title: Selective reduction in body fat mass and plasma leptin induced by angiotensin-converting enzyme inhibition in rats.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  METHODS
  In total, 16 male Sprague-Dawley rats aged 10 weeks at the start of the study.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Howard Florey Institute and Centre for Neuroscience, The University of Melbourne, Victoria, Australia. michael.mathai@vu.edu.au
authors.forename: M L
authors.initials: ML
authors.lastname: Mathai
authors.forename: S
authors.initials: S
authors.lastname: Naik
authors.forename: A J
authors.initials: AJ
authors.lastname: Sinclair
authors.forename: H S
authors.initials: HS
authors.lastname: Weisinger
authors.forename: R S
authors.initials: RS
authors.lastname: Weisinger
mesh_terms: D015502:Absorptiometry, Photon; D000273:Adipose Tissue / Q000187:drug effects*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001823:Body Composition; D001835:Body Weight; D015519:Bone Density; D004435:Eating; D020738:Leptin / Q000097:blood*; D008297:Male; D020913:Perindopril / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D020738:Leptin; D020913:Perindopril