Fig 1: miR-210-3p inhibition rescue DIO mice from glucose intolerance and insulin resistance.A, schematic diagram showing control inhibitor LNA or miR-210 inhibitor LNA administration in the visceral adipose tissue of 12 weeks HFD mice. B, H&E staining of VAT section of control inhibitor LNA or miR-210 inhibitor LNA-treated HFD mice. Scale bar represents 200 μm. C and D, immunofluorescence imaging (C) and fluorescent intensity quantification analyses (D) of GLUT4 (green), and FABP4 (red) in the VAT section of control inhibitor LNA and miR-210 inhibitor administered HFD mice, (n = 4), ∗p < 0.05, ∗∗∗p < 0.001, ns = not significant. Scale bar represents 200 μm. E and F, GLUT4 mRNA expression analyses (E) and western blotting (F) analyses in the visceral adipose tissue (VAT) of control inhibitor LNA or miR-210 inhibitor LNA-treated HFD mice, (n = 4), ∗∗p < 0.01 by Student’s t test. G, miR-210-3p expression in the visceral adipose tissue of control inhibitor LNA or miR-210 inhibitor LNA mice (n = 4). H, miR-210-3p expression in the ATM-derived EVs isolated from the VAT of control inhibitor or miR-210-3p inhibitor LNA–administered HFD mice (n = 4), ∗∗∗∗p < 0.0001 by Student’s t test. I, miR-210-3p expression in the EVs isolated from the serum of control inhibitor LNA and miR-210-3p inhibitor LNA–administered HFD mice, (n = 4), ∗p < 0.05 by Student’s t test. J–L, glucose tolerance test (GTT) (J), insulin tolerance test (ITT) (K), and HOMA of insulin resistance (HOMA-IR) (L) analyses were performed in HFD mice injected with control inhibitor LNA or miR-210 inhibitor LNA (n = 4). ∗p < 0.05, ∗∗p < 0.01, ns= not significant by two-way ANOVA and ∗p < 0.05 by student’s t test. Data are expressed as means ± SD. ATM, adipose tissue macrophage; EV, extracellular vesicle; HOMA-IR, homeostatic model assessment for insulin resistance; LNA, locked nucleic acid.