Fielder P J, Talamantes F
Endocrinology. 1987 Aug;121(2):493-7. doi: 10.1210/endo-121-2-493.
The lipolytic activities of three structurally related mouse hormones, placental lactogen II (mPL-II), GH (mGH), and PRL (mPRL), and human PL (hPL) were investigated. Adipose tissue was obtained from virgin and day 12 and day 16 pregnant mice. Lipolytic activity was assessed by the ability of the hormones to stimulate glycerol release from fat explants in the presence of dexamethasone and by the ability of the hormones to sensitize adipose tissue to the lipolytic stimulus theophylline. In the first experiment, adipose tissue explants were incubated in Krebs-Ringer buffer with 0.0, 0.1, 0.5, 1.0, 5.0, and 10.0 micrograms/ml hormone for 4 h. mGH was lipolytic at a concentration of 0.5 micrograms/ml or greater in adipose tissue from both virgin and pregnant mice. mPRL was lipolytic at a concentration of 5.0 micrograms/ml or greater in adipose tissue from virgin mice. In adipose tissue from pregnant mice mPRL was not lipolytic in day 12 tissue, but it was lipolytic at a concentration of 5.0 micrograms/ml in day 16 tissue. mPL-II and hPL did not stimulate glycerol release in mouse adipose tissue from virgin or pregnant mice. In the second experiment preincubating adipose tissue from virgin mice in the presence of 0.5 or 5.0 micrograms/ml mGH significantly increased the ability of the tissue to respond to theophylline; however, mGH did not induce this response in adipose tissue from pregnant mice, mPRL, mPL-II, and hPL did not increase theophylline-induced lipolysis in adipose tissue from either virgin or pregnant mice. These results indicate that two lipolytic mechanisms are activated in adipose tissue from mice; mGH can activate both mechanisms, whereas mPRL can activate only one.
对三种结构相关的小鼠激素,即胎盘催乳素II(mPL-II)、生长激素(mGH)和催乳素(mPRL)以及人胎盘催乳素(hPL)的脂解活性进行了研究。脂肪组织取自未孕小鼠以及妊娠第12天和第16天的小鼠。通过在存在地塞米松的情况下激素刺激脂肪外植体释放甘油的能力以及激素使脂肪组织对脂解刺激物茶碱敏感的能力来评估脂解活性。在第一个实验中,将脂肪组织外植体在含有0.0、0.1、0.5、1.0、5.0和10.0微克/毫升激素的 Krebs-Ringer 缓冲液中孵育4小时。在未孕和妊娠小鼠的脂肪组织中,mGH在浓度为0.5微克/毫升或更高时具有脂解作用。mPRL在未孕小鼠脂肪组织中浓度为5.0微克/毫升或更高时具有脂解作用。在妊娠小鼠的脂肪组织中,mPRL在第12天的组织中无脂解作用,但在第16天的组织中浓度为5.0微克/毫升时具有脂解作用。mPL-II和hPL在未孕或妊娠小鼠的脂肪组织中均未刺激甘油释放。在第二个实验中,在0.5或5.0微克/毫升mGH存在下预孵育未孕小鼠的脂肪组织,显著增加了组织对茶碱的反应能力;然而,mGH在妊娠小鼠的脂肪组织中未诱导这种反应,mPRL、mPL-II和hPL在未孕或妊娠小鼠的脂肪组织中均未增加茶碱诱导的脂解作用。这些结果表明,小鼠脂肪组织中激活了两种脂解机制;mGH可激活两种机制,而mPRL仅能激活一种。