Abstract
Activation of renin–angiotensin system (RAS) plays a key role in the maintenance of blood pressure, fluid, and electrolyte homeostasis through the action of the vasoactive peptide angiotensin II (Ang II). RAS has now been recognized to play an important role in metabolic diseases. Evidence from both animal and clinical studies suggest that blockade of RAS by reducing the synthesis of Ang II or its binding to angiotensin type 1 receptor (AT1R) via angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARBs) prevents the activation of inflammatory signaling mechanism involved in obesity-associated metabolic disorders. Conversely, angiotensin converting enzyme 2 (ACE2)/Ang-(1–7)/Mas receptor (MasR) axis has been proposed as counter regulatory arm with effects opposite to those produced by ACE/Ang II/AT1R. This review summarizes the relevant studies enlightening the role of RAS in obesity-associated disorders with emphasis on the inhibitory effect of ACEi and ARBs on ACE/Ang II/AT1R and stimulation of ACE2/Ang-(1–7)/MasR axis in obesity.
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