BRAIN LIPOPROTEIN-LIPASE IS RESPONSIVE TO NUTRITIONAL AND HORMONAL MODULATION
BRAIN LIPOPROTEIN-LIPASE IS RESPONSIVE TO NUTRITIONAL AND HORMONAL MODULATION
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DOI：
10.1016/0026-0495(87)90124-7
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发表时间：
1987-10-01
影响因子：
9.8
通讯作者：
GULLI, R
中科院分区：
文献类型：
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作者：
GAVIN, LA;CAVALIERI, RR;GULLI, R
最近在大鼠脑中描述了功能性脂蛋白脂肪酶活性。本研究旨在进一步表征脑脂蛋白脂肪酶（肝素释放成分）的生物学意义，并阐明其调控因子。对空腹和糖尿病大鼠（链脲佐菌素100 mg/kg BW IP）组织（脑、脂肪和心脏）肝素释放脂蛋白脂肪酶进行了比较研究。空腹（96小时）和糖尿病（10天）均显著降低脑（皮质）（P < 0.05）和脂肪（附睾脂肪垫）（P < 0.001）脂蛋白脂肪酶活性。相比之下，空腹和糖尿病组心肌酶活性显著升高（P < 0.001）。再喂养（96小时嘌呤食物）和胰岛素替代（96小时）分别逆转了禁食和糖尿病引起的组织脂蛋白脂肪酶的变化。血清胰岛素浓度变化与脂肪脂蛋白脂肪酶变化呈正相关，与脑、心脂蛋白脂肪酶变化无相关性。此外，虽然T3治疗使与禁食和糖尿病相关的低T3状态正常化，但它对研究组织中的酶活性没有影响。然而，随后的研究表明，甲状腺功能减退（甲状腺切除术后2周）显著降低脑脂蛋白脂肪酶活性（P < 0.001），增加脂肪酶（P < 0.025）和心脏酶（P < 0.025）活性。T3置换（0.8 .亩）g/100 BW/d，持续1周)逆转甲状腺功能减退的影响。然而，脑酶活性与血清T3之间的关系是非线性的，因为甲亢倾向于降低脑LPL活性。这些研究表明，大鼠皮质肝素释放脂蛋白脂肪酶对禁食、糖尿病和甲状腺功能减退有反应。虽然胰岛素和T3分别逆转了糖尿病和甲状腺功能减退对皮质LPL的影响，但激素对酶活性的直接影响还有待于进一步的体外研究。脑和脂肪LPL对禁食和糖尿病的反应是一致的，而甲状腺功能减退对各自酶反应的影响是不一致的。本研究提示皮质脂蛋白可能在脑脂质代谢中发挥重要作用。
Functional lipoprotein lipase activity was recently described in rat brain. The present study was performed to further characterize the biologic significance of brain lipoprotein lipase (heparin releasable component) and elucidate regulatory factors. Comparative studies were performed on tissue (brain, adipose, and heart) heparin releasable lipoprotein lipase in the fasted and diabetic (streptozotocin 100 mg/kg BW IP) rat. Both fasting (96 hours) and diabetes (ten days) significantly decreased brain (cortical) (P < .05) and adipose (epididymal fat pad) (P < .001) lipoprotein lipase activity. In contrast, heart muscle enzyme activity was significantly increased (P < .001) in response to fasting and diabetes. Refeeding (Purine chow 96 hours) and insulin replacement (96 hours) reversed these changes in tissue lipoprotein lipase consequent to fasting and diabetes, respectively. There was a positive correlation between the changes in serum insulin concentration and adipose lipoprotein lipase, but there was no correlation between this parameter and brain or heart lipoprotein lipase. In addition, although T3 therapy normalized the low T3 state associated with both fasting and diabetes, it had no effect on the enzyme activity in the studied tissues. However, subsequent studies demonstrated that hypothyroidism (2 weeks post thyroidectomy) significantly decreased brain lipoprotein lipase activity (P < .001) and increased both the adipose (P < .025) and heart (P < .025) enzyme activity. T3 replacement (0.8 .mu.g/100 BW/d for 1 week) reversed the effects of hypothyroidism. However, the relationship between brain enzyme activity and serum T3 was nonlinear as hyperthyroidism tended to reduce brain LPL activity. These studies demonstrate that rat cortex heparin releasable lipoprotein lipase is responsive to fasting, diabetes, and hypothyroidism. Although both insulun and T3 reversed, respectively, the effects of diabetes and hypothyroidism on cortex LPL, confirmation of direct hormone effects on enzyme activity must await future in vitro studies. The brain and adipose LPL response to fasting and diabetes was concordant, whereas the effect of hypothyroidism on the respective enzymatic responses was discordant. This study does indicate that cortical lipoprotein could play an important role in brain lipid metabolism.