Divergent Regulation of Hepatic Glucose and Lipid Metabolism by Phosphoinositide 3-Kinase via Akt and PKCλ/ζ

Abstract

(Cell Metabolism 3, 343–353; May 2006) Due to an error in assembling the final figures of the manuscript, the middle panel in the top half of Figure 1D, representing PIP3 immunostaining for insulin-stimulated L-p85αKO mice, was accidentally duplicated and inserted in the top left corner in place of the panel showing PIP3 staining for the control insulin-stimulated FLOX mice. In the new version of Figure 1D, we have replaced the latter panel with a correct version of the PIP3 staining in the insulin-stimulated FLOX mice. The authors apologize for any confusion that this error may have caused. Divergent regulation of hepatic glucose and lipid metabolism by phosphoinositide 3-kinase via Akt and PKCλ/ζTaniguchi et al.Cell MetabolismMay, 2006In BriefAlthough the class IA phosphoinositide 3-kinase (PI3K) pathway is central to the metabolic actions of insulin, its mechanism of action is not well understood. To identify the role of the PI3K pathway in insulin regulation of hepatic function, we ablated the expression of both major regulatory subunits of PI3K by crossing mice lacking Pik3r1 in liver with Pik3r2 null mice, creating liver-specific double knockout mice (L-p85DKO). L-p85DKO mice failed to activate PI3K or generate PIP3 upon insulin stimulation or activate its two major effectors, Akt and PKCλ/ξ. Full-Text PDF Open Archive