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
Copyright policy )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
In their article, Kumar et al. (1) demonstrated the importance of mTORC2 for the insulin-induced glucose transport and lipolysis in adipocytes. They also discussed the mechanisms of the fat-cell–specific deletion of rictor and alterations in the insulin signaling pathway, leading to systemic insulin resistance. They suggested that the increased serum nonesterified fatty acid levels in FRic−/− mice are the mediators for the impairment of the whole-body insulin sensitivity (1). Previously, Cybulski et …
Mice, Knockout, Online Letters to the Editor, Protein Serine-Threonine Kinases, Lipid Metabolism, Mice, Glucose, Rapamycin-Insensitive Companion of mTOR Protein, Adipokines, Adipose Tissue, Liver, Animals, Insulin, Carrier Proteins, Energy Metabolism, Muscle, Skeletal, Signal Transduction
Mice, Knockout, Online Letters to the Editor, Protein Serine-Threonine Kinases, Lipid Metabolism, Mice, Glucose, Rapamycin-Insensitive Companion of mTOR Protein, Adipokines, Adipose Tissue, Liver, Animals, Insulin, Carrier Proteins, Energy Metabolism, Muscle, Skeletal, Signal Transduction
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