Research Paper Volume 12, Issue 17 pp 17150—17166

Figure 5. LNK deficiency altered insulin signaling and the expression of GLUT-4 protein in adipose tissues in obesity-induced insulin resistance model. (A, B) Representative images of immunohistochemical stain of GLUT4 in adipose tissue were shown (HFD: LNK^-/- n=7, WT n=6; NCD: LNK^-/- n=6, WT n=7. Five images were quantified per mouse). (C, D) LNK impairs IRS1 serine phosphorylation, PI3K tyrosine phosphorylation, Akt serine phosphorylation and AS160 threonine phosphorylation as shown by WB in HFD-fed mice visceral adipose tissue (LNK^-/- n=7, WT n=6 with three replicates. Representative images were shown). (E, F) GLUT4 expression and IRS1 serine phosphorylation, PI3K tyrosine phosphorylation, Akt serine phosphorylation and AS160 threonine phosphorylation as shown by WB in NCD-fed mice adipose tissue (LNK^-/- n=6, WT n=7 with three replicates. Representative images were shown). (G) LNK deficiency improves glucose uptake in primary adipocyte from mice after HFD feeding for 16 weeks (n=6 per group). The primary adipocytes were differentiated into mature adipocytes and were then stimulated by LY294002 (50 μM) and insulin (10 μM) for 30 min or insulin (10 μM) for 30 min alone. Scale bars: 100 μm. Data were shown as mean ± SD. Statistical analysis was performed by ANOVA (B and G) and Student’s t-test (D and F). *p < 0.05, **p < 0.01, ***p < 0.001.