Research on Effects of Arsenic on Glucose Transportation of Insulin Sensitivity
|Course||Human Anatomy and Embryology|
|Keywords||3T3-L1 preadipocytes Differentiation Arsenic trioxide Insulin resistance Mechanism|
Objective: different concentrations of arsenic (NaAsO2) insulin-dependent glucose transporter, and to further explore its possible mechanism. Methods: (1) induction of 3T3-L1 preadipocytes; Oil Red O staining of mature adipocytes: extract oil red O dye, in the spectrophotometer at a wavelength of 490nm detection of absorbance (A) Quantitative analysis of arsenic in the 3T3-L1 ago adipocyte differentiation; (2) the MTT detect arsenic proliferation of 3T3-L1 preadipocytes and adipocytes and vitality; (3) detection of arsenic on glucose oxidase 3T3-L1 fat cell glucose consumption ; (4) immunofluorescence cytochemistry assay arsenic 3T3-L1 fat cells, glucose transporter 4 (GLUT4) translocation; (5) Western-blot detection of arsenic on 3T3-L1 fat cells GLUT4 and NF.kBp65 expression; (6) ELISA detection of arsenic on the content of 3T3-L1 fat cells Gang sub-IL-6, IL-8 and TNF-a expression. Results: (1) 3T3-L1 preadipocytes were fibroblast-like adherent growth, induction of differentiation into mature adipocytes after oil red O staining, the results show that red lipid droplets, identified by fat cells. Spectrophotometer ended often groups and arsenic group absorbance values, arsenic group oil red O absorbance values ??(0.34 ± 0.05) was significantly lower than the normal group (0.78 ± 0.13), the difference between the two was statistically significant (p lt; 0.05); (2) different concentrations of AS203 3T3-L1 preadipocytes and adipocytes proliferation and activity of students K: results of low concentrations of arsenic (5 micromol / L or less) 3T3.L1 proliferation of preadipocytes performance to promote the role of On the contrary, above this concentration inhibits cell proliferation; different concentrations of arsenic on the differentiation of 3T3-Ll preadipocytes was restrained, and compared to the normal group, the difference was statistically significant (p <; 0.051, and showed a certain amount of activity relationship (3) the role of the different concentrations of arsenic (of 1,5,10,15,20 mol / L) in 3T3-L1 fat cells inhibited adipocyte glucose consumption for 48h glucose consumption were 4.57 ± 0.72,2.99 ± 0.64 , 2.32 ± 0.53,2.00 ± 0.66,1.56 ± 0.29, and were lower than the normal group (p LT; 0.05), glucose consumption were reduced with the increase of the concentration of arsenic (P lt; 0.05). 1μmol / L insulin stimulation, stained arsenic group 3T3-L1 fat cells compared to the consumption of glucose and insulin group was statistically significant (P lt; 0.01) (4) Lee ended compared to the normal group, arsenic exposure group 3T3-L1 fat cells the GLUT4 translocation block, in the case of insulin-stimulated Bu dye arsenic group GLUT4 in fluorescent particles on the membrane was significantly lower than the insulin group (P lt; 0.01). (5) Arsenic inhibition of the expression of GLUT4 protein (P lt; 0.05) and promote of nuclear factor NF.kBp65 the expression (p lt; 0.01): (6) IL-6, IL-8 and TNF-alpha expression with the increase of the concentration and effect of arsenic (24, 48 72h) extension increased (p lt; 0.05), and dose-dependent manner. conclusions: (1) the success of 3T3-L1 preadipocytes induced differentiation of 3T3-L1 fat cells; (2) in 3T3-L1 fat cells Low concentrations of arsenic (5 micromol / L or less) (3) Arsenic inhibition of 3T3-L1 preadipocytes proliferation, high concentrations of arsenic can contribute to inhibit the proliferation of 3T3-L1 preadipocytes differentiation; different concentrations of arsenic dampen demand. fat cells consume glucose and GLUT4 translocation and expression; (4) arsenic reduced sensitivity to insulin induced insulin resistance, and its molecular mechanism may be provided with the nuclear NF-kappa B, IL-6, IL-8 and TNF- associated with a high expression of.