The role of impaired adipogenesis in insulin resistance among non-obese individuals

Figures

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  FIGURE 1. Comparison of the proliferation percentage (A) and adipogenic capacity (B) between thigh and buccal fat tissue. (C) Immunofluorescence imaging: Nuclei stained with DAPI (blue) and lipid droplets visualized using LipidTOX (red).

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  FIGURE 2. Proliferation of preadipocytes, pooled from both depots, from insulin sensitive (IS) and insulin resistant (IR) individuals, and effect of TNF-α/metformin + insulin on preadipocyte proliferation percent in both groups. Data are presented as mean ± SEM; Differences between IS and IR were tested by independent-sample t-test; *p < 0.05. The proliferation percentage was normalized to untreated cells.

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  FIGURE 3. (a) Adipogenic capacity of differentiated preadipocytes pooled from both depots derived from IS and IR lean/overweight individuals. (b,c) Effect of TNF-α/metformin + insulin on preadipocyte differentiation. (d) Immunofluorescence imaging: Nuclei stained with DAPI (blue) and lipid droplets visualized using LipidTOX (red). Data are presented as mean ± SEM; Differences between IS and IR were tested by independent-sample t-test; *p < 0.05.

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  FIGURE 4. Secreted levels of IL-6, IL-8, IL-1RA, IL-1 beta, IL-10, IL-22, MCP-1 were compared between IS and IR-derived differentiated adipocytes pooled from both depots. Cytokine levels were normalized by dividing cytokine levels to the cell number. Data are presented as mean ± SEM; Differences between IS and IR were tested by independent-sample t-test; *p < 0.05.

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  FIGURE 5. Level of phosphorylated IRS-1, 70S6K, GSK3α/β, BAD, PTEN, AKT, S6RP, and mTOR were measured in differentiating adipocytes derived from insulin sensitive (IS) and insulin resistant (IR) individuals pooled from both depots. Data are presented as Mean ± SEM. *P < 0.05, Independent and paired samples t-test.

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  FIGURE 6. Level of secreted IL-6 and IL-8 in IS and IR differentiated preadipocytes pooled from both depots and derived from lean/overweight individuals and after treatment with TNF-α or metformin. Cytokine levels were normalized by dividing cytokine levels to the cell number and then normalized to the mean of untreated group. Data are presented as mean fold change ±SEM; Differences were tested by ANOVA/Kruskal Wallis followed by post hocFriedman/Dunnett test; *p < 0.05, **p < 0.01.

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  FIGURE 7. Insulin signaling pathway of differentiated adipocytes pooled from both depots and derived from IS and IR lean/overweight individuals after treatment with TNF-α or metformin + insulin. Fold changes in response to TNF-α or metformin treatment are shown. Data are presented as mean ± SEM; Differences between IS and IR were tested by independent-sample t-test; *p < 0.05.