The kinase AKT has been regarded as an obligate intermediate in the insulin signaling pathway that suppresses glucose production by inhibiting the transcription factor forkhead box O1 (FoxO1) after meals. A new study shows that, without AKT-FoxO1 signaling, insulin still contributes to postprandial responses, revealing an AKT-independent pathway for insulin action that might be exploited to treat metabolic disease (pages 388–395).
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Cheng, Z., White, M. The AKTion in non-canonical insulin signaling. Nat Med 18, 351–353 (2012). https://doi.org/10.1038/nm.2694
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DOI: https://doi.org/10.1038/nm.2694
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