Collier G R, Chisholm K, Sykes S, Dryden P A, O'Dea K
J Nutr. 1985 Nov;115(11):1471-6. doi: 10.1093/jn/115.11.1471.
Glucose and insulin responses to oral and intravenous glucose (1 g/kg body weight) were measured after consumption of a high fat (HF) or low fat (LF) diet for 3 wk in conscious rats with implanted intravenous and intra-arterial catheters. The HF diet resulted in impaired glucose tolerance and insulin resistance after both oral and intravenous glucose; the effect was more pronounced after oral glucose. In an attempt to understand the basis of the impairment of glucose tolerance after consuming the HF diet, the activity of hepatic glucokinase and the rate of intestinal glucose uptake were also measured. The more severe impairment of glucose tolerance by oral rather than intravenous administration was not explained by an increased rate of intestinal glucose uptake. Indeed, there was a small but significant reduction in the rate of jejunal glucose uptake in the HF rats. However, the greatly reduced activity of hepatic glucokinase in the HF rats was consistent with a reduced capacity for hepatic glucose uptake, which may have contributed significantly to the impaired glucose tolerance. The effects of the HF diet on the insulin response to glucose were much more pronounced after oral rather than intravenous glucose administration. This indicated that the HF diet may have stimulated the enteroinsular axis. However, it is also possible that the particularly high circulating insulin levels, resulting from oral glucose in the HF rats, were a direct response to hyperglycemia, secondary to reduced glucose removal.
在植入静脉和动脉导管的清醒大鼠中，给予高脂（HF）或低脂（LF）饮食3周后，测量口服和静脉注射葡萄糖（1 g/kg体重）后的葡萄糖和胰岛素反应。HF饮食导致口服和静脉注射葡萄糖后葡萄糖耐量受损和胰岛素抵抗；口服葡萄糖后的影响更明显。为了了解食用HF饮食后葡萄糖耐量受损的基础，还测量了肝葡萄糖激酶的活性和肠道葡萄糖摄取率。口服而非静脉给药导致的葡萄糖耐量更严重受损，并非由肠道葡萄糖摄取率增加所致。事实上，HF大鼠空肠葡萄糖摄取率有小幅但显著的降低。然而，HF大鼠肝葡萄糖激酶活性大幅降低与肝葡萄糖摄取能力下降一致，这可能是导致葡萄糖耐量受损的重要原因。HF饮食对葡萄糖胰岛素反应的影响在口服葡萄糖后比静脉注射葡萄糖后更明显。这表明HF饮食可能刺激了肠胰岛轴。然而，也有可能是HF大鼠口服葡萄糖后循环胰岛素水平特别高，是对高血糖的直接反应，继发于葡萄糖清除减少。
