Consumo de semente de linhaça durante a lactação afeta peso e nível de hemoglobina na prole de ratas

OBJETIVO: Avaliar os efeitos do consumo da semente de linhaça durante a lactação sobre o peso corporal, indicadores hematológicos e massa de gordura visceral dos filhotes de ratas na idade adulta. MÉTODOS: Foram utilizadas 16 ratas Wistar que, após o parto, foram divididas em dois grupos que receberam, durante a lactação, as seguintes dietas: grupo-controle (GC), ração à base de caseína, e grupo linhaça (GL), ração à base de caseína contendo 25% de semente de linhaça. Ao desmame, os filhotes machos passaram a receber ração comercial até a idade adulta, quando foram sacrificados aos 170 dias de vida para coleta de sangue e avaliação da massa de gordura visceral. RESULTADOS: Foi encontrado menor peso corporal da prole do GL (GL = 42,69±3,06 g; GC = 47,31±4,72 g; p = 0,036) ao desmame. Aos 170 dias de idade foram observados menores valores na hemoglobina do GL (GL = 12,30±1,28 g/dL; GC = 13,88±0,91 g/dL; p = 0,02). Não foram verificadas diferenças estatísticas na massa de gordura visceral entre os grupos. CONCLUSÕES: O consumo materno da ração à base de semente de linhaça durante a lactação promoveu menor peso ao desmame e níveis menores de hemoglobina na idade adulta quando comparados ao GC

Food for healthier aging: power on your plate

Inflammageing is a persistent low-level inflammatory burden that accompanies age-related dysregulation of the immune system during normative aging and within the diseasome of aging. A healthy diet containing a balanced amount of macronutrients, vitamins and minerals, adequate in calories and rich in poly(phenols), has an essential role in mitigating the effects of inflammageing and extending healthspan through modulation of the activity of a range of factors. These include transcription factors, such as nuclear factor erythroid-derived 2 related factor 2 (Nrf2) and nuclear factor-κB (NF-kB), the inflammasome and the activities of the gut microbiota. The aim of this narrative review is to discuss the potential of food to ameliorate the effects of the diseasome of aging

Can diet modulate trimethylamine N-oxide (TMAO) production? What do we know so far?

Background: Trimethylamine N-oxide (TMAO) is a metabolite that has attracted attention due to its positive association with several chronic non-communicable diseases such as insulin resistance, atherosclerotic plaque formation, diabetes, cancer, heart failure, hypertension, chronic kidney disease, liver steatosis, cardiac fibrosis, endothelial injury, neural degeneration and Alzheimer's disease. TMAO production results from the fermentation by the gut microbiota of dietary nutrients such as choline and carnitine, which are transformed to trimethylamine (TMA) and converted into TMAO in the liver by flavin-containing monooxygenase 1 and 3 (FMO1 and FMO3). Considering that TMAO is involved in the development of many chronic diseases, strategies have been found to enhance a healthy gut microbiota. In this context, some studies have shown that nutrients and bioactive compounds from food can modulate the gut microbiota and possibly reduce TMAO production. Objective: This review has as main objective to discuss the studies that demonstrated the effects of food on the reduction of this harmful metabolite. Methods: All relevant articles until November 2020 were included. The articles were searched in Medline through PubMed. Results: Both the food is eaten acutely and chronically, by altering the nature of the gut microbiota, influencing colonic TMA production. Furthermore, hepatic production of TMAO by the flavin monooxygenases in the liver may also be influenced by phenolic compounds present in foods. Conclusion: The evidence presented in this review shows that TMAO levels can be reduced by some bioactive compounds. However, it is crucial to notice that there is significant variation among the studies. Further clinical studies should be conducted to evaluate these dietary components’ effectiveness, dose, and intervention time on TMAO levels and its precursors

Associação entre níveis de ferritina e peroxidação lipídica em pacientes em hemodiálise

Resumo Introdução: A suplementação de ferro é uma das importantes recomendações em pacientes com doença renal crônica (DRC), contudo, uma sobrecarga desse mineral pode contribuir para o estresse oxidativo, condição essa bastante relacionada com o risco cardiovascular nesses pacientes. Objetivo: O objetivo desse trabalho foi investigar se os níveis de ferritina estão associados ao estresse oxidativo avaliado pelo malondialdeído (MDA) em pacientes em hemodiálise (HD). Métodos: Vinte pacientes em tratamento de HD (55,0 ± 15,2 anos, tempo de diálise de 76,5 ± 46,3 meses, IMC 23,6 ± 3,0 kg/m2) foram comparados com 11 indivíduos saudáveis (50,9 ± 8,0 anos, IMC 23,8 ± 1,9 kg/m2). O nível de MDA foi medido pela reação com o ácido tiobarbitúrico e os dados bioquímicos de rotina foram obtidos por meio do prontuário médico. Resultados: Os pacientes em HD apresentaram elevados níveis de MDA (13,2 ± 5,3 nmol/mL) quando comparados aos indivíduos saudáveis (5,1 ± 2,7 nmol/mL; p < 0,01). Doze pacientes (60%) apresentaram valores de ferritina superiores a 500 ng/mL e houve correlação positiva entre ferritina e MDA nos pacientes HD (r = 0,66; p = 0,005; n = 17). Conclusão: O excesso dos estoques de ferro em pacientes em HD resulta em um aumento da peroxidação lipídica e, consequentemente, contribui para um maior estresse oxidativo nesses pacientes

Dysbiosis in Patients with Chronic Kidney Disease: Let Us Talk About Vitamin K

PURPOSE OF REVIEW: This narrative review aimed to summarize the current evidence on the connection between dysbiosis and vitamin K deficiency in patients with chronic kidney disease (CKD). The presence of dysbiosis (perturbations in the composition of the microbiota) has been described in several non-communicable diseases, including chronic kidney disease, and it has been hypothesized that dysbiosis may cause vitamin K deficiency. Patients with CKD present both vitamin K deficiency and gut dysbiosis; however, the relationship between gut dysbiosis and vitamin K deficiency remains to be addressed. RECENT FINDINGS: Recently, few studies in animals have demonstrated that a dysbiotic environment is associated with low production of vitamin K by the gut microbiota. Vitamin K plays a vital role in blood coagulation as well as in the cardiovascular and bone systems. It serves as a cofactor for γ-glutamyl carboxylases and thus is essential for the post-translational modification and activation of vitamin K-dependent calcification regulators, such as osteocalcin, matrix Gla protein, Gla-rich protein, and proteins C and S. Additionally, vitamin K executes essential antioxidant and anti-inflammatory functions. Dietary intake is the main source of vitamin K; however, it also can be produced by gut microbiota. This review discusses the effects of uremia on the imbalance in gut microbiota, vitamin K-producing bacteria, and vitamin K deficiency in CKD patients, leading to a better understanding and raising hypothesis for future clinical studies

From bench to the hemodialysis clinic: protein-bound uremic toxins modulate NF-\kappaB/Nrf2 expression

International audiencePURPOSE: Uremic toxins produced by gut microbiota (indoxyl sulfate-IS, p-cresyl sulfate-p-CS, and indole-3-acetic acid-IAA) accumulate in hemodialysis (HD) patients and exhibit potent inflammatory effects. However, the impact of these toxins on nuclear E2-related factor 2 (Nrf2) and nuclear factor-kappa B (NF-kappaB) expression in HD patients remains poorly defined. The aim of this study was to evaluate the association between uremic toxins and Nrf2/NF-kappaB expression in vitro (RAW 264.7 macrophage-like cells) and in peripheral blood mononuclear cells from HD patients. METHODS: Uremic toxins, C-reactive protein (CRP), interleukin-6 (IL-6) and malondialdehyde (MDA) levels were measured in fifteen HD patients and nine healthy individuals. RAW 264.7 macrophage-like cells were incubated with IS, as a prototype of protein-bound uremic toxin. Nrf2 and NF-kappaB expressions were analyzed by RT-qPCR. RESULTS: HD patients presented high levels of inflammatory markers, MDA and uremic toxins. In addition, they presented high NF-kappaB and low Nrf2 expression. Uremic toxins were positively correlated with NF-kappaB expression (IS, rho = 0.58, p \textless 0.003; p-CS, rho = 0.71, p \textless 0.001; IAA, rho = 0.62, p \textless 0.001) and negatively with Nrf2 (IS, rho = - 0.48, p = 0.01; p-CS, rho = - 0.46, p \textless 0.02). Uremic toxins also exhibited positive correlations with CRP and MDA levels. Multivariate analysis revealed that p-CS is a determinant factor of NF-kappaB expression. In RAW 264.7 culture, NF-kappaB mRNA expression was stimulated by IS, while Nrf2 was downregulated. CONCLUSIONS: Thus, uremic toxins may stimulate NF-kappaB mRNA and decrease Nrf2 expression in HD patients and, consequently, trigger inflammation and oxidative stress