Lee J J, Smith P J, Fried S K
Department of Nutritional Sciences, Cook College, Rutgers University, New Brunswick, NJ 08901-8525, USA.
J Nutr. 1998 Jun;128(6):940-6. doi: 10.1093/jn/128.6.940.
The aim of this study was to delineate the mechanisms by which varying periods of starvation decrease lipoprotein lipase (LPL) activity in rat adipose tissue. LPL mRNA levels and rates of LPL synthesis, degradation and secretion were compared in adipocytes from male rats that had been fed or starved for 1 or 3 d. The decreased LPL activity after 3 d of starvation (-76%) was explained mainly by a 50% decrease in the relative abundance of LPL mRNA levels (P < 0.05) and a parallel 50% decrease in relative rates of LPL biosynthesis (P < 0.05). In contrast, starvation for 1 d decreased total LPL activity by 47% (P < 0.05) but did not affect LPL mRNA levels or relative rates of LPL biosynthesis. Pulse-chase studies demonstrated that 1 d of starvation increased the rate of degradation of newly synthesized LPL (P < 0.05) and markedly decreased its secretion into the medium (P < 0.05). A decrease in overall protein synthesis also contributed to the decreased LPL activity after 1 and 3 d of starvation. We conclude that the relative importance of pre- and post-translational mechanisms in regulating adipose tissue LPL activity depends on the duration of starvation. During short-term starvation, degradation of newly synthesized LPL is an important determinant to its secretion from the adipocyte and hence its functional activity at the capillary endothelium.
本研究的目的是阐明饥饿不同时期降低大鼠脂肪组织中脂蛋白脂肪酶（LPL）活性的机制。比较了喂食或饥饿1天或3天的雄性大鼠脂肪细胞中LPL mRNA水平以及LPL合成、降解和分泌的速率。饥饿3天后LPL活性降低（-76%），主要原因是LPL mRNA水平相对丰度降低了50%（P < 0.05），LPL生物合成相对速率平行降低了50%（P < 0.05）。相比之下，饥饿1天使总LPL活性降低了47%（P < 0.05），但不影响LPL mRNA水平或LPL生物合成的相对速率。脉冲追踪研究表明，饥饿1天增加了新合成LPL的降解速率（P < 0.05），并显著降低了其向培养基中的分泌（P < 0.05）。整体蛋白质合成的减少也导致饥饿1天和3天后LPL活性降低。我们得出结论，翻译前和翻译后机制在调节脂肪组织LPL活性中的相对重要性取决于饥饿的持续时间。在短期饥饿期间，新合成LPL的降解是其从脂肪细胞分泌的重要决定因素，因此也是其在毛细血管内皮细胞功能活性的重要决定因素。
