Stress-induced cardiometabolic perturbations, increased oxidative stress and ACE/ACE2 imbalance are improved by endurance training in rats.

AIMS: To investigate the effects of endurance training on stress-induced cardiometabolic perturbations given the elevated release of stress hormones and subsequent glucose homeostasis perturbations. MATERIALS AND METHODS: Rats were randomized into non-trained rats, rats submitted to endurance training, non-trained rats submitted to stress, and trained rats submitted to stress. Endurance training was applied for 8 weeks, while chronic stress was applied at the 4th, 5th, and 6th weeks of the training period. Two weeks after the last stressor stimuli, rats were euthanized, and blood and heart were collected for biochemical tests. KEY FINDINGS: Exacerbated corticosterone levels were observed in both stressed groups, and chronic stress per se impaired glucose tolerance and insulin sensitivity. Training reduced circulating adrenaline, even though noradrenaline levels were elevated in the blood and heart of trained rats. While stress-induced high circulating serotonin levels were further increased by endurance training, cardiac serotonin levels were attenuated in trained rats. Endurance training mitigated the stress-induced higher circulating lipids. Cardiac TBARs and GPx activity increased in trained rats while CAT and GPx were reduced in response to chronic stress. Endurance training not only attenuated the stress-induced higher circulating ACE/ACE2 ratio but also reduced ACE/ACE2 balance in the heart. Glucose intolerance, insulin resistance, and altered stress hormones release were linked to impairment of cardiometabolic responses, elevated oxidative stress, and dysregulation of ACE/ACE2 ratio. SIGNIFICANCE: Endurance training mitigated the stress-related pathophysiological responses, which could be related to improvements in the antioxidant capacity and the balance of ACE/ACE2 activity.

Açai (Euterpe oleracea Mart.) Upregulates Paraoxonase 1 Gene Expression and Activity with Concomitant Reduction of Hepatic Steatosis in High-Fat Diet-Fed Rats.

Açai (Euterpe oleracea Mart.), a fruit from the Amazon region, has emerged as a promising source of polyphenols. Açai consumption has been increasing owing to ascribed health benefits and antioxidant properties; however, its effects on hepatic injury are limited. In this study, we evaluated the antioxidant effect of filtered açai pulp on the expression of paraoxonase (PON) isoforms and PON1 activity in rats with nonalcoholic fatty liver disease (NAFLD). The rats were fed a standard AIN-93M (control) diet or a high-fat (HF) diet containing 25% soy oil and 1% cholesterol with or without açai pulp (2 g/day) for 6 weeks. Our results show that açai pulp prevented low-density lipoprotein (LDL) oxidation, increased serum and hepatic PON1 activity, and upregulated the expression of PON1 and ApoA-I in the liver. In HF diet-fed rats, treatment with açai pulp attenuated liver damage, reducing fat infiltration and triglyceride (TG) content. In rats receiving açai, increased serum PON1 activity was correlated with a reduction in hepatic steatosis and hepatic injury. These findings suggest the use of açai as a potential therapy for liver injuries, supporting the idea that dietary antioxidants are a promising approach to enhance the defensive systems against oxidative stress.