Response to Comment on: Kumar et al. Fat Cell–Specific Ablation of Rictor in Mice Impairs Insulin-Regulated Fat Cell and Whole-Body Glucose and Lipid Metabolism. Diabetes 2010;59:1397–1406

  1. Thurl E. Harris4
  1. 1Department of Molecular Physiology and Biophysics and the Center for Stem Cell Biology, Vanderbilt University Medical Center, Nashville, Tennessee; the
  2. 2Department of Medicine, Division of Endocrinology, University of Virginia Health System, Charlottesville, Virginia; the
  3. 3Department of Medicine, Division of Endocrinology, Metabolism and Diabetes, University of Massachusetts Medical School, Worcester, Massachusetts; and the
  4. 4Department of Pharmacology, University of Virginia Health System, Charlottesville, Virginia
  1. Corresponding author: Anil Kumar, anil.k.laxman{at}vanderbilt.edu.

We appreciate Dr. Erol's (1) interest in our article describing the phenotype of fat cell–specific rictor knockout (FRic−/−) mice (2). Dr. Erol suggested that RBP4 may play a role in the development of insulin resistance in FRic−/− mice. RBP4 is an adipokine, whose elevated expression in, and secretion from, adipocytes correlates with the development of insulin resistance in various animal models including the fat cell–specific GLUT4 knockout (G4A−/−) mice (3). Elevated circulating levels of RBP4 have also been demonstrated in …

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