Ong J M, Simsolo R B, Saghizadeh M, Goers J W, Kern P A
Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Metabolism. 1995 Dec;44(12):1596-605. doi: 10.1016/0026-0495(95)90081-0.
Lipoprotein lipase (LPL) is found in adipose tissue and muscle, and is important for the uptake of triglyceride-rich lipoproteins from plasma. This study examined the regulation of LPL in adipose tissue and muscle by exercise training in combination with the fed or fasted state. After training male rats on a treadmill for 6 weeks, LPL activity, mass, and mRNA levels were measured in adipose tissue, heart, soleus, and extensor digitorum longus (EDL) muscles and compared with levels in sedentary rats. Tissue LPL was measured as the heparin-released (HR) and cellular-extracted (EXT) fractions 16 hours following the last bout of exercise, during which time some animals were fasted and others were allowed free access to food. Training led to an increase in HR LPL activity and LPL protein mass in soleus and EDL, but had no effort on adipose tissue and heart LPL. The increase in soleus LPL with exercise was in the HR fraction only, whereas the increase in EDL LPL with training was in both the HR and EXT fractions. All these changes in LPL activity were accompanied by similar changes in LPL immunoreactive mass. However, there were no changes in LPL mRNA levels with training. Feeding induced a large increase in adipose tissue LPL activity and mass in both the HR and EXT fractions: however, there was no change in mRNA levels. In heart, feeding yielded a decrease in HR but no consistent change in EXT activity or mass, and a consistent decrease in mRNA levels. As compared with control rats, trained rats demonstrated different responses to feeding in all tissues, especially in soleus and EDL. Whereas feeding had no effect on LPL in soleus and EDL of control rats, feeding induced a decrease in HR and EXT LPL in the soleus of trained rats. In addition, feeding yielded a significant decrease in EXT LPL of the EDL of trained rats. Thus, these data demonstrate that adipose tissue and heart LPL are highly regulated by feeding and are not responsive to long-term exercise training. On the other hand, skeletal muscle LPL is increased in trained rats, but this increase is blunted considerably by feeding following the last bout of exercise. These changes in LPL activity and mass are mostly unaccompanied by changes in LPL mRNA levels, demonstrating that much physiologic regulation occurs posttranscriptionally.
脂蛋白脂肪酶（LPL）存在于脂肪组织和肌肉中，对从血浆中摄取富含甘油三酯的脂蛋白很重要。本研究通过结合进食或禁食状态下的运动训练，考察了脂肪组织和肌肉中LPL的调节情况。在跑步机上训练雄性大鼠6周后，测量脂肪组织、心脏、比目鱼肌和趾长伸肌（EDL）肌肉中的LPL活性、质量和mRNA水平，并与久坐不动的大鼠进行比较。在最后一次运动后16小时，将组织LPL测定为肝素释放（HR）和细胞提取（EXT）部分，在此期间，一些动物禁食，另一些动物可自由进食。训练导致比目鱼肌和EDL中HR LPL活性和LPL蛋白质量增加，但对脂肪组织和心脏LPL无影响。运动后比目鱼肌LPL的增加仅在HR部分，而训练后EDL LPL的增加在HR和EXT部分均有。LPL活性的所有这些变化都伴随着LPL免疫反应性质量的类似变化。然而，训练后LPL mRNA水平没有变化。进食导致脂肪组织LPL活性和质量在HR和EXT部分均大幅增加：然而，mRNA水平没有变化。在心脏中，进食导致HR降低，但EXT活性或质量没有一致变化，mRNA水平持续降低。与对照大鼠相比，训练大鼠在所有组织中对进食表现出不同反应，尤其是在比目鱼肌和EDL中。虽然进食对对照大鼠比目鱼肌和EDL中的LPL没有影响，但进食导致训练大鼠比目鱼肌中HR和EXT LPL降低。此外，进食使训练大鼠EDL中的EXT LPL显著降低。因此，这些数据表明，脂肪组织和心脏LPL受进食高度调节，对长期运动训练无反应。另一方面，训练大鼠骨骼肌LPL增加，但在最后一次运动后进食会使这种增加显著减弱。LPL活性和质量的这些变化大多不伴随LPL mRNA水平的变化，表明许多生理调节发生在转录后。
