Department of Food Science and Nutrition, The Catholic University of Korea, Bucheon, South Korea.
J Physiol Biochem. 2010 Sep;66(3):197-203. doi: 10.1007/s13105-010-0024-8. Epub 2010 Jun 10.
Clenbuterol, a beta(2)-adrenergic receptor (beta(2)-AR) selective agonist, has been shown to decrease body fat in animals and can induce apoptosis in adipose tissue in mice. We hypothesized that direct actions of a beta-adrenergic receptor agonist on adipocytes could trigger the observed apoptotic effect. The hypothesis was inspected by investigating the direct effect of clenbuterol on apoptosis, adipogenesis, and lipolysis in vitro using the 3T3-L1 cell line and rat primary adipocytes. Cells were treated with 10(-9) to 10(-5) M clenbuterol depending on the experiments. There was no apoptotic effect of clenbuterol both in 3T3-L1 cells and rat primary adipocytes. Adipogenesis monitored by Oil Red O staining and AdipoRed assay was modestly decreased by clenbuterol treatment (p < 0.05). In fully differentiated primary adipocytes, clenbuterol increased basal lipolysis compared with the control (p < 0.01). In summary, direct stimulation of beta(2)-AR by clenbuterol does not cause apoptosis in adipocytes, despite a direct lipolytic stimulation and attenuation of adipogenesis.
克仑特罗，一种β2-肾上腺素能受体（β2-AR）选择性激动剂，已被证明可减少动物体脂肪，并可诱导小鼠脂肪组织凋亡。我们假设β-肾上腺素能受体激动剂对脂肪细胞的直接作用可能触发观察到的凋亡效应。该假设通过使用 3T3-L1 细胞系和大鼠原代脂肪细胞在体外研究克仑特罗对凋亡、脂肪生成和脂肪分解的直接作用来检验。根据实验，细胞用 10-9 到 10-5 M 的克仑特罗处理。在 3T3-L1 细胞和大鼠原代脂肪细胞中，克仑特罗均无凋亡作用。用油红 O 染色和 AdipoRed 测定法监测脂肪生成，克仑特罗处理使脂肪生成适度减少（p < 0.05）。在完全分化的原代脂肪细胞中，与对照相比，克仑特罗增加了基础脂肪分解（p < 0.01）。总之，尽管直接刺激β2-AR 可引起脂肪细胞的直接脂肪分解刺激和脂肪生成减弱，但不会导致脂肪细胞凋亡。
