Wellington de Almeida

Background/Objectives: Type 2 Diabetes Mellitus (T2DM) is characterized by hyperglycemia, increased risk of cardiovascular diseases, and oxidative imbalances. This study aimed to investigate the impact of dietary supplementations with ‘Arinto’ grape pomace flour (GPF) (WGPF) and ‘Touriga Nacional’ GPF (RGPF) in an animal model of T2DM. Methods: T2DM was induced by a high-fat diet (HFD) for 28 days and a single dose of streptozotocin (STZ) (35 mg/kg) on the 21st day. Forty adult male Wistar rats were divided into five groups: Control (CT), T2DM, T2DM + Metformin (250 mg/kg), T2DM + 10% ‘Arinto’ GPF (WGPF), and T2DM + 10% ‘Touriga Nacional’ GPF (RGPF). On the 21st day of the experimental protocol, animals were submitted to an oral glucose tolerance test. An oral glucose tolerance test, oxidative stress parameters, biochemical analysis, and pancreas histological analyses were performed. Results: T2DM impaired glucose tolerance, elevated serum triglycerides and cholesterol, increased oxidative damage in the liver, and induced pancreatic histological abnormalities. However, supplementation with WGPF and RGPF demonstrated positive effects, mitigating glycemic and lipid disruptions, ameliorating oxidative stress, and protecting pancreatic Islets β-cells. Conclusions: Our findings highlight the protective effects of WGPF and RGPF in the adverse impacts of T2DM. Additionally, our study emphasizes the innovative use of grape pomace, a winemaking by-product, promoting sustainability by transforming waste into functional foods with significant health benefits.

Neonatal hypoxia‐ischemia (HI) can lead to cognitive impairments and motor dysfunction. Acrobatic exercises (AE) were proposing as therapeutic option to manage HI motor deficits, however, the cognitive effects after this treatment is still poorly understood. Therefore, we evaluated the effects of AE protocol on memory impairments and brain plasticity markers after Rice‐Vannucci hypoxia‐ischemia rodent model. Wistar rats on the 7^th postnatal day (PND) were submitted to HI model and after weaning (PND22) were trained for 5 weeks with AE protocol, then subsequently submitted to cognitive tests. Our results showed recovery in novel object recognition (NOR) memory, but not, spatial Morris Water Maze (WM) memory after AE treatment in HI rats. BDNF and synaptophysin neuroplasticity markers indicate plastic alterations in the hippocampus and striatum, with maintenance of synaptophysin despite reduction of total volume tissue, besides, hippocampal HI‐induced ipsilateral BDNF increased and striatum contralateral BDNF decreased was noted. Nevertheless, the exercise promoted functional recovery and seems to be a promising strategy for HI treatment, however, future studies identifying neuroplastic pathway for this improvement are needed.

Methylphenidate (MPH) is a stimulant drug mainly prescribed to treat cognitive impairments in attention-deficit/hyperactivity disorder (ADHD). We demonstrated that neonatal hypoxia-ischemia (HI) induced attentional deficits in rats and MPH administration reversed these deficits. However, MPH effects on memory deficits after the HI procedure have not been evaluated yet. We aimed to analyze learning and memory performance of young hypoxic-ischemic rats after MPH administration and associate their performance with brain-derived neurotrophic factor (BDNF) levels in the prefrontal cortex and hippocampus. Male Wistar rats were divided into four groups (n=11–13/group): control saline (CTS), control MPH (CTMPH), HI saline (HIS) and HIMPH. The HI procedure was conducted at post-natal day (PND) 7 and memory tasks between PND 30 and 45. MPH administration (2.5 mg/kg, i.p.) occurred 30 min prior to each behavioral session and daily, for 15 days, for the BDNF assay (n=5–7/group). As expected, hypoxic-ischemic animals demonstrated learning and memory deficits in the novel-object recognition (NOR) and Morris water maze (MWM) tasks. However, MPH treatment did not improve learning and memory deficits of these animals in the MWM—and even disrupted the animals’ performance in the NOR task. Increased BDNF levels were found in the hippocampus of HIMPH animals, which seem to have been insufficient to improve memory deficits observed in this group. The MPH treatment was not able to improve memory deficits resulting from the HI procedure considering a dose of 2.5 mg/kg. Further studies investigating different MPH doses would be necessary to determine a dose–response relationship in this model.

Clinical studies show that physical exercise has anxiolytic and pro-cognitive properties for both healthy individuals and psychiatric patients. Most of these data refer to the effects of aerobic exercise. However, other modalities such as resistance exercise deserve more attention because they may also modulate brain function. This study aimed to compare the effects of an aerobic exercise protocol on a treadmill and a resistance exercise protocol on a ladder apparatus on anxiety-like behavior, cognitive flexibility, and neuroplasticity parameters in healthy animals. Adult male Wistar rats were divided into three groups: sedentary control, aerobic training, and resistance training. Subsequently, they were evaluated in the elevated plus-maze (EPM), light-dark box, and modified hole board (mHB) tests. The expressions of synaptophysin and postsynaptic plasticity protein 95 in the dorsal and ventral hippocampus were analyzed by immunofluorescence. The results demonstrated an anxiolytic effect promoted by exercise in the EPM, particularly in the animals submitted to aerobic training, and a mild pro-learning effect of both exercise modalities was observed in the mHB test. All groups showed similar outcomes in the other evaluations. Therefore, the exercise modalities investigated in the present study did not provide considerable modifications to such aspects of the emotional/cognitive functions and neuroplasticity under physiological contexts. Perhaps the two types of exercise acted in neurobiological pathways not analyzed in this study, or the effects may emerge under pathological contexts. These hypotheses should be tested in future studies.

In an attempt to propose an animal model that reproduces in rats the phenotype of cerebral palsy, this study evaluated the effects of maternal exposure to bacterial endotoxin associated with perinatal asphyxia and sensorimotor restriction on gait pattern, brain and spinal cord morphology. Two experimental groups were used: Control Group (CTG) − offspring of rats injected with saline during pregnancy and Cerebral Palsy Group (CPG) − offspring of rats injected with lipopolysaccharide during pregnancy, submitted to perinatal asphyxia and sensorimotor restriction for 30 days. At 29 days of age, the CPG exhibited coordination between limbs, weight‐supported dorsal steps or weight‐supported plantar steps with paw rotation. At 45 days of age, CPG exhibited plantar stepping with the paw rotated in the balance phase. An increase in the number of glial cells in the primary somatosensory cortex and dorsal striatum were observed in the CPG, but the corpus callosum thickness and cross‐sectional area of lateral ventricle were similar between studied groups. No changes were found in the number of motoneurons, glial cells and soma area of the motoneurons in the ventral horn of spinal cord. The combination of insults in the pre, peri and postnatal periods produced changes in hindlimbs gait pattern of animals similar to those observed in diplegic patients, but motor impairments were attenuated over time. Besides, the greater number of glial cells observed seems to be related to the formation of a glial scar in important sensorimotor brain areas.