长程高脂肪膳食对大鼠空腹血糖及糖耐量的影响

研究了单纯高脂膳食喂养对大鼠空腹血糖(Fasting plasma glucose,FPG)及葡萄糖耐量(Glucose tolerancetest,GTT)的影响,旨在模拟与现代人生活饮食结构及发病情况更为接近的糖调节异常动物模型.取正常SD大鼠100只喂以普通饲料或高脂饲料14mo,动态监测动物体重及空腹血糖的变化,并分别在第5、8、10、14mo时用糖耐量试验观察葡萄糖耐量减退(IGT)的情况.结果显示,高脂喂养第1~14个月过程中,雄性大鼠的体重较普食组均未出现显著增加,而雌性大鼠体重仅在喂养第5~8个月期间较普食组增加了10%~15%;与普食组相比,在喂养高脂膳食第1~5个月中雌雄两性大鼠空腹血糖均显著升高,在喂养第5~10个月中雄性葡萄糖耐量显著减退,但雌性动物则未出现明显的IGT,至第14个月时雄性IGT与普食组的差异消失.研究表明,单纯高脂膳食虽不能诱发糖尿病,但可出现较典型的IFG空腹血糖受损和IGT现象,且以雄性动物造模更为适宜,喂养时间以10mo以内为宜.由于单纯高脂喂养更接近自然人群发病过程,因此,此种模型将为糖调节受损发生机制及其早期干预的研究提供新的动物模型.图2表1参12

Effect of Long-term High-fat Diet on Fasting Glucose and Glucose Tolerance in Rats

The effect of long-term high-fat diet(HF)on fasting glucose and glucose tolerance in rats was observed and studied to establish a stable animal model which can simulate a natural pathophysiological process similar to impaired glucose regulation for humans.100 SD rats were randomly divided into control group and enriched HF group,and were fed with free access to food and water for 14 months.Body weight and fasting glucose levels were measured every month,and intraperitoneal glucose tolerance test was performed in the 5,8,10 and 14th months after HF feeding.During HF feeding from the 1st to 14th month,body weight of males was not significantly increased,while that of females slightly increased by 10%~15% from 5th to 8th month.Compared with the control group,the fasting glucose levels of the HF group of both genders were significantly increased from the 1st to 5th month,whereas only males showed significantly impaired glucose tolerance(IGT)from the 5th to 10th month.However,the difference in IGT of males was diminished with prolonged HF feeding.Although HF alone could not cause diabetes in rats,it did induce impaired fasting glucose and IGT.Male rats were better for recapturing the matabolic features of impaired glucose regulation.Due to the close resemblance in the natural pathophysiological process to human type 2 diabetes,easy experiment and low cost,this animal model will be useful for future mechanistic study on early glucose dysregulation and its prevention.Fig 2,Tab 1,Ref 12