Karlsson C, Lindell K, Ottosson M, Sjöström L, Carlsson B, Carlsson L M
Research Centre for Endocrinology and Metabolism, Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
J Clin Endocrinol Metab. 1998 Nov;83(11):3925-9. doi: 10.1210/jcem.83.11.5276.
Angiotensin II regulates blood pressure and may affect adipogenesis and adipocyte metabolism. Angiotensin II is produced by cleavage of angiotensinogen by renin and angiotensin-converting enzyme in the circulation. In addition, angiotensin II may be produced in various tissues by enzymes of the renin-angiotensin system (RAS) or the nonrenin-angiotensin system (NRAS). We have analyzed the expression of angiotensinogen and enzymes required for its conversion to angiotensin II in human adipose tissue. Northern blot demonstrated angiotensinogen expression in adipose tissue from nine obese subjects. Western blot revealed a distinct band of expected size of the angiotensinogen protein (61 kDa) in isolated adipocytes. RT-PCR, followed by Southern blot, demonstrated renin expression in human adipose tissue. Angiotensin-converting enzyme messenger RNA was detected by RT-PCR, and the identity of the PCR products was verified by restriction enzyme cleavage. Transcripts for cathepsin D and cathepsin G, components of the NRAS, were detected by RT-PCR, verified by restriction enzyme cleavage. We conclude that human adipose tissue expresses angiotensinogen and enzymes of RAS and NRAS. This opens the possibility that angiotensinogen-derived peptides, produced in adipose tissue itself, may affect adipogenesis and play a role in the pathogenesis of obesity.
血管紧张素II调节血压,并可能影响脂肪生成和脂肪细胞代谢。血管紧张素II是由肾素和血管紧张素转换酶在循环中裂解血管紧张素原产生的。此外,血管紧张素II可能由肾素-血管紧张素系统(RAS)或非肾素-血管紧张素系统(NRAS)的酶在各种组织中产生。我们分析了血管紧张素原及其转化为血管紧张素II所需酶在人脂肪组织中的表达。Northern印迹法显示了9名肥胖受试者脂肪组织中血管紧张素原的表达。Western印迹法在分离的脂肪细胞中显示出一条预期大小的血管紧张素原蛋白(61 kDa)的明显条带。RT-PCR后进行Southern印迹法,证明了肾素在人脂肪组织中的表达。通过RT-PCR检测到血管紧张素转换酶信使RNA,并通过限制性内切酶切割验证了PCR产物的同一性。通过RT-PCR检测到NRAS的组织蛋白酶D和组织蛋白酶G的转录本,并通过限制性内切酶切割进行了验证。我们得出结论,人脂肪组织表达血管紧张素原以及RAS和NRAS的酶。这开启了一种可能性,即脂肪组织自身产生的血管紧张素原衍生肽可能影响脂肪生成并在肥胖发病机制中起作用。