Angiotensin converting enzyme inhibition lowers body weight and improves glucose tolerance in C57BL/6J mice maintained on a high fat diet

Weisinger, Richard S., Stanley, Tracy K., Begg, Denovan P., Weisinger, Harrison S., Spark, Kylie J. and Jois, Markandeya 2009, Angiotensin converting enzyme inhibition lowers body weight and improves glucose tolerance in C57BL/6J mice maintained on a high fat diet, Physiology & behavior, vol. 98, no. 1-2, pp. 192-197.

Attached Files
Name Description MIMEType Size Downloads

Title Angiotensin converting enzyme inhibition lowers body weight and improves glucose tolerance in C57BL/6J mice maintained on a high fat diet
Author(s) Weisinger, Richard S.
Stanley, Tracy K.
Begg, Denovan P.
Weisinger, Harrison S.
Spark, Kylie J.
Jois, Markandeya
Journal name Physiology & behavior
Volume number 98
Issue number 1-2
Start page 192
End page 197
Publisher Elsevier Inc.
Place of publication Amsterdam, The Netherlands
Publication date 2009-08-04
ISSN 0031-9384
Keyword(s) angiotensin II
captopril
diet-induced obesity
adiposity
Summary The renin–angiotensin system (RAS) is functional within adipose tissue and angiotensin II, the active component of RAS, has been implicated in adipose tissue hypertrophy and insulin resistance. In this study, captopril, an angiotensin converting enzyme (ACE) inhibitor that prevents angiotensin II formation, was used to study the development of diet-induced obesity and insulin resistance in obesity prone C57BL/6J mice. The mice were fed a high fat diet (w/w 21% fat) and allowed access to either water or water with captopril added (0.2 mg/ml). Body weight was recorded weekly and water and food intake daily. Glucose tolerance was determined after 11–12 weeks. On completion of the study (after 16 weeks of treatment), the mice were killed and kidney, liver, epididymal fat and extensor digitorum longus muscle (EDL) were weighed. Blood samples were collected and plasma analysed for metabolites and hormones. Captopril treatment decreased body weight in the first 2 weeks of treatment. Food intake of captopril-treated mice was similar to control mice prior to weight loss and was decreased after weight loss. Glucose tolerance was improved in captopril-treated mice. Captopril-treated mice had less epididymal fat than control mice. Relative to body weight, captopril-treated mice had increased EDL weight. Relative to control mice, mice administered captopril had a higher plasma concentration of adiponectin and lower concentrations of leptin and non-esterified fatty acids (NEFA). The results indicate that captopril both induced weight loss and improved insulin sensitivity. Thus, captopril may eventually be used for the treatment of obesity and Type 2 diabetes.
Language eng
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2009, Elsevier Inc.
Persistent URL http://hdl.handle.net/10536/DRO/DU:30041050

Document type: Journal Article
Collection: School of Medicine
Connect to link resolver
 
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.

Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 33 times in TR Web of Science
Scopus Citation Count Cited 42 times in Scopus
Google Scholar Search Google Scholar
Access Statistics: 45 Abstract Views, 1 File Downloads  -  Detailed Statistics
Created: Wed, 14 Dec 2011, 09:48:37 EST by Leanne Swaneveld

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.