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Am J Physiol Endocrinol Metab 297: E490-E494, 2009. First published June 2, 2009; doi:10.1152/ajpendo.00140.2009
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Reversal of high pancreatic islet and white adipose tissue blood flow in type 2 diabetic GK rats by administration of the β3-adrenoceptor inhibitor SR-59230A

U. S. Pettersson, J. Henriksnäs, and L. Jansson

Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden

Submitted 4 March 2009 ; accepted in final form 29 May 2009

Previous studies have shown that the Goto-Kakizaki (GK) rat, a nonobese type 2 diabetes model, has an increased white adipose tissue (WAT) and islet blood flow when compared with control rats. The aim of the study was to examine if these increased blood flow values in GK rats could be affected by the β3-adrenoceptor antagonist SR-59230A. We measured organ blood flow with a microsphere technique 10 min after administration of SR-59230A (1 mg/kg body wt), or the corresponding volume of 0.9% NaCl solution (1 ml/kg body wt) in rats anaesthetized with thiobutabarbital. The GK rat had an increased blood flow in all intra-abdominal adipose tissue depots except for the sternal fat pad compared with Wistar-Furth (WF) rats. However, no differences were seen in the blood perfusion of subcutaneous white or brown adipose tissue. The blood flow was also increased in both the pancreas and in the islets in the GK rat compared with WF rats. SR-59230A treatment affected neither WAT nor pancreatic blood flow in WF rats. In GK rats, on the other hand, SR-59230A decreased both WAT and islet blood flow values to values similar to those seen in control WF rats. The whole pancreatic blood flow was not affected by SR-59230A administration in GK rats. Interestingly, the brown adipose tissue blood flow in GK rats increased after SR-59230A administration. These results suggest that β3-adrenoceptors are involved in regulation of blood flow both in islet and in adipose tissue.

microsphere; in vivo; Goto-Kakizaki



Address for reprint requests and other correspondence: U. Pettersson, Uppsala Univ., Dept. of Medical Cell Biology, BMC, Husargatan 3, Box 571, SE-75123 Uppsala, Sweden (e-mail: ulrika.pettersson{at}mcb.uu.se)







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