Skip to main content
. 2014 Feb 7;289(12):8473–8483. doi: 10.1074/jbc.M113.546242

FIGURE 2.

FIGURE 2.

Cavin-1 deficiency results in reduced isoproterenol-stimulated lipolysis, loss of insulin-stimulated glucose uptake, decreased fatty acid uptake and incorporation, and impaired fat tolerance. A, serum free glycerol levels and free fatty acid levels in wild-type and knock-out mice before and 20 min after isoproterenol administration (10 mg/kg) (n = 5–6). B, basal and β-adrenergic receptor agonist-stimulated (isoproterenol, 1 μm) lipolysis, was measured as glycerol release over a 2-h period for isolated primary adipocytes from WT and Cavin-1-null mice. The lipolytic rate was normalized to adipocyte cell number (n = 6–7). C, primary adipocytes were treated with 1 nm insulin or not and 2-DOG uptake was determined as described under “Experimental Procedures” (n = 4). D, relative cell-associated radioactivity incorporation of oleate into lipid over a 60-min period in WT and Cavin-1-null adipocytes (n = 3). E, initial uptake kinetics of 33.3 μm [3H]oleate into adipocytes, 15 s and 30 s from WT and Cavin-1-null mice (n = 4). F, oral fat tolerance test: mice were fasted for 16 h, followed by an oral bolus of olive oil (20 μl/g BW). Aliquots of tail vein blood were sampled at the times indicated after gavage for the determination of plasma TG levels (n = 4–5). Data are expressed as the mean ± S.E. *, p < 0.05; **, p < 0.01; ***, p < 0.001 for WT versus KO.