Sodoyez J C, Sodoyez-Goffaux F
Service d'Endocrinologie, CHU Sart Tilman, Liège, Belgique.
Presse Med. 1992 Sep 9;21(28):1336-9.
Zucker obese rats (fa/fa), aged 8 to 10 weeks, were treated orally by benfluorex (2 x 25 mg.kg-1, day-1) for 2 weeks and were compared with a control group of the same age treated with placebo. Benfluorex induced a break in the weight curve, a significant fall in serum triglycerides, blood glucose and plasma insulin and in the insulin content of the pancreas. Following intrajugular injection of iodine 123 labelled insulin, the liver of the treated animals bound 25 percent more insulin than the liver of control animals. Conversely, the renal clearance of insulin of the treated animals was reduced in comparison to the placebo group. These studies confirm that, in an animal model of obesity associated with insulin resistance, benfluorex exerts a marked hypolipidemic effect and improves insulin resistance. They also demonstrate an increased targeting of insulin towards hepatic receptors either due to an increase in the hepatic blood flow or to an increase in the number of hepatic receptors or to an increase in the affinity of these receptors. However, speculative considerations make this last mechanistic hypothesis somewhat improbable.
8至10周龄的Zucker肥胖大鼠（fa/fa），口服苯氟雷司（2×25毫克·千克⁻¹，每日一次），持续2周，并与相同年龄接受安慰剂治疗的对照组进行比较。苯氟雷司导致体重曲线中断，血清甘油三酯、血糖、血浆胰岛素以及胰腺胰岛素含量显著下降。经颈静脉注射碘123标记的胰岛素后，治疗组动物肝脏结合的胰岛素比对照组动物肝脏多25%。相反，与安慰剂组相比，治疗组动物胰岛素的肾脏清除率降低。这些研究证实，在与胰岛素抵抗相关的肥胖动物模型中，苯氟雷司具有显著的降血脂作用，并改善胰岛素抵抗。它们还表明，胰岛素对肝脏受体的靶向作用增强，这可能是由于肝血流量增加、肝脏受体数量增加或这些受体的亲和力增加所致。然而，从推测的角度来看，最后这个机制假设有几分不太可能。
