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Journal of Lipid Research, Vol. 50, 740-748, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Methods

FAT/CD36 expression is not ablated in spontaneously hypertensive rats

Arend Bonen^1,*, Xiao-Xia Han^*, Narendra N. Tandon, Jan F. C. Glatz, James Lally^*, Laelie A. Snook^* and Joost J. F. P. Luiken

^* Department of Human Health and Nutritional Sciences University of -Guelph, Guelph, Ontario, N1G 2W1, Canada
Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories 9900 Medical Center Drive, Rockville, MD 20850, Maastricht University, 6200-MD Maastricht, The Netherlands
Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, The Netherlands

Published, JLR Papers in Press, December 9, 2008.

These studies were supported in part by grants from the Canadian Institutes of Health Research (AB), the Natural Sciences and Engineering Research Council of Canada (AB), the Heart and Stroke Foundation of Ontario (AB), The Netherlands Heart Foundation grant 2002.T049 (JG), the Netherlands Organization for Health Research and Development (NWO-ZonMw grant 40-00812-98-03075) (JL and JG), and the European Commission (Integrated Project LSHM-CT-2004-005272, Exgenesis) (JL and JG), and the Canada Research Chair program (AB). J.J.F.P. Luiken was the recipient of a VIDI-Innovational Research Grant from the Netherlands Organization of Scientific Research (NWO-ZonMw Grant 016.036.305). J.F.C. Glatz is the Netherlands Heart Foundation Professor of Cardiac Metabolism. A. Bonen is the Canada Research Chair in Metabolism and Health.

¹ To whom correspondence should be addressed. e-mail: abonen{at}uoguelph.ca

There is doubt whether spontaneously hypertensive rats (SHR; North American strain) are null for fatty acid translocase (FAT/CD36). Therefore, we examined whether FAT/CD36 is expressed in heart, muscle, liver and adipose tissue in SHR. Insulin resistance was present in SHR skeletal muscle. We confirmed that SHR expressed aberrant FAT mRNAs in key metabolic tissues; namely, the major 2.9 kb transcript was not expressed, but 3.8 and 5.4 kb transcripts were present. Despite this, FAT/CD36 protein was expressed in all tissues, although there were tissue-specific reductions in FAT/CD36 protein expression and plasmalemmal content, ranging from 26–85%. Fatty acid transport was reduced in adipose tissue (–50%) and was increased in liver (+47%). Normal rates of fatty acid transport occurred in heart and muscle, possibly due to compensatory upregulation of plasmalemmal fatty acid binding protein (FABPpm) in red (+123%) and white muscle (+110%). In conclusion, SHRs (North American strain) are not a natural FAT/CD36 null model, the North American strain of SHR express FAT/CD36, albeit at reduced levels.

Supplementary key words muscle • heart • liver adipose • tissue • glucose transport • fatty acid transport

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