Mathai M L, Naik S, Sinclair A J, Weisinger H S, Weisinger R S
Howard Florey Institute and Centre for Neuroscience, The University of Melbourne, Victoria, Australia.
Int J Obes (Lond). 2008 Oct;32(10):1576-84. doi: 10.1038/ijo.2008.126. Epub 2008 Aug 12.
There is emerging evidence that angiotensin stimulates adipocyte differentiation and lipogenesis. This study tested the hypothesis that inhibition of angiotensin II by treatment with an angiotensin-converting enzyme inhibitor, perindopril, would reduce fat mass in rats.
After a 12-day baseline, rats were divided into two groups: one was untreated and the other received perindopril (1.2 mg kg(-1) per day) in drinking water for 26 days.
In total, 16 male Sprague-Dawley rats aged 10 weeks at the start of the study.
Plasma leptin was measured in samples collected at baseline, half-way through and at the end of treatment. Body weight, food and water intake were measured daily throughout the experiment. Body fat mass, bone and lean mass were determined by dual energy X-ray absorptiometry (DEXA) at the end of the treatment period.
Daily food intake was the same in both groups throughout the study. By the end of treatment, animals receiving perindopril showed a modest reduction in weight gain relative to the untreated animals (62.4+/-5.0 g vs 73.0+/-4.0 g; P<0.05). DEXA analysis showed that body composition was greatly altered and the perindopril-treated group had 26% less body fat mass than the untreated group (61.0+/-5.2 g vs 44.4+/-4.2 g; P<0.01). The reduction in body fat mass was correlated with reductions in the weight of both the epididymal and retroperitoneal fat pads (P<0.001). Similarly, plasma leptin was reduced by perindopril treatment (4.64+/-0.56 ng ml(-1)) compared to the untreated group (8.27+/-1.03 ng ml(-1); P<0.001). In contrast, there were no differences in lean or bone mass between the two groups.
Oral treatment with perindopril selectively reduced body fat mass without influencing daily food intake. In contrast, there were no differences in lean or bone mass between the two groups.
越来越多的证据表明血管紧张素可刺激脂肪细胞分化和脂肪生成。本研究检验了以下假设：通过使用血管紧张素转换酶抑制剂培哚普利进行治疗来抑制血管紧张素II，可减少大鼠的脂肪量。
在12天的基线期后，将大鼠分为两组：一组不进行治疗，另一组在饮水中给予培哚普利（每天1.2 mg·kg⁻¹），持续26天。
本研究开始时共有16只10周龄的雄性斯普拉格-道利大鼠。
在基线期、治疗中期和治疗结束时采集的样本中测量血浆瘦素。在整个实验过程中每天测量体重、食物和水的摄入量。在治疗期结束时通过双能X线吸收法（DEXA）测定体脂肪量、骨骼和瘦体重。
在整个研究过程中，两组的每日食物摄入量相同。到治疗结束时，接受培哚普利治疗的动物相对于未治疗的动物体重增加适度减少（62.4±5.0 g对73.0±4.0 g；P<0.05）。DEXA分析表明身体组成发生了很大变化，培哚普利治疗组的体脂肪量比未治疗组少26%（61.0±5.2 g对44.4±4.2 g；P<0.01）。体脂肪量的减少与附睾和腹膜后脂肪垫重量的减少相关（P<0.001）。同样，与未治疗组（8.27±1.03 ng·ml⁻¹）相比，培哚普利治疗使血浆瘦素降低（4.64±0.56 ng·ml⁻¹；P<0.001）。相比之下，两组之间的瘦体重或骨骼质量没有差异。
口服培哚普利可选择性减少体脂肪量，而不影响每日食物摄入量。相比之下，两组之间的瘦体重或骨骼质量没有差异。
