findings reveal that XN can be a therapeutic agent against liver metabolic changes in T1D, playing a possible role in the insulin receptor pathways.
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