Oscarsson J, Ottosson M, Edén S
Department of Physiology, University of Göteborg, Sweden.
J Endocrinol Invest. 1999;22(5 Suppl):2-9.
Lipoprotein lipase (LPL) is a key enzyme in the regulation of the flux of fatty acids. LPL hydrolyses triglycerides in chylomicrons and very-low-density lipoproteins (VLDL), forming intermediate- (IDL) and low-density lipoproteins (LDL). Hepatic lipase (HL) is a related enzyme with a more restricted tissue distribution than LPL; HL is mainly engaged in the turnover of IDL and of high-density lipoproteins (HDL). Both enzymes can be released from their endothelial sites by heparin and their activities measured separately in post-heparin plasma (PHP). The PHP-LPL activity decreases in hypophysectomized rats and this effect is reversed by growth hormone (GH) therapy. However, GH seems to have no effect, or an inhibitory effect, on PHP-LPL activity in humans. Muscle and adipose tissues are the main sources of PHP-LPL activity. One week of GH therapy of hypophysectomized rats increases skeletal muscle and heart LPL activity. In this model, GH has little or no effect on LPL activity in adipose tissue. However, GH has been shown to decrease LPL activity in isolated rat adipose tissue. Insulin-like growth factor-I therapy decreases and insulin therapy increases LPL activity in adipose tissue of hypophysectomized rats, whereas these therapies have no effect on LPL activity in muscle tissue. The LPL activity in human adipose tissue is reduced both in vivo and in vitro after administration of GH while the LPL mRNA level is unchanged. The effect of GH on HL activity has been studied in PHP and liver. Several studies in the rat indicate that GH increases PHP-HL and liver HL activity, at least partly at the level of mRNA expression. In humans, GH has been shown to have variable effects on PHP-HL activity; this variability is probably to some extent dependent on different experimental set-ups. Although GH therapy increases hepatic secretion of VLDL, serum triglyceride levels decrease as a result of GH therapy in the hypophysectomized rat. An increase in HL and LPL activity by GH therapy is in line with these findings. In summary, GH is involved in the regulation of both LPL and HL activity but the effects and mechanisms of action of GH in the regulation of LPL and HL activity in different tissues are not yet fully elucidated.
脂蛋白脂肪酶（LPL）是调节脂肪酸通量的关键酶。LPL水解乳糜微粒和极低密度脂蛋白（VLDL）中的甘油三酯，形成中间密度脂蛋白（IDL）和低密度脂蛋白（LDL）。肝脂肪酶（HL）是一种相关酶，其组织分布比LPL更局限；HL主要参与IDL和高密度脂蛋白（HDL）的代谢。两种酶都可被肝素从其内皮部位释放出来，并可在肝素后血浆（PHP）中分别测量其活性。垂体切除大鼠的PHP-LPL活性降低，生长激素（GH）治疗可逆转这种效应。然而，GH似乎对人类的PHP-LPL活性没有影响，或有抑制作用。肌肉和脂肪组织是PHP-LPL活性的主要来源。对垂体切除大鼠进行一周的GH治疗可增加骨骼肌和心脏的LPL活性。在这个模型中，GH对脂肪组织中的LPL活性几乎没有影响或没有影响。然而，已证明GH可降低离体大鼠脂肪组织中的LPL活性。胰岛素样生长因子-I治疗可降低垂体切除大鼠脂肪组织中的LPL活性，胰岛素治疗可增加其活性，而这些治疗对肌肉组织中的LPL活性没有影响。给予GH后，人体脂肪组织中的LPL活性在体内和体外均降低，而LPL mRNA水平不变。已在PHP和肝脏中研究了GH对HL活性的影响。在大鼠中的几项研究表明，GH可增加PHP-HL和肝脏HL活性，至少部分是在mRNA表达水平上。在人类中，已证明GH对PHP-HL活性有不同的影响；这种变异性可能在某种程度上取决于不同的实验设置。尽管GH治疗可增加VLDL的肝脏分泌，但垂体切除大鼠接受GH治疗后血清甘油三酯水平会降低。GH治疗导致HL和LPL活性增加与这些发现一致。总之，GH参与LPL和HL活性的调节，但GH在不同组织中调节LPL和HL活性的作用和机制尚未完全阐明。
