The role of 1, 25-dihydroxyvitamin D3 in palmitic acid induced insulin resistance in human umbilical vein endothelial cells
WANG Liang1, DONG Sisi1, CHEN Jing2, WU Xiaoying1, RUAN Luya1, PAN Youjin1, HU Yunliang3, ZHENG Chao1
1.Department of Endocrinology, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325027, China; 2.Department of Clinical Laboratory, Women and Children’s Health Care Hospital of Linyi, Linyi 276000, China; 3.Department of Clinical Laboratory, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325027, China
WANG Liang,DONG Sisi,CHEN Jing, et al. The role of 1, 25-dihydroxyvitamin D3 in palmitic acid induced insulin resistance in human umbilical vein endothelial cells[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2020, 50(5): 377-381.
Abstract： Objective: To investigate the effect of 1, 25-dihydroxyvitamin D3 [1, 25(OH)2D3] on the insulin resistance of human umbilical vein endothelial cells (HUVECs) induced by palmitic acid (PA) and its possible mechanism. Methods: HUVECs were cultured in DMEM medium containing (0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9 mmol/L) PA to establish insulin resistance endothelial cell model. 0, 0.01, 0.1, 1, 10, 100 nmol/L 1, 25(OH)2D3 intervention, nitrate/nitrite fluorescence kit to determine the content of NO, Western blot to determine the expression of pAkt and penos protein. The expression of VDR and ET-1 was detected by qPCR. Results: after HUVECs were cultured with 0.6 mmol/L PA for 18 hours, the glucose concentration in the culture medium was significantly lower than that in the control group, the cell viability was reduced, and the endothelial cell model of insulin resistance was established. The NO content of HUVECs in PA group was lower than that in control group (P<0.05). After the intervention of 1 nmol/L 1, 25(OH)2D3 on insulin resistant endothelial cells, the protein expression of peNOS and pAkt increased significantly (P<0.05), and the mRNA expression of ET1 decreased significantly (P<0.05). Conclusion: 1, 25(OH)2D3 can increase the expression of peNOS and pAkt, increase the production of NO and decrease the expression of ET-1, which may have a protective effect on insulin resistant vascular endothelial cells.
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