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. 2007 Feb 22;117(3):739–745. doi: 10.1172/JCI30400

Figure 4. PKCε ASO therapy improves hepatic insulin signaling and preserves insulin receptor kinase activity.

Figure 4

Insulin receptor (IR) tyrosine phosphorylation, IRS2 tyrosine phosphorylation, and AKT2 activity were assessed in the basal, fasted state, and after 20 minutes of hyperinsulinemic-euglycemic clamping. (A) Insulin receptor tyrosine phosphorylation. (B) IRS2 tyrosine phosphorylation. *P < 0.05 versus saline; †P < 0.05 versus control ASO. (C) AKT2 activity. †P < 0.05 versus control ASO. (D) Immunoprecipitation of the insulin receptor also precipitates PKCε and vice versa. (E) Incubation of active insulin receptor kinase with increasing molar ratios of PKCε results in a dose-dependent decrease in insulin receptor kinase activity. (F) Activity of lecithin-purified insulin receptor kinase from rats fed a normal low-fat diet and high-fat-fed (HFF) rats treated with saline, control ASO, and PKCε ASO. #P < 0.01 versus HFF/saline; ΧP < 0.001 versus HFF.