Xanthohumol Restores Hepatic Glucolipid Metabolism Balance in Type 1 Diabetic Wistar Rats.

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.