LBP-4a improves insulin resistance via translocation and activation of GLUT4 in OLETF rats

• Published in: Food & function 2014-04, Vol.5 (4), p.811-82
• Main Authors: Zhao, Rui, Qiu, Bing, Li, Qingwang, Zhang, Tao, Zhao, Hui, Chen, Zhibao, Cai, Yaping, Ruan, Hongsheng, Ge, Wenzhong, Zheng, Xiaoliang
• Format: Article
• Language: English
• Subjects: Adipocytes - drug effects; Adipocytes - metabolism; Animals; Diabetes Mellitus, Type 2 - drug therapy; Diabetes Mellitus, Type 2 - metabolism; Drugs, Chinese Herbal - administration & dosage; Drugs, Chinese Herbal - isolation & purification; Glucose Transporter Type 4 - metabolism; Humans; Insulin Resistance; Lycium - chemistry; Male; Protein Transport; Rats; Rats, Inbred OLETF
• ISSN: 2042-6496; 2042-650X
• DOI: 10.1039/c3fo60602c

Lycium barbarum polysaccharide (LBP) has been shown to ameliorate insulin resistance, but the identification of compounds from LBP and the mechanisms have not been clarified. In this study, LBP-4a was purified from Lycium barbarum by DEAE cellulose and Sephadex G-100 column chromatography, and the effects of LBP-4a on insulin resistance were investigated. The results indicated that LBP-4a caused translocation of the glucose transporter isoform 4 (GLUT4) to the cell surface, which in turn stimulated glucose uptake, and the effect was sensitive to wortmannin, an inhibitor of phosphoinositol 3-kinase (PI3-K), and SB203580, an inhibitor of p38 mitogen activated protein kinase (p38 MAPK (α, β)). Furthermore, the effects of LBP-4a on p38 MAPK activities were abrogated by pretreatment of rat adipocytes using SB203580. In summary, LBP-4a improved insulin resistance via translocation and activation of GLUT4 in OLETF rats, and the activation of PI3-K and p38 MAPK contributed to these effects. Stimulation of glucose transport by LBP-4a consists of two events: PI3-Kinase-dependent translocation and p38 MAPK-dependent stimulation of the intrinsic activity of GLUT4.