Figure 6. Loss of miR‐183 and miR‐96 protects mice from diet‐induced obesity and glucose intolerance.
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ARepresentative photographs of WT and DKO mice after HFD feeding for 2 months. Scale bar: 1 cm.
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B, CBody 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).
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DConcentration 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).
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ERelative mRNA expression of FoxO1, PDK4, and ATGL in GAS muscles of WT and DKO mice fed with HFD for 2 months (n = 5).
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FWestern blot analysis of FoxO1, PDK4, p‐PDHA1, PDHA1, and ATGL in GAS muscles of WT and DKO mice fed with HFD for 2 months.
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G, HRelative 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).
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IFasting blood glucose levels (left) and random blood glucose levels (right) in WT and DKO mice after HFD feeding (n = 10–11).
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JGlucose 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.