期刊
JOURNAL OF LIPID RESEARCH
卷 50, 期 4, 页码 740-748出版社
ELSEVIER
DOI: 10.1194/jlr.M800237-JLR200
关键词
muscle; heart; liver adipose; tissue; glucose transport; fatty acid transport
资金
- Canadian Institutes of Health Research
- Natural Sciences and Engineering Research Council of Canada
- Heart and Stroke Foundation of Ontario
- The Netherlands Heart Foundation [2002.T049]
- Netherlands Organization for Health Research and Development [40-00812-9803075]
- European Commission [LSHM-CT-2004-005272]
- Canada Research Chair program
- VIDI-Innovational Research Grant
- Netherlands Organization of Scientific Research [016.036.305]
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.-Bonen, A., X-X. Han, N. N. Tandon, J. F. C. Glatz, J. Lally, L. A. Snook, and J. J. F. P. Luiken. FAT/CD36 expression is not ablated in spontaneously hypertensive rats. J. Lipid Res. 2009. 50: 740-748. Supplementary
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