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. 2021 Aug 6;22(9):e52247. doi: 10.15252/embr.202052247

Figure 6. Loss of miR‐183 and miR‐96 protects mice from diet‐induced obesity and glucose intolerance.

Figure 6

  • A
    Representative photographs of WT and DKO mice after HFD feeding for 2 months. Scale bar: 1 cm.
  • B, C
    Body weight, body weight gain after HFD feeding (B) and tissue weight of iWAT and eWAT (C) of WT and DKO mice fed with HFD for 2 months (n = 10–11).
  • D
    Concentration of serum triglyceride (TAG) (left) and non‐esterified fatty acid (NEFA) (right) in WT and DKO mice after HFD feeding for 2 months (n = 5).
  • E
    Relative mRNA expression of FoxO1, PDK4, and ATGL in GAS muscles of WT and DKO mice fed with HFD for 2 months (n = 5).
  • F
    Western blot analysis of FoxO1, PDK4, p‐PDHA1, PDHA1, and ATGL in GAS muscles of WT and DKO mice fed with HFD for 2 months.
  • G, H
    Relative mRNA expression of PGC1α, PLIN5 (G), and HSL (H) in GAS muscles of WT and DKO mice fed with HFD for 2 months (n = 5).
  • I
    Fasting blood glucose levels (left) and random blood glucose levels (right) in WT and DKO mice after HFD feeding (n = 10–11).
  • J
    Glucose tolerance test (GTT) and area under the curve (AUC) data for GTT in WT and DKO mice after HFD feeding (n = 10–11).

Data information: Means ± SEM are shown for all panels. *P < 0.05 versus control; **P < 0.01 versus control; ***P < 0.001 versus control (Student’s t‐test). All experiments were performed at least three times, and representative data are shown.

Source data are available online for this figure.