Supplementary Materials

Supplementary Materials for:

Reversal of diet-induced obesity and insulin resistance by inducible genetic ablation of GRK2

Rocio Vila-Bedmar, Marta Cruces-Sande, Elisa Lucas, Hanneke L. D. M. Willemen, Cobi J. Heijnen, Annemieke Kavelaars, Federico Mayor Jr.,* Cristina Murga*

*Corresponding author. E-mail: cmurga{at}cbm.csic.es (C.M.); fmayor{at}cbm.csic.es (F.M.)

This PDF file includes:

  • Fig. S1. Characterization of an obese and insulin-resistant phenotype after 8 weeks of HFD, before tamoxifen treatment, and quantification of tamoxifen-induced GRK2 depletion.
  • Fig. S2. HFD-induced weight gain in control mice compared with SD-fed mice.
  • Fig. S3. CreER expression or translocation to the nucleus does not affect body weight gain or insulin-induced phosphorylation of AKT in muscle, eWAT, or liver.
  • Fig. S4. The abundance of components in or inhibitors of the insulin signaling pathway is not changed upon GRK2 loss in muscle or liver.
  • Fig. S5. CreER expression or translocation to the nucleus does not affect lipid accumulation in the liver.
  • Fig. S6. Decreased abundance of inflammation markers in the liver upon tamoxifen-induced GRK2 loss.
  • Table S1. Primers used for RT-PCR analysis.

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Citation: R. Vila-Bedmar, M. Cruces-Sande, E. Lucas, H. L. D. M. Willemen, C. J. Heijnen, A. Kavelaars, F. Mayor Jr., C. Murga, Reversal of diet-induced obesity and insulin resistance by inducible genetic ablation of GRK2. Sci. Signal. 8, ra72 (2015).

© 2015 American Association for the Advancement of Science