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. 2019 Dec 29;21(2):e49473. doi: 10.15252/embr.201949473

Figure 5. Adult onset, liver‐specific deletion of Raptor attenuates insulin resistance (IR) and glucose intolerance induced by DOCK5 knockdown in HFD‐fed mice.

Figure 5

Eight‐week‐old male Raptorflox/flox mice (Raptorflox/flox Cre+) were fed a HFD for 12 weeks and injected with AAV8‐shDOCK5 ± AAV8‐Cre or AAV8‐GFP (at a dose of 3 × 1011 vg/200 μl/mouse) via the tail vein 14 days prior to the in vivo study.
  1. Schematic representation of the strategy used to produce liver‐specific Raptor knockout (L‐Raptor KO) mice.
  2. Fasting and fed blood glucose 14 days post‐infection.
  3. Blood glucose levels and AUC during glucose tolerance tests.
  4. Blood glucose levels and AUC during insulin tolerance tests.
  5. Glucose infusion rate (GIR).
  6. Glucose disposal rate (GDR).
  7. Hepatic glucose production (HGP).
  8. Percentage of suppression of hepatic glucose production (HGP).
Data information: AUC, the area under the curve for glucose. Data are means ± SEM (n = 5–6 mice for each group). P‐values were determined with t‐test, **< 0.01 versus GFP group; # < 0.05, ## < 0.01 versus shDOCK5 group.