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
- 1Department of Molecular Physiology and Biophysics and the Center for Stem Cell Biology, Vanderbilt University Medical Center, Nashville, Tennessee; the
- 2Department of Medicine, Division of Endocrinology, University of Virginia Health System, Charlottesville, Virginia; the
- 3Department of Medicine, Division of Endocrinology, Metabolism and Diabetes, University of Massachusetts Medical School, Worcester, Massachusetts; and the
- 4Department of Pharmacology, University of Virginia Health System, Charlottesville, Virginia
- Corresponding author: Anil Kumar, .
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 …