Krähenbühl L, Bürgi U
University Clinic of Internal Medicine, Inselspital, Bern, Switzerland.
Horm Metab Res Suppl. 1987;17:20-2.
The decreased basal and catecholamine stimulated lipolysis in adipocytes from hypothyroid rats can be increased by thyroid hormone (TH) treatment. In the present study it was investigated whether this TH effect is mediated via nuclear receptors and synthesis of new proteins or via other mechanisms. Epinephrine stimulated lipolysis was measured in vitro in isolated white adipocytes. Decreased lipolysis in adipocytes from hypothyroid rats was increased to euthyroid levels when the animals received one dose of 15 micrograms triiodothyronine (T3)/100 g body weight (BW) iv 15 h before the adipocytes were prepared for the in vitro measurement of lipolysis. No effect of T3 on lipolysis could be seen when the T3 was given only 10 min. before obtaining adipose tissue for the in vitro measurements. The stimulation of lipolysis several hours after the administration of T3 could be abolished by the protein synthesis blocker cycloheximide. These data and our previous demonstration of nuclear T3 receptors in rat adipocytes are compatible with the assumption that the enhancement of lipolysis by TH is mediated via a mechanism involving nuclear TH receptors and synthesis of new proteins.
甲状腺功能减退大鼠脂肪细胞中基础脂解和儿茶酚胺刺激的脂解作用降低,甲状腺激素(TH)治疗可使其增加。在本研究中,研究了这种TH效应是通过核受体和新蛋白质的合成介导,还是通过其他机制介导。在体外测定分离的白色脂肪细胞中肾上腺素刺激的脂解作用。当动物在制备用于体外脂解测量的脂肪细胞前15小时静脉注射一剂15微克三碘甲状腺原氨酸(T3)/100克体重(BW)时,甲状腺功能减退大鼠脂肪细胞中降低的脂解作用增加到甲状腺功能正常水平。当仅在获取用于体外测量的脂肪组织前10分钟给予T3时,未观察到T3对脂解的影响。蛋白质合成阻断剂环己酰亚胺可消除T3给药数小时后对脂解的刺激作用。这些数据以及我们之前在大鼠脂肪细胞中证明的核T3受体与以下假设一致,即TH对脂解的增强作用是通过涉及核TH受体和新蛋白质合成的机制介导的。