Shiau Y F, Holtzapple P G
Am J Physiol. 1980 Apr;238(4):E364-70. doi: 10.1152/ajpendo.1980.238.4.E364.
We have previously shown that glucose metabolism plays an important role in modifying intestinal fatty acid esterification. Because it is well known that glucose metabolism is under insulin regulation, we examined the effect of insulin on intestinal fatty acid esterification. Insulin pretreatment led to a marked decrease in in vitro intestinal fatty acid esterification, but this decrease was abolished by maintaining blood glucose above 80 mg/dl. Addition of insulin to the incubation medium failed to produce any effect on intestinal fatty acid esterification. The decreased fatty acid esterification on hypoglycemic rats was not associated with changes in fatty acid uptake or lipid esterifying enzyme activities. However, there was a significant increase in the production of volatile metabolites of fatty acid. We conclude that 1) insulin itself has no effect on intestinal fatty acid esterification, 2) the effects observed in this study are due to insulin-induced hypoglycemia, 3) hypoglycemia does not alter intestinal fatty acid uptake or intrinsic esterification activity, but leads to preferential oxidation rather than esterification of fatty acid by the small intestine, and 4) the critical blood glucose concentration needed to maintain normal esterification in the rat was approximately at 80 mg/dl.
我们之前已经表明,葡萄糖代谢在调节肠道脂肪酸酯化过程中发挥着重要作用。由于众所周知葡萄糖代谢受胰岛素调控,我们研究了胰岛素对肠道脂肪酸酯化的影响。胰岛素预处理导致体外肠道脂肪酸酯化显著降低,但通过将血糖维持在80mg/dl以上,这种降低被消除。向孵育培养基中添加胰岛素未能对肠道脂肪酸酯化产生任何影响。低血糖大鼠脂肪酸酯化的降低与脂肪酸摄取或脂质酯化酶活性的变化无关。然而,脂肪酸挥发性代谢产物的产生显著增加。我们得出以下结论:1)胰岛素本身对肠道脂肪酸酯化没有影响;2)本研究中观察到的效应是由胰岛素诱导的低血糖所致;3)低血糖不会改变肠道脂肪酸摄取或内在酯化活性,但会导致小肠优先氧化而非酯化脂肪酸;4)维持大鼠正常酯化所需的临界血糖浓度约为80mg/dl。