Activation of hypothalamic S6 kinase mediates diet-induced hepatic insulin resistance in rats
J. Clin. Invest. Hiraku Ono, et al. 118:2959 doi:10.1172/JCI34277 [
Go to this article.]
Figure 4Hypothalamic overexpression of CA-S6K and functional validation in GT1-7 hypothalamic cells. (
A) Construction of CA-S6K. (
B) Adenovirus-infected GT1-7 cells were stimulated with insulin for 30 min. Serine phosphorylations in the basal state (0 nM insulin) of S6, IRS-1, and eIF4B were increased to maximal levels (comparable to LacZ expression with 100 nM insulin) by CA-S6K overexpression (
P < 0.01;
n = 2). The ratios of phosphoproteins to total proteins, and of phosphoproteins to actin, were statistically analyzed. Representative bands are shown. (
C) Expression of CA-S6K in the MBH. MBH tissue lysates obtained 12 d after viral injection were immunoblotted with anti-S6K, anti–M5-Flag, or anti–β-gal antibodies. (
D) S6K activity in MBH samples. **
P < 0.01 versus LacZ.
