中文摘要：

目的 探讨代谢综合征（MS）大鼠肠系膜脂肪组织中肾素-血管紧张素系统（RAS）变化及拮抗血管紧张素Ⅱ（AngⅡ）对脂肪细胞成脂作用的影响。方法 30只8周龄健康雄性Wistar大鼠随机分为MS组和正常对照组，分别给予高脂饲料和普通饲料喂养24周，造成MS模型后，取出肠系膜脂肪组织，应用RT-PCR和Western blot法检测脂肪组织中mRNA和蛋白质表达。同时，将前脂肪细胞（3T3-L1）进行诱导分化，油红O染色观察脂滴形成情况，比率荧光倒置显微镜检测脂肪细胞内钙水平（[Ca^2＋]i）。给予AngⅡ刺激，并观察血管紧张素Ⅱ受体阻断剂（ARB）坎地沙坦或血管紧张素转换酶抑制剂（ACEI）巯甲丙脯酸对脂滴形成及细胞内钙水平（[ca^2＋]i）的作用。结果 MS大鼠肠系膜脂肪组织的血管紧张素原（ACT）、血管紧张素转换酶（ACE）和血管紧张素Ⅱ受体亚型1（AT1R）表达均显著高于正常对照组（P〈0．05，P〈0．01）；未诱导前脂肪细胞和经AngⅡ处理的成熟脂肪细胞未见明显脂滴形成，给予ACEI和ARB的成熟脂肪细胞有明显的脂滴形成；AngⅡ可致前脂肪细胞内钙水平（[Ca^2＋]i）显著增加（P〈0．01），巯甲丙脯酸和坎地沙坦可阻断其效应，而对成熟脂肪细胞，AngⅡ介导的细胞内钙水平（[ca^2＋]i）升高受到抑制，但坎地沙坦能恢复AngⅡ的效应，巯甲丙脯酸与AngⅡ组比较细胞内钙水平（[Ca^2＋]i）差异无显著性。结论 代谢综合征大鼠肠系膜脂肪组织中RAS系统处于激活状态，拮抗RAS能恢复脂肪细胞的基本功能。

英文摘要：

Objective To investigate the renin-angiotensin system （BAS） in mesenteric adipose tissues and effect of angiotensin Ⅱ on adipocyte differentiation. Methods Thirty normal 8-week-old male Wistar rats were divided into groups on normal diet and high-fat diet. The rats on high-fat diet for 24 weeks developed the metabolic syndrome respectively. The mRNA and protein expression of mesenteric adipose tissue were measured by reverse transeription-polymerase chain reaction （BT-PCR） and Western blot. Lipid drop in 3T3- L1 preadipocytes and mature adipocytes were observed using oil-red O staining. The fluorescence microscope was used to detect eytosolic-free calcium in 3T3-L1 predipocytes and mature adipoeytes. Results The expressions of angiotensinogen, angiotensin converting enzyme, angiotensin Ⅱ receptor type 1 in mesenterie adipose tissue were significantly increased in rats with metabolic syndrome compared with those in rats on normal diet （P 〈 0. 05, P 〈 0. 01 ）. After administration of angiotensin Ⅱ , no lipid droplet in 3T3-L1 preadipocytes and adipoeytes were observed, however, intensive lipid droplet in adipoeyte was found after administration of captopril and candesartan. Angiotensin Ⅱ increased the intracellular-free calcium concentration in preadipocytes （P 〈0. 01 ）, which was blocked by captopril and candesartan; in contrast, angiotensin Ⅱ effect was blunt in mature adipocyte. Captopril and candesartan partially recovered the angiotensin Ⅱ -mediated increase of cytosolic-free calcium. Conclusion RAS in the mesenteric adipose tissues is active in rats with metabolic syndrome, and antagonization of RAS can recover the lipogenesis of adipocyte.