实验性肥胖动物模型

金硫葡萄糖(GTG)、汞硫葡萄糖均可用于制作下丘脑损伤性肥胖动物模型,而钠硫葡萄糖则可对抗GTG对下丘脑腹内侧核的破坏,故不宜使用。GTG肥胖鼠,小肠对葡萄糖(G)吸收率加快其原因可能与肥胖伴有血糖改变及胰岛素升高有关。整体实验四氧嘧啶糖尿病鼠小肠对G吸收率降低,用胰岛素治疗G吸收增加的现象,在离体小肠吸收G实验中未观察到,故肥胖高胰岛素可能通过改变血糖水平继发性影响G吸收。 谷氨酸一钠虽也可以引起大鼠腹股沟脂肪垫增长,但常伴活的过度及视网膜损害,故不宜用于制作肥胖模型。胰岛素小量多次注射可以刺激食欲使进食量增加,体重增长,肌肉增多。

EXPERIMENTAL ANIMAL MODEL OF OBESITY

Obesity lias been produced in male mice by the injection of gold thio-glucose ( GTG ) or mercury thioglucose. Histological examination confirmed tbe destruction of the ventromedial nuclei in the mice treated with these two drugs, Sodium thioglucose was found to be able to prevent the GTG-induced damage and obesity development. At the end of the thirteenth week after injections of GTG, the weights of the inguinal fat pads of the treated mice were greatly increased as compared with the untreated mice. In GTG-treated mice, there was a distinct increase in glucose absorption from the intestine as measured in vivo. Since obesity is accompanied by hyperinsulinaemia, we would conclude that increased intestinal absorption of glucose in the GTG-obesity mice was related with insulin. The intestinal absorption of glucose in the alloxan-diabetic rats was greatly decreased as measured in vivo. But the glucose absorption of the alloxan-diabetic rats was not decreased as measured in vitro. There was a linear relationship between the blood sugar level and the absorptiverate of glucose. The insulin control was not in a direct manner to theactive transport system for glucose but an indirect manner, probably secondary to the changes of blood sugar level. Besides, the obese rats were accompanied by hyperinsulinaemia as measured by the serum RIA method and the gastrocnemius muscle capacity of the obese rats was decreased as compared with control rats. Experimental animal models can also be produced by insulin or monosodium glutamate.