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Objective To study the antidiabetic effects and the underlying molecular mechanisms of Lycium barbarum polysaccharide(LBP) and its DEAE cellulose elution fraction LBP-IV in diabetic rats induced by high fat diet(HFD) and streptozotocin(STZ). Methods After ig administration of LBP-IV [50, 100, and 200 mg/(kg·d)] and LBP [100 mg/(kg·d)] once daily for consecutive 4 weeks to diabetic rats, the glucose and lipids in blood, m RNA expression of phosphoenolpyruvate carboxykinase(PEPCK), sterol regulatory element binding-protein-1c(SREBP-1c), and fatty acid synthase(FAS) in liver were determined. Results Ig administration of LBP and LBP-IV significantly decreased the levels of blood glucose, Hb A1 c, TC, TG, and LDL-C, as well as the hepatic m RNA expression of PEPCK, SREBP-1c, and FAS, whereas significantly increased the oral glucose tolerance of diabetic rats. Conclusion The findings suggest that the antidiabetic effects of LBP and LBP-IV are associated with the decreased hepatic m RNA expression of PEPCK, SREBP-1c, and FAS in HFD-STZ induced diabetic rats.
Objective To study the antidiabetic effects and the underlying molecular mechanisms of Lycium barbarum polysaccharide (LBP) and its DEAE cellulose elution fraction LBP-IV in diabetic rats induced by high fat diet (HFD) and streptozotocin (STZ). Methods After ig administration of LBP -IV [50, 100, and 200 mg / (kg · d)] and LBP [100 mg / (kg · d)] once daily for consecutive 4 weeks to diabetic rats, the glucose and lipids in blood, m RNA expression of Results Ig administration of LBP and LBP-IV significantly decreased the levels of blood glucose, Hb (PEPCK), sterol regulatory element binding-protein-1c (SREBP-1c), and fatty acid synthase (FAS) A1 c, TC, TG, and LDL-C, as well as the hepatic m RNA expression of PEPCK, SREBP-1c, and FAS, and a significantly increased the oral glucose tolerance of diabetic rats. Conclusion The findings suggest that the antidiabetic effects of LBP and LBP-IV are associated with the decreased hepatic m RNA exp ression of PEPCK, SREBP-1c, and FAS in HFD-STZ induced diabetic rats.