Accumulation of fat deposits in muscle tissue is strongly linked to the onset of insulin resistance, a hallmark of Type 2 diabetes. Identifying the muscle-specific molecular pathways that contribute to insulin resistance may lead to potential therapies that reduce the risks and complications for Type 2 diabetes and other obesity-related disorders. This month in the JCI, a study led by Daniel Kelly at the Sanford Burnham Prebys Medical Discovery Institute determined that the transcription factor MondoA regulates key pathways controlling glucose uptake and fat accumulation in muscle cells. Deactivation of MondoA led to reductions in the levels of two proteins that suppress insulin signaling. In mice, inhibiting MondoA also led to enhancements in glucose uptake and insulin signaling as well as improved glucose tolerance. These findings indicate that pathways regulated by MondoA are potential therapeutic targets for preventing and treating obesity-related insulin resistance.
TITLE: MondoA coordinately regulates skeletal myocyte lipid homeostasis and insulin signaling
Daniel P. Kelly
Sanford Burnham Prebys Medical Discovery Institute
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