Using a congenital mouse model of lipodystrophy, the authors observed that administration of leptin under the skin was not as potent as lower doses administered directly to the central nervous system, which were able to correct the metabolic abnormalities associated with lipodystrophy. Furthermore, using microarray technology, the authors identified repression of the enzyme SCD-1 as a mechanism of leptin action to improve fatty liver degeneration. These findings may have profound effects on the progression of leptin treatment strategies for metabolic diseases.

TITLE: Site and mechanism of leptin action in a rodent form of congenital lipodystrophy

AUTHOR CONTACT:
Jeffrey M. Friedman
The Rockefeller University, New York, New York, USA.
Phone: (212) 327-8800
Fax: (212) 327-7420
E-mail: friedj@mail.rockefeller.edu

View the PDF of this article at: https://www.the-jci.org/press/19511.pdf

Enzyme Akt is critical for stabilizing thrombus formation after vessel injury

The activation of platelets contributes to the formation of thrombi in the circulation, which block arteries and can cause heart attack and stroke. Interested in the role of the serine/threonine kinase, Akt, in platelet activation, Donna Woulfe and colleagues from the University of Pennsylvania examined platelets from normal and Akt2-deficient mice. In the February 2 issue of the Journal of Clinical Investigation the authors report that platelets from Akt2-deficient mice, but not Akt1-deficient mice, have defects in aggregation, secretion, and thrombus formation. Furthermore, Akt2 was shown to be more highly expressed in mouse platelets than Akt1. The data indicate that Akt is needed for optimal platelet aggregat
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
2-Feb-2004