Rannels D E, Sahms R H, Watkins C A
Am J Physiol. 1979 Apr;236(4):E421-8. doi: 10.1152/ajpendo.1979.236.4.E421.
Metabolism of lung proteins was investigated in rats starved 3 days or made diabetic with streptozotocin. Body weight was below normal in both groups, but lung weight decreased only in starved animals. Total lung protein and RNA (mg/lung) decreased during starvation and diabetes. Protein concentration (mg/g) was unchanged in either group of animals; RNA concentration decreased only during starvation. Protein synthesis, estimated in lungs perfused in situ, was reduced 22% in starvation, but remained unchanged in diabetes. Inhibition of protein synthesis was accounted for by loss of RNA. Ribosomal profiles were unchanged by starvation, suggesting an unaltered relationship between rates of peptide-chain initiation and elongation in vivo. Activity of an eIF-2-like initiation factor decreased during starvation in proportion to the loss of RNA. In diabetes, factor activity remained normal. Thus, starvation but not streptozotocin-induced diabetes, reduced the capacity of the lung to synthesize protein. No evidence for reduced efficiency of synthesis was observed.
对饥饿3天或用链脲佐菌素诱导糖尿病的大鼠的肺蛋白代谢进行了研究。两组动物的体重均低于正常水平,但只有饥饿动物的肺重量下降。饥饿和糖尿病期间,肺总蛋白和RNA(mg/肺)减少。两组动物的蛋白质浓度(mg/g)均未改变;仅在饥饿期间RNA浓度下降。通过原位灌注肺来估计的蛋白质合成,在饥饿时减少了22%,但在糖尿病时保持不变。蛋白质合成的抑制是由RNA的损失引起的。饥饿对核糖体图谱没有影响,这表明体内肽链起始和延伸速率之间的关系未改变。一种类似eIF-2的起始因子的活性在饥饿期间随着RNA的损失而按比例下降。在糖尿病中,该因子活性保持正常。因此,饥饿而非链脲佐菌素诱导的糖尿病降低了肺合成蛋白质的能力。未观察到合成效率降低的证据。