FOOD SCIENCE ›› 2021, Vol. 42 ›› Issue (17): 170-176.doi: 10.7506/spkx1002-6630-20200824-310

• Nutrition & Hygiene • Previous Articles     Next Articles

Effect of Sweet Corncob Polysaccharide on Glucose Metabolism in Insulin Resistant HepG2 Cells

MA Yongqiang, HAN Ye, ZHANG Kai, WANG Xin, WANG Zhili   

  1. (1. College of Food Engineering, Harbin University of Commerce, Harbin 150076, China; 2. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150080, China)
  • Published:2021-09-29

Abstract: Objective: To investigate the effect of a polysaccharide isolated from sweet corncob (designated SCP-80-I) on glucose metabolism in insulin resistant (IR) HepG2 cells. Methods: The optimal conditions for inducing IR in HepG2 cells were established and applied. The IR cells were incubated for 24 h in the presence of different concentrations of SCP-80-I (50, 100, 200 and 400 μg/mL) to evaluate the effect of the polysaccharide on glucose uptake as well as assess the cytotoxicity by methyl thiazolyl tetrazolium (MTT) assay. Biomarkers of oxidative stress, including superoxide dismutase (SOD) activity, malondialdehyde (MDA) and reactive oxygen species (ROS) levels, were measured. In addition, intracellular glycogen accumulation and the activities of rate-limiting enzymes for glycolysis (hexokinase, HK; pyruvate kinase, PK) were determined. Results: Treatment with 1 × 10-6 mol/L insulin for 24 hours was the optimal condition for the formation of IR HepG2 cells. SCP-80-I significantly increased glucose uptake in IR HepG2 cells (P < 0.01), and the cell viability increased first and then decreased with increasing SCP-80-I concentration. The contents of MDA and ROS decreased, and the activities of SOD, HK and PK and intracellular glycogen contents increased in the SCP-80-I intervention group (200 μg/mL) compared with the model control group (P < 0.01). Conclusion: The hypoglycemic effect of SCP-80-I may be related to the alleviation of oxidative stress-induced liver injury and the improvement of glucose metabolism in IR liver cells.

Key words: diabetes mellitus; HepG2 cells; insulin resistance; sweet corncob polysaccharide; glucose metabolism

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