Jones B H, Standridge M K, Taylor J W, Moustaïd N
Physiology Program, University of Tennessee, Knoxville 37996-1900, USA.
Am J Physiol. 1997 Jul;273(1 Pt 2):R236-42. doi: 10.1152/ajpregu.1997.273.1.R236.
Synthesis of angiotensin II (ANG II) has recently been described in adipose cells and has been linked to regulation of adiposity. Angiotensinogen (AGT), the substrate from which ANG II is formed, was previously shown to be elevated in adipose tissue of obese (ob/ob and db/db) mice and regulated by nutritional manipulation. It is unknown, however, whether overexpression of adipose AGT can be extended to other models of obesity and whether hormonal and/or nutritional factors directly regulate AGT expression in adipocytes. We investigated these possibilities by analyzing AGT mRNA levels in adipose tissue of obese Zucker rats, viable yellow (Avy) mice, and humans and by treating 3T3-L1 adipocytes with insulin, glucose, and a beta-adrenergic agonist. We demonstrate that AGT mRNA is decreased by approximately 50 and 80%, respectively, in adipose tissue of obese vs. lean Zucker rats and Avy mice. We also report that AGT is expressed at variable levels in human adipose tissue. Finally, we show that AGT mRNA is upregulated by insulin and downregulated by beta-adrenergic stimulation in adipocytes.
最近在脂肪细胞中发现了血管紧张素II（ANG II）的合成，并且其与肥胖的调节有关。血管紧张素原（AGT）是形成ANG II的底物，先前已证明在肥胖（ob/ob和db/db）小鼠的脂肪组织中其水平升高，并受营养调控。然而，尚不清楚脂肪AGT的过表达是否能扩展到其他肥胖模型，以及激素和/或营养因素是否直接调节脂肪细胞中AGT的表达。我们通过分析肥胖Zucker大鼠、存活黄色（Avy）小鼠和人类脂肪组织中的AGT mRNA水平，以及用胰岛素、葡萄糖和β-肾上腺素能激动剂处理3T3-L1脂肪细胞来研究这些可能性。我们证明，与瘦的Zucker大鼠和Avy小鼠相比，肥胖大鼠和Avy小鼠脂肪组织中的AGT mRNA分别降低了约50%和80%。我们还报告说，AGT在人类脂肪组织中的表达水平各不相同。最后，我们表明胰岛素可上调脂肪细胞中AGT mRNA的表达，而β-肾上腺素能刺激则使其下调。
