Xu B, Berkich D A, Crist G H, LaNoue K F
Department of Cellular and Molecular Physiology, Milton S. Hershey Medical Center, Pennsylvania State University College of Medicine, Hershey 17033-0850, USA.
Am J Physiol. 1998 Feb;274(2):E271-9. doi: 10.1152/ajpendo.1998.274.2.E271.
The A1 adenosine receptor (A1ar) antagonist 1,3-dipropyl-8-(p-acrylic)-phenylxanthine (BW-1433) was administered to lean and obese Zucker rats to probe the influence of endogenously activated A1ars on whole body energy metabolism. The drug induced a transient increase in lipolysis as indicated by a rise in serum glycerol in obese rats. The disappearance of the response by day 7 of chronic studies was accompanied by an increase in A1ar numbers. Glucose tolerance tests were administered to rats treated with BW-1433. Peak serum insulin levels and areas under glucose curves (AUGs) were 34 and 41% lower in treated obese animals than in controls, respectively, and 19 and 39% lower in lean animals. With chronic administration (6 wk), AUGs decreased 47 and 33% in obese and lean animals, respectively. There was no effect of BW-1433 in either lean or obese rats on weight gain or percent body fat. Thus the major sustained influence of whole body A1ar antagonism in both lean and obese animals was an increase in whole body glucose tolerance at lower levels of insulin.
将A1腺苷受体（A1ar）拮抗剂1,3 - 二丙基 - 8 -（对 - 丙烯酸）- 苯基黄嘌呤（BW - 1433）给予瘦型和肥胖型Zucker大鼠，以探究内源性激活的A1ar对全身能量代谢的影响。该药物导致肥胖大鼠血清甘油升高，表明脂肪分解出现短暂增加。在慢性研究的第7天，这种反应消失，同时A1ar数量增加。对用BW - 1433处理的大鼠进行葡萄糖耐量试验。与对照组相比，经处理的肥胖动物的血清胰岛素峰值水平和葡萄糖曲线下面积（AUGs）分别降低了34%和41%，瘦型动物分别降低了19%和39%。长期给药（6周）后，肥胖和瘦型动物的AUGs分别降低了47%和33%。BW - 1433对瘦型或肥胖型大鼠的体重增加或体脂百分比均无影响。因此，在瘦型和肥胖型动物中，全身A1ar拮抗作用的主要持续影响是在较低胰岛素水平下提高全身葡萄糖耐量。
