SENSITIVITY OF BETA-CELLS TO STREPTOZOTOCIN IN LEAN AND OBESE RATS
SENSITIVITY OF BETA-CELLS TO STREPTOZOTOCIN IN LEAN AND OBESE RATS
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DOI：
10.1055/s-0028-1093413
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发表时间：
1978-01-01
影响因子：
2.2
通讯作者：
BRAY, GA
中科院分区：
文献类型：
--
作者：
INOUE, S;BRAY, GA
实验[2]已经验证了肥胖可能会增加胰腺对致糖尿病药物的敏感性的假设。在第一个实验中，瘦和下丘脑肥胖（VMH）大鼠注射15，25或35毫克/公斤的链脲佐菌素。VMH肥胖大鼠显示出剂量相关的血糖升高，但瘦大鼠仅显示出最高剂量的葡萄糖升高。所有接受35 mg/kg链脲佐菌素的肥胖大鼠均死于酮症酸中毒，6只接受25 mg/kg链脲佐菌素的肥胖大鼠中有3只患糖尿病（2只酮症酸中毒）。在瘦大鼠中，只有3只患上轻度糖尿病。25和35 mg/kg链脲佐菌素1周后，肥胖大鼠血清胰岛素水平显着下降，但在瘦大鼠没有变化。在第二个实验中，瘦大鼠接受单剂量的链脲佐菌素（25毫克/公斤）1周前下丘脑病变。随后将动物分成4组（VMH-高脂肪饮食：VMH-低脂肪饮食：假手术-高脂肪饮食：假手术-低脂肪饮食）。高脂饮食喂养的VMH-肥胖大鼠显示葡萄糖逐渐升高。除假手术组外，其余各组均表现为糖耐量受损。7周后，每只大鼠再给予5 mg链脲佐菌素。随后的血清葡萄糖升高与体重相关。高脂饮食的6只肥胖大鼠中有5只发生糖尿病，低脂饮食的肥胖大鼠中有3只发生糖尿病，高脂饮食的假手术大鼠中有2只发生糖尿病。没有一只瘦老鼠患上糖尿病。胰腺β-细胞在肥胖症发展后可能比β-葡萄糖细胞更易受致糖尿病剂如链脲佐菌素的影响。瘦肉动物的细胞。
Experiments [2] have tested the hypothesis that pancreatic sensitivity to diabetogenic agents may be increased by obesity. In the 1st experiment, lean and hypothalamic obese (VMH) rats were injected with 15, 25 or 35 mg/kg of streptozotocin. The VMH-obese rats showed a dose-related rise in blood glucose but the lean rats only showed a rise in glucose with the highest dose. All obese rats which received 35 mg/kg of streptozotocin died of ketoacidosis, and 3 of the 6 obese rats receiving 25 mg/kg of streptozotocin became diabetic (2 with ketoacidosis). Among the lean rats, only 3 became mildly diabetic. Serum insulin levels were decreased significantly with 25 and 35 mg/kg 1 wk after streptozotocin in the obese rats, but there was no change in the lean rats. In the 2nd experiment, lean rats received a single dose of streptozotocin (25 mg/kg) 1 wk before hypothalamic lesions. Animals were subsequently divided into 4 groups (VMH-high fat diet: VMH-low fat diet: Sham-high fat diet: Sham-low fat diet). The VMH-obese rats fed a high fat diet showed a progressive rise in glucose. All groups except the sham-operated rats fed the low fat diet, showed impaired glucose tolerance. After 7 wk, an additional 5 mg of streptozotocin was given to each rat. The subsequent rise of serum glucose was weight-related. Diabetes developed in 5 of the 6 obese rats on the high fat diet, in 3 of the obese rats on the low fat diet and in 2 of the sham-operated rats on the high fat diet. None of the lean rats became diabetic. The pancreatic .beta.-cells may be more susceptible to a diabetogenic agent, such as streptozotocin after the development of obesity than the .beta.-cells of lean animals.