Butzner J D, Brockway P D, Meddings J B
Gastrointestinal Research Group, University of Calgary, Alberta, Canada.
Am J Physiol. 1990 Dec;259(6 Pt 1):G940-6. doi: 10.1152/ajpgi.1990.259.6.G940.
We examined sodium-dependent glucose transport, membrane lipid composition, and membrane fluidity in microvillus membrane vesicles isolated from the distal intestine of infant rabbits subjected to protein-energy malnutrition and age-matched controls. In vesicles from malnourished animals, sodium-dependent glucose transport was significantly enhanced, as evidenced by a twofold increase in maximal transport capacity, Jmax. Carrier affinity for glucose, as assessed by the Km of the transport process, was unaffected. These alternations were associated with marked changes in microvillus membrane composition. Malnourished animals had an increase in the lipid-to-protein ratio of the microvillus membrane, which suggests that malnutrition might be associated with either a reduction in membrane protein or an increase in membrane lipid. This would be expected to increase the fluidity of the microvillus membrane. However, we observed no differences in either the static or dynamic component of membrane fluidity, using multiple fluorescent probes, between dietary groups. Further analysis of membrane lipids was undertaken to establish whether quantitative differences in lipid subclasses could explain this discrepancy. We found that nutrient deprivation produced numerous alterations in membrane lipids. The major findings were an increase in both the cholesterol-to-phospholipid and phosphatidylethanolamine-to-phosphatidylcholine ratios. Both alterations would be expected to decrease membrane fluidity and presumably represent a compensatory response to the loss of membrane protein. Thus chronic postnatal protein-energy malnutrition initiates several adaptive responses that include major alterations in the chemical composition of the microvillus membrane. The resulting effect preserves efficient glucose transport and maintains the physical properties of the microvillus membrane.
我们检测了从患蛋白质-能量营养不良的幼兔远端肠道分离的微绒毛膜囊泡以及年龄匹配的对照动物的微绒毛膜囊泡中的钠依赖性葡萄糖转运、膜脂质组成和膜流动性。在营养不良动物的囊泡中，钠依赖性葡萄糖转运显著增强，最大转运能力Jmax增加了两倍就证明了这一点。通过转运过程的Km评估的载体对葡萄糖的亲和力未受影响。这些变化与微绒毛膜组成的显著改变有关。营养不良的动物微绒毛膜的脂质与蛋白质比率增加，这表明营养不良可能与膜蛋白减少或膜脂质增加有关。这有望增加微绒毛膜的流动性。然而，我们使用多种荧光探针观察到，不同饮食组之间在膜流动性的静态或动态成分上均无差异。对膜脂质进行了进一步分析，以确定脂质亚类的定量差异是否可以解释这种差异。我们发现营养剥夺导致膜脂质发生了许多变化。主要发现是胆固醇与磷脂的比率以及磷脂酰乙醇胺与磷脂酰胆碱的比率均增加。这两种变化都有望降低膜流动性，大概代表了对膜蛋白损失的一种补偿反应。因此，出生后慢性蛋白质-能量营养不良引发了几种适应性反应，包括微绒毛膜化学成分的重大改变。其结果是保持了高效的葡萄糖转运并维持了微绒毛膜的物理性质。
