Enalapril and treadmill running reduce adiposity, but only the latter causes adipose tissue browning in mice.


Giori IG(1), Magliano DC(2), Alexandre-Santos B(1)(2), Fernandes T(3)(4), Oliveira EM(3)(4), Vieira CP(5), Conte-Junior CA(5), Ceddia RB(6), Nobrega ACL(1)(3), Frantz EDC(1)(2)(3).
Author information:
(1)Laboratory of Exercise Sciences, Fluminense Federal University, Niteroi, Rio de Janeiro, Brazil.
(2)Laboratory of Morphological and Metabolic Analyses, Fluminense Federal University, Niteroi, Rio de Janeiro, Brazil.
(3)National Institute for Science and Technology, INCT Physical
(In)activity and Exercise, CNPq, Niteroi, Rio de Janeiro, Brazil.
(4)Laboratory of Biochemistry and Molecular Biology of Exercise, School of Physical Education and Sport, University of Sao Paulo, São Paulo, State of São Paulo, Brazil.
(5)Department of Food Technology, Faculty of Veterinary, Fluminense Federal University, Niteroi, Rio de Janeiro, Brazil.
(6)Muscle Health Research Center, School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada.


This study investigated whether regulation of the renin-angiotensin system (RAS) by enalapril and/or aerobic exercise training (AET) causes browning of the subcutaneous white adipose tissue (sWAT). C57BL/6 mice were fed either a standard chow or a high-fat (HF) diet for 16 weeks. At Week 8, HF-fed animals were divided into sedentary (HF), enalapril (HF-E), AET (HF-T), and enalapril plus AET (HF-ET) groups. Subsequently, sWAT was extracted for morphometry, determination of RAS expression, and biomarkers of WAT browning. The HF group displayed adipocyte hypertrophy and induction of the classical RAS axis. Conversely, all interventions reduced adiposity and induced the counterregulatory RAS axis. However, only AET raised plasma irisin, increased peroxisome proliferator-activated receptor-γ coactivator-1α, and uncoupling protein-1 levels, and the expression of PR-domain containing 16 in sWAT. Therefore, we concluded that AET-induced sWAT browning was independent of the counterregulatory axis shifting of RAS in HF diet-induced obesity.