Taking KLF9 to "Cort" for crimes against metabolism.

Taking KLF9 to "Cort" for crimes against metabolism.
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DOI:
10.1172/jci128481
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发表时间:
2019-04
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
David R. Sweet;Liyan Fan;M. Jain
David R. Sweet;Liyan Fan;M. Jain
中科院分区:
其他
文献类型:
--
作者:
David R. Sweet;Liyan Fan;M. Jain

文献摘要

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糖皮质激素(GC)对于适当的血糖控制至关重要,但过量可导致高血糖症和糖尿病。在本期JCI中,Cui等人阐明了GC在生理和疾病环境中利用转录因子Krüppel样因子9(KLF 9)调节糖异生的机制。他们报告说,KLF9是一种GC诱导因子,最终增加增殖物激活受体γ共激活因子1 α(PGC1α)的转录,导致肿瘤异生。鉴于GC诱导的糖尿病的高发病率,该信号传导轴的鉴定不仅提供了关键的科学见解,而且为接受慢性GC治疗的患者提供了预防性治疗的基础。
Glucocorticoids (GCs) are essential for proper glycemic control, but in excess, can lead to hyperglycemia and diabetes. In this issue of the JCI, Cui et al. elucidate a mechanism by which GCs regulate gluconeogenesis utilizing the transcription factor Krüppel-like factor 9 (KLF9) in physiology and disease settings. They report that KLF9 is a GC-inducible factor that ultimately increases the transcription of proliferator-activated receptor γ coactivator 1 α (PGC1α), resulting in gluconeogenesis. Given the high incidence of GC-induced diabetes, identification of this signaling axis provides, not only critical scientific insight, but also a foundation for preventative therapies for patients receiving chronic GC treatment.