EFFECT OF SHORT-TERM CONSUMPTION OF A HIGH-FAT DIET ON GLUCOSE-TOLERANCE AND INSULIN SENSITIVITY IN THE RAT
EFFECT OF SHORT-TERM CONSUMPTION OF A HIGH-FAT DIET ON GLUCOSE-TOLERANCE AND INSULIN SENSITIVITY IN THE RAT
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DOI：
10.3177/jnsv.33.377
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发表时间：
1987-10-01
影响因子：
1.6
通讯作者：
ODEA, K
中科院分区：
文献类型：
--
作者：
CHISHOLM, KW;ODEA, K
高脂肪、低碳水化合物饮食损害葡萄糖耐量和降低胰岛素敏感性的机制尚不清楚。为了澄清这一问题，在喂食高脂肪（HF: 66%能量为脂肪）或低脂肪（LF: 12%能量为脂肪）两周后，对大鼠的肝脏和骨骼肌静脉内葡萄糖耐量和胰岛素作用进行了检测。两种饲粮的P/S比（多不饱和脂肪与饱和脂肪之比）均为1.3。高脂肪饮食导致静脉葡萄糖耐量轻度损害。在持续胰岛素反应的情况下，餐后血糖水平升高。体外胰岛素刺激下HF大鼠比目鱼肌的葡萄糖利用明显减少，这表明[14C]葡萄糖掺入肌糖原减少。相反，葡萄糖的肌肉脂肪生成不受饮食成分的影响。HF和LF大鼠的胰岛素与比目鱼肌的结合没有差异，表明胰岛素受体结合与受体后代谢事件之间存在解离。在体内，饮食成分不影响增加的[14C]葡萄糖负荷并入肌糖原或脂质。然而，HF饮食与[14C]葡萄糖在肝脏脂质和糖原中的掺入减少有关，并且在较小程度上减少了体内脂肪组织脂质的掺入。这些结果表明，HF饮食损害糖耐量的机制主要来自肝脏。葡萄糖摄取减少，继发于葡萄糖激酶活性降低，可能导致肝脏葡萄糖利用减少。
The mechanism by which the consumption of high fat, low carbohydrate diets impair glucose tolerance and decrease insulin sensitivity is poorly understood. In an attempt to clarify this question, intravenous glucose tolerance and insulin action in the liver and skeletal muscle were examined in rats after two weeks feeding of either a high fat (HF: 66% energy as fat) or a low fat (LF: 12% energy as fat) diet. Both diets had a P/S ratio (ratio of polyunsaturated to saturated fat in the diet) of 1.3. The high fat diet resulted in mild impairment of intravenous glucose tolerance. Postprandial glucose levels were elevated in the presence of a sustained insulin response. In vitro insulin-stimulated glucose utilization was decreased significantly in soleus muscle of HF rats, as indicated by decreased [14C]glucose incorporation into muscle glycogen. In contrast, muscle lipogenesis from glucose was not affected by dietary composition. There was no difference in insulin binding to soleus muscle of HF and LF rats, indicating a dissociation between insulin receptor binding and post-receptor metabolic events. Dietary composition did not influence the incorporation of increasing [14C]glucose loads into muscle glycogen or lipid in vivo. However, the HF diet was associated with reduced incorporation of [14C]glucose into lipids and glycogen in the liver and, to a smaller extent, reduced incorporation into adipose tissue lipids in vivo. These results suggest that the mechanism by which HF diets impaired glucose tolerance was mainly hepatic in origin. Decreased glucose uptake, secondary to reduced glucokinase activity, may result in a reduction in glucose utilization in the liver.