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Articles in PresS, published online ahead of print May 28, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00011.2002
Submitted on January 15, 2002
Accepted on May 6, 2002
1 Kinesiology, University of Waterloo, Waterloo, Ontario, Canada; Physiology, Maastricht University, Maastricht, Limburg, The Netherlands
2 Kinesiology, University of Waterloo, Waterloo, Ontario, Canada
3 Agriculuture, Food and Nutritional Sciences, University of Alberta, Edmonton, Alberta, Canada
4 GlaxoSmithKline, Miami, Florida, USA
5 Thrombosis Research Laboratory, Otsuka Maryland Research Institute, Rockville, Maryland, USA
6 Physiology, Maastricht University, Maastricht, Limburg, The Netherlands
* To whom correspondence should be addressed. E-mail: abonen{at}healthy.uwaterloo.ca.
We have examined the effects of STZ-induced diabetes (moderate and severe) on fatty acid transport and fatty acid transporter (FAT/CD36 and FABPpm) expression, at the mRNA and protein level, as well as their plasmalemmal localization. These studies have shown that with STZ induced diabetes a) fatty acid transport across the plasma membrane is increased in heart, skeletal muscle and adipose tissue, and is reduced in liver, b) changes in fatty acid transport are generally not associated with changes in fatty acid transporter mRNA's, except in the heart, c) increases in fatty acid transport in heart and skeletal muscle occurred with concomitant increases in plasma membrane FAT/CD36, while in contrast, the increase and decrease in fatty acid transport in adipose tissue and liver were accompanied by concomitant increments and reductions in plasma membrane FABPpm,respectively. Finally, d) the increases in plasma membrane transporters (FAT/CD36 in heart and skeletal muscle; FABPpm in adipose tissue) were attributable their increased expression, while in liver the reduced plasma membrane FABPpm appeared to be due to its relocation within the cell in the face of a slightly increased expression. Taken together, STZ-induced changes in FA uptake demonstrate a complex and tissue-specific pattern, involving different fatty acid transporters in different tissues, in combination with different underlying mechanisms to alter their surface abundance.
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