Li Xiaopeng, Sui Yong, Wu Qian, Xie Bijun, Sun Zhida
College of Food Science and Technology, Huazhong Agricultural University , Wuhan 430070, China.
Institute for Farm Products Processing and Nuclear-Agricultural Technology, Hubei Academy of Agricultural Science , Wuhan 430064, China.
J Agric Food Chem. 2017 May 17;65(19):3801-3810. doi: 10.1021/acs.jafc.7b00233. Epub 2017 May 8.
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.
本研究调查了莲房原花青素低聚物（LSOPC）和合生元（双歧杆菌Bb-12和低聚木糖）对高脂和链脲佐菌素（STZ）诱导的糖尿病的保护作用。给予LSOPC或合生元对正常小鼠的血糖没有影响。用LSOPC治疗12周可显著降低血糖、游离脂肪酸（FFA）、内毒素和糖化血红蛋白（GHbA1c），并改善葡萄糖稳态、脂质代谢和胰岛素水平。此外，给予LSOPC可显著逆转肝脏、骨骼肌和白色脂肪组织（WAT）中mTOR和p66的增加。LSOPC显著增加肝脏、骨骼肌和WAT中的葡萄糖摄取和糖酵解，同时改善棕色脂肪组织（BAT）中的产热，并抑制肝脏中的糖异生和脂肪生成。此外，合生元增强了LSOPC的改善作用。这些发现表明，LSOPC和合生元可能通过p66-mTOR信号通路调节外周靶组织中的葡萄糖代谢。
