Abstract:In Korea, soy (Glycine max (L.) Merr.) leaves are eaten as a seasonal vegetable or pickled in soy sauce. Ethyl acetate extracts of soy leaves (EASL) are enriched in pterocarpans and have potent α-glucosidase inhibitory activity. This study investigated the molecular mechanisms underlying the anti-diabetic effect of EASL in C57BL/6J mice with high-fat diet (HFD)-induced type 2 diabetes. Mice were randomly divided into normal diet (ND), HFD (60 kcal% fat diet), EASL (HFD with 0.56% (wt/wt) EASL), and Pinitol (HFD with 0.15% (wt/wt) pinitol) groups. Weight gain and abdominal fat accumulation were significantly suppressed by EASL. Levels of plasma glucose, HbA1c, and insulin in the EASL group were significantly lower than those of the HFD group, and the pancreatic islet of the EASL group had greater size than those of the HFD group. EASL group OPEN ACCESSMolecules 2014, 19 18494 up-regulated neurogenin 3 (Ngn3), paired box 4 (Pax4), and v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA), which are markers of pancreatic cell development, as well as insulin receptor substrate 1 (IRS1), IRS2, and glucose transporter 4 (GLUT4), which are related to insulin sensitivity. Furthermore, EASL suppressed genes involved in hepatic gluconeogenesis and steatosis. These results suggest that EASL improves plasma glucose and insulin levels in mice with HDF-induced type 2 diabetes by regulating β-cell proliferation and insulin sensitivity.

These data suggest that the novel TCR-targeting LMP1 might allow the potential design of T-cell-based immunotherapeutic strategies against EBV-positive malignancies.

Yellow-soybean-leaf extract includes kaempferol glycosides and pheophorbides that reduce obesity and plasma glucose levels. This study researched the molecular mechanisms underlying the glucose-lowering effect of the extract of blacksoybean leaves (EBL), which mainly contains quercetin glycosides and isorhamnetin glycosides, in mice with high-fat-diet (HFD)-induced obesity and diabetes and in HepG2 cells. Twelve weeks of EBL supplementation decreased body weight and fasting glucose, glycated hemoglobin, insulin, triglyceride, and nonesterified fatty acid levels. Histological analyses manifested that EBL suppressed hepatic steatosis. Interestingly, EBL significantly improved plasma adiponectin levels and increased adiponectin-receptor-gene (AdipoR1 and AdipoR2) expression in the liver. EBL restored the effects of HFD on hepatic AMPactivated protein kinase (AMPK) and on the family of peroxisome proliferator-activated receptors (PPARα, PPARδ, and PPARγ), which are associated with fatty acid metabolism and are downstream of the adiponectin receptors. Hence, EBL effectively diminished hyperglycemia and hepatic steatosis through enhancing adiponectin-induced signaling and AMPK activation in the liver.

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