Hyperinsulinemia, glucose intolerance, and dyslipidemia induced by acute inhibition of phosphoinositide 3-kinase signaling in the liver
J. Clin. Invest. Kazuaki Miyake, et al. 110:1483 doi:10.1172/JCI15880 [Go to this article.]

Figure 3
Effects of Δp85 expression in the liver on insulin-induced activation of signaling molecules in skeletal muscle and adipose tissue. DNPI3K and LacZ mice were deprived of food for 16 hours and then injected with insulin (+) or saline (–). Skeletal muscle (left panels) and adipose tissue (right panels) were removed 2 minutes later, homogenized, and subjected to analysis of the abundance and tyrosine phosphorylation of the IR, IRS-1, or IRS-2 (a), of the association of PI 3-K activity with IRS-1 or IRS-2 (b), and of phosphorylation of Akt (c) as described in the legend to Figure 2. Data in a and c are representative of results obtained from three mice; those in b are means ± SEM of values from four mice. *P < 0.05, **P < 0.01 versus the corresponding value for LacZ mice.