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. 2023 Mar 15;299(5):104611. doi: 10.1016/j.jbc.2023.104611

Figure 2.

Figure 2

Loss of cell surface heparan sulfate interactions during adipogenesis reduce glucose uptake. A, Ndst1−/− cells have a significantly reduced glucose uptake potential relative to WT adipocytes (two-way ANOVA, n = 2; one representative experiment out of 3). B, heparin treatment (100 μg/ml) reduces glucose uptake potential relative to WT adipocytes (two-way ANOVA, n = 2; one representative experiment out of 3). C, heparin treatment does not further reduce Ndst1−/− adipocytes ability to access glucose (n = 2, one representative experiment out of 3). D, primary adipocytes derived from murine subcutaneous white adipose tissue (sWAT) stromal vascular cells presented with reduced glucose uptake when co-incubated with heparin during adipogenesis (two-way ANOVA, n = 2). E, stimulation of mature adipocytes (day 6) with insulin (20 nM) leads to equal signaling transduction via AKT phosphorylation regardless of HSPG interaction modulation (n = 3). F, glucose transporter 4 protein (GLUT4) is similarly expressed at the cell surface of WT and HSPG inhibited adipocytes (n = 3). Data are presented as mean ± SD, ∗p < 0.05; #p <0.05 relative to WT with no insulin stimulation. Hep, Heparin; HSPG, HS proteoglycan; Ndst1, N-deacetylase-N-sulfotransferase 1.