Conditional disruption of IκB kinase 2 fails to prevent obesity-induced insulin resistance
J. Clin. Invest. Mathias Röhl, et al. 113:474 doi:10.1172/JCI18712 [Go to this article.]

Figure 4
Glucose metabolism in obese IKK2-deficient mice. (a) Random-fed blood glucose concentrations in male GTG-treated animals of the indicated genotype. Data represent the mean ± SEM of at least six animals in each group. Statistical analysis revealed no significant differences between the groups (unpaired Student’s t test). (b) Plasma insulin concentrations in lean and obese mice, given as mean ± SEM of at least 16 animals in each group (*P < 0.05). (c) Plasma insulin concentrations in male GTG-treated animals of the indicated genotype. Data represent the mean ± SEM of at least six animals in each group. Statistical analysis revealed no significant differences between the groups (unpaired Student’s t test). (d) The results of glucose-tolerance tests in male lean mice (filled squares), GTG-treated mice (open squares), and mice fed a high-fat diet (filled circles). Data represent the mean ± SEM of at least 12 animals in each group (*P < 0.05, **P < 0.01, unpaired Student’s t test). (e) The results from glucose-tolerance tests in male GTG-treated animals. Data represent the mean ± SEM of at least six animals in each group (IKK2^WT mice, filled diamonds; IKK2^Het mice, filled squares; IKK2^Mus mice, open squares; IKK2^Het/Mus mice, open diamonds). (f) The results from glucose-tolerance tests in male animals exposed to a high-fat diet. Data represent the mean ± SEM of at least six animals in each group (IKK2^WT mice, filled diamonds; IKK2^Het mice, filled squares; IKK2^Mus mice, open squares; IKK2^Het/Mus mice, open circles).