Figure 6. Deletion of liver Raptor attenuates the role of the DOCK5 deficiency on gluconeogenesis and insulin signaling in vivo and vitro .

Male Raptor^flox/flox mice (8 weeks) were fed a HFD for 12 weeks and injected with AAV8‐GFP or AAV8‐shDOCK5 or AAV8‐shDOCK5+ AAV8‐Cre via the tail vein.

• A
  The mRNA and protein expression of PEPCK and G6Pase in the liver.
• B
  Total and phosphorylated InsR, IRS‐1^Ser1101, and Akt in the liver.
• C
  The levels of DOCK5 and Raptor protein, and total and phosphorylated mTOR and S6K1 in the liver.
• D–F
  MPHs from Raptor^flox/flox mice were infected with Ad‐GFP or Ad‐shDOCK5 or Ad‐shDOCK5+ Ad‐Cre. The lysates were immunoblotted with the indicated antibodies or β‐actin. (D) The expression of PEPCK and G6Pase mRNA and protein. (E) Total and phosphorylated InsR, IRS‐1^Ser1101, and Akt. (F) The levels of DOCK5 and Raptor protein, and total and phosphorylated mTOR and S6K1.

Data information: Data are means ± SEM (n = 2 mice for each group or 1 cell cultures). P‐values were determined with Student's t‐test, **P < 0.01 versus GFP group; ^# P < 0.05, ^## P < 0.01 versus shDOCK5 group.