ent of insulin action in the liver. Masato Kasuga and colleagues at Kobe University, Japan, have found that mice deficient in the hepatic enzyme PKC-lambda have increased overall insulin sensitivity, yet their blood glucose concentration remained within normal limits. The authors demonstrated a link between the altered expression of the sterol regulatory element-binding protein SREBP-1c gene and its target genes, and defective PKC-lambda signaling. Restoration of PKCl expression in the liver restored SREBP-1c expression and insulin sensitivity to normal. This study suggests that reagents that block PKC-lambda signaling specifically in the liver might consequently ameliorate insulin resistance.

TITLE: PKC-lambda in liver mediates insulin-induced SREBP-1c expression and determines both hepatic liver content and overall insulin sensitivity

AUTHOR CONTACT:
Masato Kasuga
Division of Diabetes and Digestive and Kidney Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.
Phone: 81-78-382-5861
Fax: 81-78-382-2080
E-mail: kasuga@med.kobe-u.ac.jp

View the PDF of this article at: https://www.the-jci.org/press/18816.pdf

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HATs off to Hop in cardiac hypertrophy

Histone acetylation, regulated by two antagonistic enzymes histone acetyltransferases (HATs) and histone deacetylases (HDACs) results in transcriptional changes and also plays a critical role in cardiac development and disease. A new study by Jonathan Epstein and colleagues from the University of Pennsylvania shows that overexpression of the atypical transcriptional co-repressor homeodomain-only protein (Hop) causes cardiac hypertrophy via recruitment of a class I HDAC. In contrast to the body of work on transcriptional mechanisms that drive cardiac hypertrophy, including class II HDACs, this report elucidates a novel gro
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
15-Sep-2003

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