The impact of high-fat diet consumption and inulin fiber supplementation on anxiety-related behaviors and liver oxidative status in female Wistar rats.

BACKGROUND: Obesity is a worldwide public health problem associated with cognitive and mental health problems in both humans and rats. Studies assessing the effect of fiber supplementation on behavioral deficits and oxidative stress caused by high-fat diet (HFD) consumption in female rats are still scarce. We hypothesized that HFD consumption would lead to anxiety-related behavior and hepatic oxidative stress and that inulin would protect against these changes. We analyzed the impact of HFD-induced obesity combined with fiber supplementation (inulin) on anxiety-related defensive behavior and hepatic oxidative stress. RESULTS: Female rats were fed a high-fat diet (HFD; 45%) for nine weeks to induce obesity. The administration of inulin was found to decrease the adiposity index in both the control and obese groups. The consumption of a HFD combined with inulin supplementation resulted in a reduction in both CAT activity and carbonylated protein levels, leading to a shift in the hepatic redox balance. Interestingly, the behavioral data were conflicting. Specifically, animals that consumed a high-fat diet and received inulin showed signs of impaired learning and memory caused by obesity. The HFD did not impact anxiety-related behaviors in the female rats. However, inulin appears to have an anxiolytic effect, in the ETM, when associated with the HFD. On the other hand, inulin appears to have affected the locomotor activity in the HFD in both open field and light-dark box. CONCLUSION: Our results show that consumption of a HFD induced obesity in female rats, similar to males. However, HFD consumption did not cause a consistent increase in anxiety-related behaviors in female Wistar rats. Treatment with inulin at the dosage used did not exert consistent changes on the behavior of the animals, but attenuated the abdominal WAT expansion and the hepatic redox imbalance elicited by high-fat diet-induced obesity.

Ivabradine restores tonic cardiovascular autonomic control and reduces tachycardia, hypertension and left ventricular inflammation in post-weaning protein malnourished rats.

Malnutrition results in autonomic imbalance and heart hypertrophy. Overexpression of hyperpolarization-activated cyclic nucleotide-gated channels (HCN) in the left ventricles (LV) is linked to hypertrophied hearts and abnormal myocardium automaticity. Given that ivabradine (IVA) has emerging pleiotropic effects, in addition to the widely known bradycardic response, this study evaluated if IVA treatment could repair the autonomic control and cardiac damages in malnourished rats. AIM: Assess the impact of IVA on tonic cardiovascular autonomic control and its relationship with hemodynamics regulation, LV inflammation, and HCN gene expression in post-weaning protein malnutrition condition. MAIN METHODS: After weaning, male rats were divided into control (CG; 22 % protein) and malnourished (MG; 6 % protein) groups. At 35 days, groups were subdivided into CG-PBS, CG-IVA, MG-PBS and MG-IVA (PBS 1 ml/kg or IVA 1 mg/kg) received during 8 days. We performed jugular vein cannulation and electrode implant for drug delivery and ECG registration to assess tonic cardiovascular autonomic control; femoral cannulation for blood pressure (BP) and heart rate (HR) assessment; and LV collection to evaluate ventricular remodeling and HCN gene expression investigation. KEY FINDINGS: Malnutrition induced BP and HR increases, sympathetic system dominance, and LV remodeling without affecting HCN gene expression. IVA reversed the cardiovascular autonomic imbalance; prevented hypertension and tachycardia; and inhibited the LV inflammatory process and fiber thickening caused by malnutrition. SIGNIFICANCE: Our findings suggest that ivabradine protects against malnutrition-mediated cardiovascular damage. Moreover, our results propose these effects were not attributed to HCN expression changes, but rather to IVA pleiotropic effects on autonomic control and inflammation.