Taylor S A, Price R G, Kang S S, Yudkin J
Diabetologia. 1980 Oct;19(4):364-72. doi: 10.1007/BF00280522.
Rats were fed on diets containing either sucrose or starch as the carbohydrate component (55%) for eight months. Diabetes was induced in animals of both groups by injecting streptozotocin (50 mg/kg body weight). Diabetic rats failed to gain weight, had enlarged kidneys, polyuria and elevated blood glucose levels. Starch and sucrose fed rats gained weight normally and had normal blood glucose levels. Sucrose fed rats had enlarged kidneys. Regional thickening of the glomerular basement membrane was present in sucrose-fed and diabetic rats but not in starch-fed controls. Glomerular basement membrane isolated from pooled kidney cortices from rats in the different experimental groups were analysed for amino acid, disaccharide and hexosamine content. Hydroxylysine (9 to 20%), hydroxyproline (21 to 24%), disaccharide (27%) and hexosamine (26%) were increased in membranes insolated from the three experimental groups, compared with starch-fed non-diabetic controls. An increase in low molecular weight components of the glomerular basement membrane of sucrose-fed and diabetic rats was observed using electrophoresis in sodium dodecyl sulphate. Significantly higher (p < 0.001) glucosyltransferase activity was present in kidney supernatants prepared from sucrose-fed (1050 +/- 60 nmol/2h/kidney) compared to starch-fed rats (510 +/- 40 nmol/2h/kidney). Sucrose feeding induces changes similar to those found in diabetes and the induction of diabetes made little difference over the feeding of sucrose alone.
将大鼠分为两组,分别喂食含蔗糖或淀粉作为碳水化合物成分(55%)的饮食,持续八个月。通过注射链脲佐菌素(50毫克/千克体重)诱导两组动物患糖尿病。糖尿病大鼠体重未增加,肾脏肿大,出现多尿且血糖水平升高。喂食淀粉和蔗糖的大鼠体重正常增加且血糖水平正常。喂食蔗糖的大鼠肾脏肿大。喂食蔗糖的大鼠和糖尿病大鼠出现肾小球基底膜局部增厚,而喂食淀粉的对照组则未出现。对从不同实验组大鼠的肾皮质中收集的肾小球基底膜进行氨基酸、二糖和己糖胺含量分析。与喂食淀粉的非糖尿病对照组相比,从三个实验组分离的基底膜中羟赖氨酸(9%至20%)、羟脯氨酸(21%至24%)、二糖(27%)和己糖胺(26%)含量增加。使用十二烷基硫酸钠电泳观察到,喂食蔗糖的大鼠和糖尿病大鼠的肾小球基底膜低分子量成分增加。与喂食淀粉的大鼠(510±40纳摩尔/2小时/肾脏)相比,喂食蔗糖的大鼠(1050±60纳摩尔/2小时/肾脏)制备的肾脏上清液中葡萄糖基转移酶活性显著更高(p<0.001)。喂食蔗糖会引发与糖尿病相似的变化,且诱导糖尿病与单独喂食蔗糖相比差异不大。