Carlos Henrique Xavier

Technological advances, easily pursued by research on ruminant nutrition, can improve animal production, prevent nutritional disorders, and increase digestibility concomitantly with reducing ingestive discrepancies. This study aimed to investigate the inclusion of crude extract of Croton urucurana (Croton) or essential oils of cashew and castor bean on in vitro and in situ degradability of Tifton 85 hay and metabolic parameters in beef cattle. The experiment was conducted at the Biological Sciences Institute (ICB) and the Veterinary School of the Federal University of Goias, Brazil. The treatments were: Control, Monensin, Croton, and Blend (essential oil composed of cashew and castor bean). We used five replicates to evaluate ruminal parameters and dry matter degradability. Blend increased dry matter degradation, indicating that forage feeds last longer in the rumen and tend to be more degraded with Blend inclusion. The assessments of ad libitum ingestion of dry matter showed that monensin treatment reduced feed intake compared to control and Croton treatments. Our results suggest that the inclusion of Blend improves the degradability of dry matter in the diet and could be a strategy of choice in diets based on low-quality forage.

Intracranial pressure (ICP) is pressure within the cranium, between 5 and 15 mmHg in a normal brain, and is influenced by the dynamic balance between brain tissue, cerebrospinal fluid (CSF) and cerebral blood volume. ICP is vital for cerebral health, impacting outcomes in various neurological conditions. Disruptions, such as cerebral haemorrhage, hydrocephalus and malignant hypertension, can lead to elevated ICP, a dangerous condition known as intracranial hypertension (IH). Systemic hypertension significantly impacts cerebral health by causing microvascular damage, dysfunction of the blood–brain barrier (BBB) and impairment of intracranial compliance (ICC). This increases the risk of IH), cerebral ischaemia, neuroinflammation and lacunar infarction, further worsening neurological dysfunction. This review describes the complex relationship between hypertension and ICP regulation, focusing on the mechanisms underlying ICP and ICC adjustments in hypertensive conditions and emphasizing the role of BBB integrity and cerebral blood flow (CBF) dynamics. It discusses how the sympathetic output might change the regulation of CBF and the maintenance of ICP, highlighting how hypertensive conditions can impair this mechanism, increasing the risk of cerebral ischaemia. The neurovascular unit, including astrocytes and microglia, plays a significant role in this process, contributing to IH in hypertensive patients. Understanding the effects of hypertension on ICP and ICC could lead to therapies aimed at preserving BBB integrity, reducing inflammation and improving cerebral compliance, potentially preventing brain dysfunction and reducing stroke risk in hypertensive patients. This review underscores the need for early detection and intervention to mitigate the severe consequences of uncontrolled hypertension on cerebral health. image

Childhood and puberty can affect metabolism, leading to tissue injury and malfunction later in life. The consumption of high-processed foods rich in salt and sugar is increasing in middle- and high-income countries, especially among young people. It is necessary to evaluate the effects of high salt and sugar levels in the youth on most injured organs during metabolic challenges. We aimed to investigate whether high-salt/sucrose intake affects whole-body development and leads to end-organ injury. Weaned male Wistar rats were divided into two groups: a control group fed a standard diet and tap water, and an experimental group (SS) fed a standard diet and a beverage containing 1·8 % NaCl and 20 % sucrose instead of tap water. The animals were treated for 60 d, starting after weaning at 21 d of age, after which the animals were subjected to glucose and insulin tolerance tests, urine collection and heart rate monitoring and euthanised for sample collection at 81 d of age. SS showed reduced body weight gain and increased food intake of sodium/sucrose solution. Interestingly, high-salt/sucrose intake led to increased body adiposity, liver lipid inclusion, heart rate and renal dysfunction. SS exhibits increased levels of PPAR alpha to counterbalance the hypertrophy of brown adipose tissue. Our findings reveal that the SS rat model exhibits non-obvious obesity with end-organ damage and preserved brown adipose tissue function. This model closely parallels human conditions with normal BMI but elevated visceral adiposity, providing a relevant tool for studying atypical metabolic disorders.

Ghrelin has effects that range from the maturation of the central nervous system to the regulation of energy balance. The production of ghrelin increases significantly during the first weeks of life. Studies have addressed the metabolic effects of liver-expressed antimicrobial peptide 2 (LEAP2) in inhibiting the effects evoked by ghrelin, mainly in glucose homeostasis, insulin resistance, and lipid metabolism. Despite the known roles of ghrelin in the postnatal development, little is known about the long-term metabolic influences of modulation with the endogenous expressed growth hormone secretagogue receptor (GHSR) inverse agonist LEAP2. This study aimed to evaluate the contribution of GHSR signalling during perinatal phases, to neurodevelopment and energy metabolism in young animals, under inverse antagonism by LEAP2_[1–14]. For this, two experimental models were used: (i) LEAP2_[1–14] injections in female rats during the pregnancy. (ii) Postnatal modulation of GHSR with LEAP2_[1–14] or MK677. Perinatal GHSR modulation by LEAP2_[1–14] impacts glucose homeostasis in a sex and phase-dependent manner, despite no effects on body weight gain or food intake. Interestingly, liver PEPCK expression was remarkably impacted by LEAP2 injections. The observed results suggests that perinatal LEAP2 exposure can modulate liver metabolism and systemic glucose homeostasis. In addition, these results, although not expressive, may just be the beginning of the metabolic imbalance that will occur in adulthood.

Background: Though maternal diabetes effects are well described in the literature, the effects of maternal diabetes in postnatal phases are often overlooked. Diabetic individuals have higher levels of circulating glycotoxins, and there is a positive correlation between maternal-derived glycotoxins and circulating glycotoxins in their progeny. Previous studies evaluated the metabolic effects of high glycotoxin exposure during lactation in adult animals. However, here we focus on the cardiovascular system of juvenile rats. Methods: For this, we used two experimental models: 1. High Methylglyoxal (MG) environment: pregnant Wistar rats were injected with PBS (VEH group) or Methylglyoxal (MG group; 60 mg/kg/day; orally, postnatal day (PND) 3 to PND14). 2. GLO-1 inhibition: pregnant Wistar rats were injected with dimethyl sulfoxide (VEH group) or a GLO-1 inhibitor (BBGC group; 5 mg/kg/day; subcutaneously, PND1–PND5). The offspring were evaluated at PND45. Results: MG offspring presented cardiac dysfunction and subtly worsened vasomotor responses in the presence of perivascular adipose tissue, without morphological alterations. In addition, an endogenous increase in maternal glycotoxins impacts offspring vasomotricity due to impaired redox status. Conclusions: Our data suggest that early glycotoxin exposure led to cardiac and vascular impairments, which may increase the risk for developing cardiovascular diseases later in life.