c-Cbl–deficient mice have reduced adiposity, higher energy expenditure, and improved peripheral insulin action
J. Clin. Invest. Juan C. Molero, et al. 114:1326 doi:10.1172/JCI21480 [Go to this article.]

Figure 6
Representative electron micrographs of soleus muscle from WT and c-Cbl–deficient mice (A), showing the subsarcolemmal mitochondria population. Scale bar: 1 μm. The histogram shows the average mitochondrial size from more than 100 mitochondria from matching sections of muscles from WT (black bars) and c-Cbl–deficient (white bars) mice. (B and C) Muscle homogenates were immunoblotted with either antibodies specific for UCP3, pSer79-ACC, ACC, and PGC1α (5 and 15 μg total protein) (B) or antibodies specific for AMPK and pThr172-AMPK (60 μg total protein) (C). The fold increase in protein levels observed in c-Cbl^–/– mice compared with WT animals, as well as the result of the statistical analysis of the data, is shown at the right of each lane. Data represent the mean ± SEM of 6 (C) or 12 (B) animals in each group. (D) Histograms show ACC phosphorylation as a ratio of total ACC (top) and AMPK phosphorylation as a ratio of total AMPK (bottom) in quadriceps from WT and c-Cbl^–/– mice. *P < 0.05, **P < 0.01.