Abstract:All vertebrate animals have developed a sophisticated regulatory system to cope with frequent and unpredictable episodes of fasting. A recent letter to Nature suggests that a switch from early gluconeogenic gene activation via CRTC2 (also known as TORC2) to late action of FOXO1 is critical to this process.
Suppression of KLF2 by FOXO1 may be a plausible mechanism of diabetic endothelial dysfunction. High-glucose-induced, FOXO1-mediated KLF2 suppression was reversed by atorvastatin, suggesting that intensive statin treatment could be a therapeutic option in diabetic vascular dysfunction.
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