Abstract
The renin-angiotensin system (RAS) has been implicated in the development of metabolic syndrome. We investigated whether the hepatic RAS is modulated by exercise training and if this modulation improves the deleterious effects of fructose overload in rats. Male Wistar rats were divided into (n = 8 each) control (CT), exercise control (CT-Ex), high fructose (HFr) and exercise high fructose (HFr-Ex) groups. Fructose-drinking rats received D-fructose (100 g L−1). After two weeks, CT-Ex and HFr-Ex rats were assigned to a treadmill training protocol at moderate-intensity for eight weeks (60 min day−1, four days/week). We assessed body mass, glucose and lipid metabolism, hepatic histopathology, ACE and ACE2 activity, angiotensin concentration, the expression profile of proteins affecting hepatic RAS, gluconeogenesis and inflammation. Neither fructose overload nor exercise training influenced body mass gain and serum ACE and ACE2 activity. The HFr group showed hyperinsulinemia, but exercise training normalized this parameter. Exercise training was effective in preventing hepatic steatosis as well as triacylglycerol and glycogen accumulation. Furthermore, exercise improved the response to the deleterious effects of HFr overload by normalizing the gluconeogenesis pathway as well as the protein levels of IL-6 and TNF-alpha. The HFr rats displayed increased hepatic ACE activity and protein expression and Ang II concentration which were attenuated by exercise training. Exercise training restored the ACE2/Ang (1-7)/Mas receptor axis. Exercise training may favor the counter-regulatory ACE2/Ang (1-7)/Mas receptor axis over the classical RAS (ACE/Ang II/AT1R axis), which could be responsible for the decrease of metabolic dysfunction and the prevention of non-alcoholic fatty liver disease (NAFLD).
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