Antonio Marcus de Andrade Paes

Introduction: Low birth weight (LBW) is an early life adversity associated with various risk factors and metabolic dysfunction throughout life. However, the role of socioeconomic factors in the association between LBW and peripubertal health in low- and middle-income countries (LMICs) remains unclear. This ecological study investigated the factors contributing to LBW and its impacts in Brazil.Methods: Data were collected from the Global Health Data Exchange as summary exposure values (SEVs), which serve as a proxy for population prevalence weighted by the relative risk. Additionally, information was sourced from official Brazilian government resources covering the years 1995 to 2017, resulting in a total of 338 state-year observations applied for temporal lagged analyses. First, we tested the SEV of 1-year lagged reproductive-age population (15–49 years) risk factors as exposures and the SEV of LBW as an outcome. In the second temporal lagged analysis, we tested the association between the SEV of LBW as the primary exposure and the SEV of high body mass index (HBMI) in peripubertal population 10 years later as the outcome. Fixed-effects multivariable linear regression models with lags were constructed, adjusting for socioeconomic covariates.Results: The exposure of the reproductive-age population to smoking, alcohol, high systolic blood pressure, and HBMI was positively associated with the SEV of LBW. A diet high in sugar-sweetened beverages (SSB diet) was also positively associated, but the association disappeared when GDP per capita and access to primary care were added to the model. Regarding the repercussions of LBW, a 1-point increase in the SEV of LBW was associated with a 1.6-point increase in HBMI in the peripubertal population (95% CI: 0.66 to 2.55). However, this association disappeared after adjusting for GDP per capita and access to primary care, indicating their confounding roles.Discussion: Our study highlights several risk factors in the adult population associated with LBW and its relationship with peripubertal HBMI. Interestingly, GDP per capita and access to primary care were found to be the socioeconomic determinants for birth outcomes as a result of exposure to the risk factors tested and the mid-term effects of LBW. These findings enhance our understanding of the role of socioeconomic factors contributing to LBW in LMICs and the need for public policies addressing healthcare and welfare to reduce the burden of LBW in LMICs.

Introdução: O presente estudo foi realizado para investigar os efeitos do carvacrol sobre parâmetros hemodinâmicos, lipídicos e inibição da Enzima Conversora de Angiotensina em animais submetidos a treinamento físico aeróbio. Métodos: Os animais foram divididos aleatoriamente em grupos: Wistar- controle normotenso tratado com sorbitol; SHR- controle hipertenso tratado com sorbitol; SHR- tratado com losartana 50mg/kg (Los -50); SHR- tratado com Carvacrol 20 mg/kg (Carv-20); SHR- treinado com exercício aeróbio 60 minutos (Exer); SHR- tratado com Carvacrol (Exercarv) + 60 minutos de exercício aeróbio. O tratamento consitiu em quatro semanas com monitoramento de peso, consumo de ração, frequência cardíaca, pressão arterial sistólica, diastólica e média. Posterior ao tratamento, foram realizadas dosagens bioquímicas para parâmetros renais, hepaticos, lípidicos e dosagens séricas de ECA I. Foram analisadas reduções significativas nos níveis pressóricos dos animais hipertensos, após o protocol de itervenção. O grupo Exercarv, apresentou maiores reduções da PA, quando comparado aos demais grupos, apresentando valores pressóricos de PAS 122,0 ± 3,8 mmHg, PAD 97 ± 3,0 mmHg, PAM 105,5 ± 2,3 mmHg. Ainda, o grupo ExerCarv ocasionou reduções nos níveis de TG, CT, VLDL, TG/HDL e CT/HDL assim como, nos níveis de ureia e AST. Resultados: O procedimento isolado com carvacrol, assim como sua combinação com treinamento físico aeróbio, teve capacidade de reduzir atividade da ECA I comparando ao grupo SHR com p<0,001. Considerações finais: Um mês de tratamento com carvacrol combinado com exercício físico aeróbio apresentaram efeito antihipertensivo, relacionado a inibição da ECA I. Além disso, o tratamento melhorou os parâmetros renais, hepáticos e lipídicos.

El concepto del Desarrollo Temprano de la Salud y la Enfermedad (del inglés Developmental Origins of Health and Disease, DOHaD) tuvo sus raíces en la década de 1980, cuando David Barker y otros investigadores contemporáneos llamaron la atención sobre las complejas interacciones entre el ambiente intrauterino y la salud a lo largo de la vida. Este enfoque innovador desafía la visión tradicional de que los factores genéticos son los únicos determinantes cruciales de la salud, reconociendo la importancia crítica de las exposiciones antes y durante el embarazo, así como en los primeros años de vida. Varios investigadores latinoamericanos comenzaron a involucrarse con el concepto DOHaD a mediados de la década de 2000, destacando la Dra. Elena Zambrano en México, el Dr. Paulo Mathias en Brasil y los Dres. Paola Casanello y Francisco Mardones en Chile.

Sugar-induced metabolic imbalances are a major health problem since an excessive consumption of saccharides has been linked to greater obesity rates at a global level. Sucrose, a disaccharide composed of 50% glucose and 50% fructose, is commonly used in the food industry and found in a range of fast, restaurant, and processed foods. Herein, we investigated the effects of a TRPC4/TRPC5 blocker, ML204, in the metabolic imbalances triggered by early exposure to sucrose-enriched diet in mice. TRPC4 and TRPC5 belong to the family of non-selective Ca⁺² channels known as transient receptor potential channels. High-sucrose (HS)-fed animals with hyperglycaemia and dyslipidaemia, were accompanied by increased body mass index. mesenteric adipose tissue accumulation with larger diameter cells and hepatic steatosis in comparison to those fed normal diet. HS mice also exhibited enhanced adipose, liver, and pancreas TNFα and VEGF levels. ML204 exacerbated hyperglycaemia, dyslipidaemia, fat tissue deposition, hepatic steatosis, and adipose tissue and liver TNFα in HS-fed mice. Normal mice treated with the blocker had greater hepatic steatosis and adipose tissue cell numbers/diameter than those receiving vehicle, but showed no significant changes in tissue inflammation, glucose, and lipid levels. The results indicate that TRPC4/TRPC5 protect against the metabolic imbalances caused by HS ingestion.

Plant-derived (poly)phenolic compounds have been undoubtedly shown to promote endocrine homeostasis through the improvement of diverse metabolic outcomes. Amongst diverse potential mechanisms, the prebiotic modulatory effects exerted by these compounds on the gut microbiota have supported their nutraceutical application in both experimental and clinical approaches. However, the comprehension of the microbiota modulatory patterns observed upon (poly)phenol-based dietary interventions is still in its infancy, which makes the standardization of the metabolic outcomes in response to a given (poly)phenol a herculean task. Thus, this narrative review sought to gather up-to-date information on the relationship among (poly)phenols intake, their modulatory effect on the gut microbiota diversity, and consequent metabolic outcomes as a supportive tool for the future design of experimental approaches and even clinical trials.

Since it acquired pandemic status, SARS-CoV-2 has been causing all kinds of damage all over the world. More than 6.3 million people have died, and many cases of sequelae are in survivors. Currently, the only products available to most of the world’s population to fight the pandemic are vaccines, which still need improvement since the number of new cases, admissions into intensive care units, and deaths are again reaching worrying rates, which makes it essential to compounds that can be used during infection, reducing the impacts of the disease. Plant metabolites are recognized sources of diverse biological activities and are the safest way to research anti-SARS-CoV-2 compounds. The present study computationally evaluated 55 plant compounds in five SARS-CoV-2 targets such Main Protease (Mpro or 3CL or MainPro), RNA-dependent RNA polymerase (RdRp), Papain-Like Protease (PLpro), NSP15 Endoribonuclease, Spike Protein (Protein S or Spro) and human Angiotensin-converting enzyme 2 (ACE-2) followed by in vitro evaluation of their potential for the inhibition of the interaction of the SARS-CoV-2 Spro with human ACE-2. The in silico results indicated that, in general, amentoflavone, 7-O-galloylquercetin, kaempferitrin, and gallagic acid were the compounds with the strongest electronic interaction parameters with the selected targets. Through the data obtained, we can demonstrate that although the indication of individual interaction of plant metabolites with both Spro and ACE-2, the metabolites evaluated were not able to inhibit the interaction between these two structures in the in vitro test. Despite this, these molecules still must be considered in the research of therapeutic agents for treatment of patients affected by COVID-19 since the activity on other targets and influence on the dynamics of viral infection during the interaction Spro x ACE-2 should be investigated.

Metabolic dysfunctions, such as hyperglycemia and insulin resistance, have been associated to cognitive impairment and dementia regardless of advanced age, although the underlying mechanisms are still elusive. Thus, this study investigates the deleterious effects of metabolic syndrome (MetS) induced by long-term exposure to a high-sucrose diet on motor and cognitive functions of male adult rats and its relationship with hippocampal endoplasmic reticulum (ER) stress. Weaned Wistar male rats were fed a high-sucrose diet until adulthood (HSD; 6 months old) and compared to both age-matched (CTR; 6 months old) and middle-aged chow-fed rats (OLD; 20 months old). MetS development, serum redox profile, behavioral, motor, and cognitive functions, and hippocampal gene/protein expressions for ER stress pro-adaptive and pro-apoptotic pathways, as well as senescence markers were assessed. Prolonged exposure to HSD induced MetS hallmarked by body weight gain associated to central obesity, hypertriglyceridemia, insulin resistance, and oxidative stress. Furthermore, HSD rats showed motor and cognitive decline similar to that in OLD animals. Noteworthy, HSD rats presented marked hippocampal ER stress characterized by failure of pro-adaptive signaling and increased expression of Chop, p21, and Parp-1 cleavage, markers of cell death and aging. This panorama resembles that found in OLD rats. In toto, our data showed that early and sustained exposure to a high-sucrose diet induced MetS, which subsequently led to hippocampus homeostasis disruption and premature impairment of motor and cognitive functions in adult rats.

The gut microbiota has been extensively investigated during the last decade because of its effects on host neuroendocrine pathways and other processes. The imbalance between beneficial and pathogenic bacteria, known as dysbiosis, may be a determining predisposing factor for many noncommunicable chronic diseases, such as obesity, type 2 diabetes mellitus, metabolic syndrome, and Alzheimer’s disease. On the other hand, interventions aiming to reestablish the balance between microbiota components have been suggested as potential preventive therapeutic strategies against these disorders. Among these interventions, dietary supplementation with (poly)phenols has been highlighted due to the modulatory effects exerted by those compounds on the gut microbiota. In addition, (poly)phenol consumption is associated with increased production of short-chain fatty acids (SCFAs), a set of microbial metabolites whose actions are ascribed to improving the abovementioned metabolic disorders. Thus, this review discusses the modulation of the gut microbiota by prebiotic (poly)phenols based on in vivo studies performed with isolated (poly)phenolic compounds, their interaction with the gut microbiota and the production of SCFAs in pursuit of the molecular mechanisms underlying the health effects of (poly)phenols on host metabolism.