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This study investigated the protective role of lotus seedpod oligomeric procyanidins (LSOPC) and synbiotics (Bifidobacterium Bb-12 and xylo-oligosaccharide) against high fat and streptozotocin (STZ)-induced diabetes. Administration of LSOPC or synbiotics had no effect on blood glucose in normal mice. Treatments with LSOPC for 12 weeks markedly reduced blood glucose, FFA, endotoxin, and GHbA1c and improved glucose homeostasis, lipid metabolism, and insulin levels. In addition, administration of LSOPC significantly reversed the increase of mTOR and p66 in liver, skeletal muscle, and white adipose tissue (WAT). LSOPC significantly increased glucose uptake and glycolysis in liver, skeletal muscle, and WAT while improving heat generation in brown adipose tissue (BAT) and inhibiting gluconeogenesis and lipogenesis in liver. Furthermore, synbiotics strengthened the improving effect of LSOPC. These findings demonstrated that LSOPC and synbiotics may regulate glucose disposal in peripheral target tissues through the p66-mTOR signaling pathway.

This study investigated the protective properties of lotus seedpod oligomeric procyanidins (LSOPC) against nonalcoholic fatty liver disease (NAFLD) and its underlying mechanism. Sprague-Dawley (SD) male rats were fed a basic diet, a high-fat diet (HFD), or HFD plus 0.2 or 0.5% (w/w) LSOPC for 12 weeks. Administration of LSOPC markedly reduced serum and hepatic biochemical parameters and protein expression of advanced glycation endproducts (AGEs). Additionally, 0.5% (w/w) LSOPC treatment remarkably reversed the increasing tendency of receptor of advanced glycation endproduct (RAGE) to normal level. Furthermore, dietary LSOPC significantly decreased the protein levels of mitogen-activated protein kinases (MAPK) and nuclear factor-kappa B (NF-κB) and down-regulated genes involved in pro-inflammatory cytokines and adhesion molecules. Taken together, these findings demonstrate that LSOPC may protect obese rats with long-term HFD-induced NAFLD against RAGE-MAPK-NF-κB signaling suppression.