Eskelson C D, Stiffel V, Owen J A, Chvapil M, Vickers A, Brendel K
Department of Surgery, University of Arizona Health Sciences Center, Tucson 85724.
Life Sci. 1988;42(15):1455-67. doi: 10.1016/0024-3205(88)90056-2.
The esterified (E) and nonesterified (NE) fatty acid level and profile in the lung, serum, and liver of rats are significantly altered after intratracheal administration of silica. The changes include a silica-specific increase of the total long chain (C16-C20:4) fatty acid content in the lung, and a decrease in the serum and liver of both groups of rats intratracheally given silica and/or saline. In the silicotic lung, arachidonate and palmitate accumulated at the highest rate. A heat-labile, high-molecular weight component from lung homogenates increases lipogenesis in isolated hepatocytes in vitro. These findings, taken together with evidence indicating increased lipogenesis in the liver of rats treated with silica under identical conditions, suggest a lung-liver communication mechanism which coordinates lipid uptake by the lung and lipid synthesis and release by the liver. The stimulatory factor identified in lung homogenates might play an important regulatory role-for hepatic lipogenesis in rats developing silicotic lungs.
经气管内注入二氧化硅后，大鼠肺、血清和肝脏中酯化（E）和非酯化（NE）脂肪酸的水平及组成会发生显著变化。这些变化包括：肺中总长链（C16 - C20:4）脂肪酸含量出现二氧化硅特异性增加，而气管内给予二氧化硅和/或生理盐水的两组大鼠的血清和肝脏中该含量均下降。在矽肺的肺组织中，花生四烯酸和棕榈酸的积累速率最高。肺匀浆中一种热不稳定的高分子量成分可在体外增加分离的肝细胞中的脂肪生成。这些发现，再加上有证据表明在相同条件下用二氧化硅处理的大鼠肝脏中脂肪生成增加，提示存在一种肺 - 肝通讯机制，该机制可协调肺对脂质的摄取以及肝脏对脂质的合成和释放。在肺匀浆中鉴定出的刺激因子可能对患矽肺大鼠的肝脏脂肪生成起重要调节作用。
