PMC:4277126 / 79223-82654
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4277126","sourcedb":"PMC","sourceid":"4277126","source_url":"http://www.ncbi.nlm.nih.gov/pmc/4277126","text":"Streptozotocin- or alloxan-induced diabetes\nLuo et al107 compared the hypoglycemic effects of LBF water decoction, crude polysaccharide extracts (crude LBPs), and purified polysaccharide fractions (LBPs) in alloxan-induced diabetic rabbits. All the three LBF extracts/fractions significantly reduced blood glucose levels in rabbits.107 The hypoglycemic effect of LBPs was more significant than those of water decoction and crude LBPs, but water and methanolic fruit extracts and crude polysaccharide extracts exhibited stronger antioxidant activity than purified polysaccharide fractions.\nZhao et al108 conducted an animal study to examine the hypoglycemic activity of LBPs in male Wistar rats with experimental diabetes. Rats were fed with HD for 3 weeks and administered intraperitoneal injection of 50 mg/kg streptozotocin to induce diabetes. Fasting plasma levels of glucose, lipids, and insulin were monitored. The content of glucose transporter type-4 (GLUT4) in gastrocnemius skeletal muscle was determined. Under anabolic condition, GLUT4 is the main carrier that transports blood glucose into muscle and adipose cells.111,112 In the nonstimulated state, GLUT4 is efficiently sequestered intracellularly. This retention prevents GLUT4 from reaching the cell surface and transporting glucose into muscle and fat cells when blood glucose levels are low.112 After a meal, when blood glucose levels rise, insulin is secreted by the pancreas, which triggers an intracellular signaling cascade, leading to the translocation of GLUT4 from intracellular compartments to the cell surface, resulting in glucose uptake and normalization of the blood glucose levels.111,112 Oral treatment of 10 mg/kg/day LBP for 3 weeks resulted in a significant decrease in the concentration of plasma triglyceride and weight in diabetic rats.108 Furthermore, LBPs markedly decreased the plasma cholesterol levels, fasting plasma insulin levels, and the postprandial glucose level at 30 minutes during oral glucose tolerance test and significantly increased the insulin sensitivity index in diabetic rats.108 Moreover, LBPs increased the level of GLUT4 in skeletal muscle under insulin stimulation. LBPs can alleviate abnormal glucose and lipid metabolism and ameliorate insulin resistance, and the mechanism may be involved in upregulation of GLUT4 and improved GLUT4 trafficking and intracellular insulin signaling.\nThe effect of oral LBP treatment on blood glucose, oxidative stress, and DNA damage was examined by Wu et al106 in male Wistar rats with experimental diabetes. Rats were fed with HD for 3 weeks and administered intraperitoneal injection of 50 mg/kg streptozotocin to induce diabetes. Oral administration of 10 mg/kg/day LBP for 4 weeks led to decreased levels of blood glucose.106 Serum MDA and NO levels were decreased by LBPs in fasting diabetic rats, and the serum level of SOD was increased by LBPs in diabetic rats.106 LBPs reduced cellular DNA damage in peripheral lymphocytes of the diabetic rats as determined by the single cell gel assay. These results suggest that LBPs can improve glucose metabolism via inhibition of oxidative stress in diabetes.\nLi17 reported that in streptozotocin-induced diabetic rats, treatment of 50–200 mg/kg LBP for 30 days significantly decreased blood glucose level and increased blood plasma insulin level. The hypoglycemic effects of LBPs are strongly related to their antioxidative 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