Commentary 10.1172/JCI128481

Taking KLF9 to “Cort” for crimes against metabolism

David R. Sweet,1,2 Liyan Fan,1,2 and Mukesh K. Jain1

1Case Cardiovascular Research Institute and University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA.

2Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA.

Address correspondence to: Mukesh K. Jain, Iris & Bert L. Wolstein Research Building, 2103 Cornell Road, Cleveland, Ohio 44106, USA. Phone: 216.368.3391; Email: mxj84@case.edu.

Find articles by Sweet, D. in: JCI | PubMed | Google Scholar

1Case Cardiovascular Research Institute and University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA.

2Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA.

Address correspondence to: Mukesh K. Jain, Iris & Bert L. Wolstein Research Building, 2103 Cornell Road, Cleveland, Ohio 44106, USA. Phone: 216.368.3391; Email: mxj84@case.edu.

Find articles by Fan, L. in: JCI | PubMed | Google Scholar

1Case Cardiovascular Research Institute and University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA.

2Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA.

Address correspondence to: Mukesh K. Jain, Iris & Bert L. Wolstein Research Building, 2103 Cornell Road, Cleveland, Ohio 44106, USA. Phone: 216.368.3391; Email: mxj84@case.edu.

Find articles by Jain, M. in: JCI | PubMed | Google Scholar

First published April 29, 2019 - More info

Published in Volume 129, Issue 6 on June 3, 2019
J Clin Invest. 2019;129(6):2178–2180. https://doi.org/10.1172/JCI128481.
© 2019 American Society for Clinical Investigation
First published April 29, 2019 - Version history

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.

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