Tissue-specific regulation of lipoprotein lipase by isoproterenol in normal-weight humans.
Tissue-specific regulation of lipoprotein lipase by isoproterenol in normal-weight humans.
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正常体重人群中异丙肾上腺素对脂蛋白脂肪酶的组织特异性调节。
DOI：
10.1152/ajpregu.1996.271.5.r1280
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Yost,TJ
中科院分区：
文献类型：
--
作者：
Eckel,RH;Jensen,DR;Schlaepfer,IR;Yost,TJ
脂蛋白脂肪酶 (LPL) 是一种水解酶，参与脂蛋白代谢和营养分配，并受到组织特异性调节。胰岛素对脂肪酶的不同调节的证据已得到证实，但 LPL 对儿茶酚胺的组织特异性反应的改变尚未在人体中进行研究。在输注 0（盐水）或 8 或 24 ng.kg-1.min-1 异丙肾上腺素的受试者中，在 2 小时内检查异丙肾上腺素（肾上腺素异丙基同系物）对人体臀部脂肪组织和股外侧肌中 LPL 的调节。向对照受试者输注生理盐水未能改变脂肪组织或骨骼肌 LPL 活性。然而，在注射生理盐水的受试者中，血浆去甲肾上腺素浓度的百分比变化与肌肉 LPL 活性的百分比变化之间呈正相关（r = 0.826，P < 0.05）。与输注盐水的对照组相比，输注异丙肾上腺素并没有改变脂肪组织或肌肉中的 LPL，但除了血浆葡萄糖、游离脂肪酸和甘油外，血浆胰岛素水平也有所增加。为了预防异丙肾上腺素引起的高胰岛素血症，采用了胰钳技术。肌肉 LPL 增加（P = 0.037），而脂肪组织 LPL 没有变化。输注 2 小时后肌肉 LPL 活性的变化与肌肉 mRNA 的变化相关（P = 0.021）。总体而言，这些研究表明，在人类中，LPL 对儿茶酚胺的反应是组织特异性的，对脂肪组织没有影响，但对骨骼肌有刺激作用。儿茶酚胺对肌肉中 LPL 的内源性调节在肌肉燃料代谢中可能很重要，并且可能与 LPL 基因水平上的 3',5'-环单磷酸腺苷和/或脂肪酸的影响有关。
Lipoprotein lipase (LPL) is a hydrolytic enzyme, involved in lipoprotein metabolism and nutrient partitioning, that is subject to tissue-specific regulation. Evidence for divergent regulation of the lipase by insulin has been demonstrated, but alterations in the tissue-specific response of LPL to catecholamines has not been studied in humans. The regulation of LPL in gluteal adipose tissue and vastus lateralis muscle by isoproterenol (epinephrine isopropyl homologue) in humans was examined over 2 h in subjects infused with 0 (saline) or 8 or 24 ng.kg-1.min-1 isoproterenol. The infusion of normal saline into control subjects failed to alter adipose tissue or skeletal muscle LPL activity. However, in the saline-infused subjects there was a positive correlation between the percent change in plasma norepinephrine concentrations and the percent change in muscle LPL activity (r = 0.826, P < 0.05). Isoproterenol infusion did not change LPL in either adipose tissue or muscle compared with saline-infused controls, but plasma insulin levels in addition to plasma glucose, free fatty acids, and glycerol were increased. To prevent the isoproterenol-induced hyperinsulinemia, a pancreatic clamp technique was utilized. An increase in muscle LPL was demonstrated (P = 0.037) with no change in adipose tissue LPL. The change in muscle LPL activity after the 2-h infusion correlated with the change in muscle mRNA (P = 0.021). Overall, these studies indicate that in humans the response of LPL to catecholamines is tissue specific with no effect in adipose tissue but a stimulation in skeletal muscle. Endogenous regulation of LPL in muscle by catecholamines could be important in muscle fuel metabolism and could relate to effects of adenosine 3',5'-cyclic monophosphate and/or fatty acids at the level of the LPL gene.