JCI Table of Contents, September 15, 2003

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

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

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

Contact: Brooke Grindlinger
Journal of Clinical Investigation

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