This study evaluated the protective role of litchi pericarp oligomeric procyanidins (LPOPC) and synbiotics (Bifidobacterium Bb-12 and xylo-oligosaccharide) against high fat and streptozotocin (STZ)-induced diabetes. LPOPC or synbiotics have no effect on blood glucose in normal mice. Treatments with LPOPC for 12 weeks significantly reduced blood glucose, FFA, endotoxin, GHbA1c and improved glucose homeostasis, lipid metabolism and insulin level. LPOPC also attenuated hyperglycemia-induced oxidative stress in serum, liver. In addition, administration of LPOPC remarkably reversed the increase of mTOR and p66^Shc in liver, skeletal muscle and white adipose tissue (WAT). LPOPC dramatically increased glucose uptake and glycolysis in liver, skeletal muscle and WAT, while inhibiting gluconeogenesis and lipogenesis in liver and improving heat generation in brown adipose tissue (BAT). Furthermore, synbiotics strengthened the improving effect of LPOPC. These findings demonstrated that LPOPC and synbiotics may regulate glucose disposal in peripheral target tissues through p66^Shc-mTOR signaling pathway.

这项研究评估了荔枝果皮寡聚原花青素（LPOPC）和合生元（双歧杆菌Bb-12和木糖寡糖）对高脂和链脲佐菌素（STZ）诱导的糖尿病的保护作用。LPOPC或合生素对正常小鼠的血糖没有影响。LPOPC治疗12周可显着降低血糖，FFA，内毒素，GHbA1c，并改善葡萄糖稳态，脂质代谢和胰岛素水平。LPOPC还减轻了高血糖引起的血清，肝脏中的氧化应激。此外，LPOPC的给药显着逆转了mTOR和p66 ^Shc的增加在肝脏，骨骼肌和白色脂肪组织（WAT）中。LPOPC显着增加了肝脏，骨骼肌和WAT中的葡萄糖摄取和糖酵解，同时抑制了肝脏中的糖异生和脂肪生成，并改善了棕色脂肪组织（BAT）的热量生成。此外，合生元增强了LPOPC的改善作用。这些发现表明，LPOPC和合生元可能通过p66 ^Shc -mTOR信号通路调节外周靶组织中的葡萄糖处置。