Tuovinen C G, Bender A E
Nutr Metab. 1975;19(3-4):161-72. doi: 10.1159/000175660.
Male rats of the ASL Wistar strain were fed from weaning on starch, fructose or carbohydrate-free diets for 4 and 12 weeks. In addition, further groups were fed for 24 weeks on starch, sucrose or carbohydrate-free diets. Livers were examined for gross composition, glucose-6-phosphatase activity and in vitro lipogenesis and glucose oxidation. Intestinal sucrase was also measured. Dietary fructose and the carbohydrate-free diet induced an enlargement of the livers after 12 weeks feeding, when expressed per 100g body weight, and at the same time, an increased fat content. Fructose caused an increase in liver glucose-6-phosphatase after 4 weeks, which persisted after 12 weeks, and a similar increase was observed after 24 weeks feeding on sucrose. Fructose produced an increase in intestinal sucrose after 4 weeks, but this did not persist and there was no increase evident after 12 weeks feeding, nor after 24 weeks feeding on sucrose. Fructose markedly depressed the in vitro lipogenesis and glucose oxidation in liver slices. This was evident after 4 weeks feeding and also after 12 weeks when the effect of age showed as a fall in both these parameters in the control group of animals. The carbohydrate-free diet caused an increase in liver glucose-6-phosphatase after 4 weeks, a smaller increase after 12 weeks, and there was no increase apparent when feeding was continued for 24 weeks. Apparently due to the absence of substrate, the intestinal sucrose activity fell to less than half after 4 weeks and to negligible levels after 12 and 24 weeks on carbohydrate-free diet. In vitro liver lipogenesis and glucose oxidation were depressed after 4 and 12 weeks in a similar way to the fructose diet. On both these diets the rise in liver glucose-6-phosphatase appeared to parallel the fall in liver lipogeneis and glucose oxidation.
将ASL品系的雄性Wistar大鼠从断奶开始分别用淀粉、果糖或无碳水化合物饮食喂养4周和12周。此外,另有几组大鼠分别用淀粉、蔗糖或无碳水化合物饮食喂养24周。对肝脏进行大体组成、葡萄糖-6-磷酸酶活性以及体外脂肪生成和葡萄糖氧化的检测。同时也测定了肠道蔗糖酶活性。喂养12周后,以每100克体重计算,膳食果糖和无碳水化合物饮食会导致肝脏肿大,同时脂肪含量增加。果糖喂养4周后肝脏葡萄糖-6-磷酸酶增加,12周后仍持续增加,而蔗糖喂养24周后也观察到类似增加。果糖喂养4周后肠道蔗糖酶增加,但未持续,喂养12周后无明显增加,蔗糖喂养24周后也未增加。果糖显著抑制肝脏切片的体外脂肪生成和葡萄糖氧化。喂养4周后以及12周后这种情况很明显,此时对照组动物由于年龄影响这两个参数均下降。无碳水化合物饮食喂养4周后肝脏葡萄糖-6-磷酸酶增加,12周后增加幅度较小,持续喂养24周后无明显增加。显然由于缺乏底物,无碳水化合物饮食喂养4周后肠道蔗糖酶活性降至不到一半,12周和24周后降至可忽略不计的水平。无碳水化合物饮食喂养4周和12周后,体外肝脏脂肪生成和葡萄糖氧化的抑制情况与果糖饮食类似。在这两种饮食中,肝脏葡萄糖-6-磷酸酶的升高似乎与肝脏脂肪生成和葡萄糖氧化的下降平行。