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25 March 2004

Fatp4 and Restrictive Dermopathy in Mice

Heidelberg scientists studying fat transport in the intestine have come across a possible key gene for severe skin disorders

What they set out to discover was how certain nutrition fats get from the intestine into the blood. What they finally came up with was something very different. Scientists at the University of Heidelberg's Hospital for Internal Medicine, in collaboration with colleagues at EMBL (Heidelberg), the German Cancer Research Centre (Heidelberg) and the University of Regensburg established that mice without Fatp4, a gene responsible for fatty acid transport, displayed extreme restrictive dermopathy. This finding may be an important contribution to the clarification of the causes of severe skin disorders in humans.

The members of the Fatp (fatty acid transport protein) family are involved in the cellular uptake of fatty acids. So far six different genes have been identified but little is known about their functions. The Heidelberg team headed by Prof. Dr. Wolfgang Stremmel, medical director of the Gastro-Enterology and Infectious Diseases Department, and senior consultant Dr. Thomas Herrmann generated so-called knockout mice without the Fatp4 gene. The scientists discovered this gene themselves six years ago and have since described it in detail.

The result of the Heidelberg experiment was surprising. Mice without Fatp4 die immediately after birth. They have horny skin, almost like a coat of armour, which severely limits the movements of the rib-cage and thus prevents the lungs from developing fully. These mice also lose nine times as much water through the skin as healthy animals.

Skin ceramides with the wrong fatty acids

Scientists from the Department of Clinical Chemistry at the University of Regensburg took a closer look at the animals. They found that the ceramides (protective substances that normally keep the skin supple and robust) contained too few long-chain fatty acids. Obviously the absence of the Fatp4 gene had impaired the fatty acid metabolism of the skin and thus brought about the hyperkeratosis observed.

This may mean that scientists now have a key to the treatment of skin disorders in humans. The Fatp4 gene in humans is very similar to that in mice and probably has a similar function. If it should transpire that people with severe skin disorders like neurodermatitis or ichthyosis have a defective Fatp4 gene, or none at all, this could trigger new approaches to therapy for such conditions.

Contact
Dr. Thomas Herrmann
Senior Consultant
Department of Internal Medicine IV
Thomas_Herrmann@med.uni-heidelberg.de

References
Herrmann T, Buchkremer F, Gosch I, Hall AM, Bernlohr DA, Stremmel W: Mouse fatty acid transport protein 4 (FATP4): Characterization of the gene and functional assessment as a very long chain acyl-CoA synthetase. Gene 2001;270:31-40.

Herrmann T, van der Hoeven F, Grone HJ, Stewart AF, Langbein L, Kaiser I, Liebisch G, Gosch I, Buchkremer F, Drobnik W, Schmitz G, Stremmel W: Mice with targeted disruption of the fatty acid transport protein 4 (Fatp 4, Slc27a4) gene show features of lethal restrictive dermopathy. J. Cell Biol, 2003; 161: 1105-1115.

The original article can be requested from contact@med.uni-heidelberg.de .

Please address any inquiries to
Dr. Annette Tuffs
Public Relations Dept. of the Faculty of Medicine
University of Heidelberg
Voßstrasse 2, Building 4040
D-69115 Heidelberg
phone: 06221/564536
fax: 06221/564544
mobile: 0170/5724725
e-mail: Annette_Tuffs@med.uni-heidelberg.de
www.med.uni-heidelberg.de

Dr. Michael Schwarz
Press Officer of the University of Heidelberg
phone: 06221/542310, fax: 54317
michael.schwarz@rektorat.uni-heidelberg.de
http://www.uni-heidelberg.de/presse/index.html


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