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Michihiro Matsumoto, Wataru Ogawa, Kazunori Akimoto, Hiroshi Inoue, Kazuaki Miyake, Kensuke Furukawa, Yoshitake Hayashi, Haruhisa Iguchi, Yasushi Matsuki, Ryuji Hiramatsu, Hitoshi Shimano, Nobuhiro Yamada, Shigeo Ohno, Masato Kasuga, Tetsuo Noda
Published in Volume 112, Issue 6
J Clin Invest. 2003; 112(6):935–944 doi:10.1172/JCI18816
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Figure 5

Effects of adenovirus-mediated restoration of PKCλ expression in the liver of mice with liver-specific PKCλ deficiency on hepatic lipid content, expression of Srebp1 in the liver, and insulin sensitivity. (a) Twenty-week-old λlox/lox or L-λKO mice (n = 7–9) were injected with PBS or with adenoviruses encoding either β-gal (LacZ) or WT PKCλ (λWT), as indicated. Total liver homogenates were subsequently subjected to immunoprecipitation and immunoblot analysis with antibodies to PKCλ (upper panel; data are representative of three experiments). Total RNA extracted from the liver was separately combined and subjected to Northern blot analysis with a probe specific for Srebp1 mRNA (middle panel), and hepatic triglyceride content was determined (lower panel; data are shown as mean ± SEM). *P < 0.05 (ANOVA). (b and c) Twelve-week-old λlox/lox or L-λKO mice were injected with PBS or with adenoviruses encoding either β-gal or WT PKCλ, after which blood glucose and plasma insulin concentrations were determined in the randomly fed state (b) or an insulin tolerance test was performed (c). Data represent mean ± SEM from six to ten mice. *P < 0.05 for the indicated comparisons (b) or for the comparison of L-λKO mice injected with the adenovirus encoding β-gal vs. all other conditions.