血管紧张素原,血管紧张素II和脂肪组织发育。

G Ailhaud, A Fukamizu, F Massiera, R Negrel, P Saint-Marc, M Teboul
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引用次数: 100

摘要

脂肪组织是血管紧张素原(AGT)的重要来源。最近的证据表明,局部肾素血管紧张素原系统(RAS)存在于人体脂肪组织中,可能与血浆RAS不同。在肥胖患者中,由于脂肪组织分泌的血浆AGT增加,血管紧张素II (angII)参与了高血压的发展。AGT通过angII在脂肪组织发育中的另一个作用得到以下支持:(i)在体外,angII刺激脂肪细胞产生和释放前列环素,这反过来促进前体细胞向脂肪细胞的分化;(ii)在体内和体外,angII和(carba)前列环素都能促进新脂肪细胞的形成;(iii)与野生型小鼠相比,AGT -/-小鼠脂肪组织发育减慢。总的来说,这些数据与AGT、angII和前列环素在脂肪组织发育中的自分泌/旁分泌机制是一致的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Angiotensinogen, angiotensin II and adipose tissue development.

Adipose tissue is an important source of angiotensinogen (AGT). Recent evidence shows that a local renin-angiotensinogen system (RAS) is present in human adipose tissue and may act as a distinct system from plasma RAS. In obese patients, the involvement of angiotensin II (angII) as a consequence of increased plasma AGT secreted from adipose tissue has been proposed in the development of hypertension. Another role of AGT via angII in the development of adipose tissue is supported by the following: (i) in vitro, angII stimulates the production and release of prostacyclin from adipocytes, which in turn promotes the differentiation of precursor cells into adipocytes; (ii) ex vivo and in vivo, both angII and (carba)prostacyclin promote the formation of new fat cells; and (iii) AGT -/- mice exhibit a slowing down of adipose tissue development, as compared to wild-type mice. Altogether the data are consistent with an autocrine/paracrine mechanism implicating AGT, angII and prostacyclin in adipose tissue development.

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