(1) Background: We examined the effect of the acute administration of olive oil (EVOO), linseed oil (GLO), soybean oil (SO), and palm oil (PO) on gastric motility and appetite in rats. (2) Methods: We assessed food intake, gastric retention (GR), and gene expression in all groups. (3) Results: Both EVOO and GLO were found to enhance the rate of stomach retention, leading to a decrease in hunger. On the other hand, the reduction in food intake caused by SO was accompanied by delayed effects on stomach retention. PO caused an alteration in the mRNA expression of NPY, POMC, and CART. Although PO increased stomach retention after 180 min, it did not affect food intake. It was subsequently verified that the absence of an autonomic reaction did not nullify the influence of EVOO in reducing food consumption. Moreover, in the absence of parasympathetic responses, animals that received PO exhibited a significant decrease in food consumption, probably mediated by lower NPY expression. (4) Conclusions: This study discovered that different oils induce various effects on parameters related to food consumption. Specifically, EVOO reduces food consumption primarily through its impact on the gastrointestinal tract, making it a recommended adjunct for weight loss. Conversely, the intake of PO limits food consumption in the absence of an autonomic reaction, but it is not advised due to its contribution to the development of cardiometabolic disorders.

O trabalho objetivou realizar revisão da literatura acerca das evidências científicas disponíveis sobre o potencial terapêutico que alguns compostos bioativos podem exercer sobre a infecção por Sars-Cov-2, a partir de testes realizados com as técnicas de docking molecular. A revisão integrativa foi realizada a partir de buscas nos bancos de dados eletrônicos acerca de publicações de artigos originais escritos em inglês e português, entre os anos de 2019 a 2021. As buscas foram realizadas nas bases de dados: Science Direct (Biblioteca virtual da Elsevier), Scielo (Scientific Electronic Library Online), Pubmed/Medline (Medical Literature Analysis and Retrievel System Online) e BVS (Biblioteca Virtual em saúde), utilizando como descritores em saúde de acordo com a plataforma DeCS/MeSH as palavras: Compostos bioativos derivados de alimentos, replicação, SARS-CoV-2, in silico, nos idiomas inglês e português, utilizando o termo ‘’and’’ como operador booleano. Após o processo de busca e seleção utilizando os critérios citados na metodologia, foram selecionados 6 artigos. Produtos naturais derivados de matrizes alimentares podem ser uma fonte valiosa de novos compostos bioativos para combater a pandemia da COVID-19. De acordo com os resultados relatados nesta revisão, vários compostos naturais, incluindo polifenóis e flavonóides, mostraram a capacidade de prevenir a replicação do SARS-CoV-2 por meio da inibição das principais proteases do vírus, para assim mitigar as consequências clínicas da infecção, de acordo com a técnica in silico utilizada.

In this narrative review, we synthesize current epidemiological and mechanistic evidence on the association between ultra-processed food (UPF) consumption, obesity, and breast cancer (BC) risk. The global increase in UPF intake has been linked to substantial metabolic alterations, including weight gain, insulin resistance, low-grade chronic inflammation, and hormonal imbalances—factors that contribute to a tumor-promoting microenvironment. Given the established role of obesity in breast carcinogenesis, understanding the intermediary role of UPFs is critical. Articles were selected from PubMed, SciELO, and ScienceDirect databases using descriptors related to ultra-processed foods, obesity, and breast cancer. The synthesis of current evidence supports the view that excessive UPFs consumption represents a modifiable and preventable risk factor for obesity and BC, underscoring the need for integrated strategies in dietary guidance, public health policy, and cancer prevention.

This study aimed to synthesize a liposomal nanoformulation containing citrinin (LP-CIT) to improve its availability and to evaluate its toxicogenomic profile, focusing on cytotoxic and genotoxic effects in breast cancer (MDA-MB-231) and non-tumorigenic mammary epithelial (MCF-10A) cell lines. The formulation was characterized by macroscopic appearance, pH, particle size, polydispersity index (PDI), zeta potential, encapsulation efficiency, and estability of nanoparticles. Citrinin content, encapsulation efficiency, and liposome stability were evaluated. Cytotoxicity was assessed using MTT, trypan blue exclusion, and flow cytometry. Cell death mechanisms were investigated by mitochondrial membrane potential analysis and expression of apoptotic markers (caspase-9 and BAX). Genotoxicity was evaluated using the comet assay. The liposomal nanosystem consisted of small unilamellar vesicles with a mean diameter of 143.3 nm, a PDI of 0.3, and a positive surface charge (+ 28.5 mV). The average was 63.69 ± 0.18% of citrinin encapsulated in liposomes with stability more than 21 days. Both free citrinin (CIT) and LP-CIT showed cytotoxic effects in MDA-MB-231 and MCF-10A cells, with lower LC₅₀ values observed for LP-CIT. Although LP-CIT induced more pronounced cytotoxic and genotoxic effects in the cancer cell line, toxic effects were also observed in non-tumorigenic cells, indicating limited selectivity. Cell death was associated with mitochondrial membrane depolarization and increased caspase-9 and BAX expression. Both formulations induced DNA damage as detected by the comet assay. Liposomal encapsulation enhanced citrinin biological activity but did not indicate tumor selectivity. Thus, this study represents a toxicogenomic assessment of citrinin and its liposomal formulation for potential therapeutic applicability.

Background: Oncological treatment remains a major clinical challenge. Despite therapeutic advances and the diversity of available approaches, many tumors continue to exhibit limited responsiveness to chemotherapy. In this context, nutrition has emerged as a promising complementary strategy to support cancer therapy. In particular, interventions based on nutritional deprivation have gained prominence due to their ability to modulate tumor metabolism, inducing alterations that may increase the sensitivity of cancer cells to conventional treatments. Accordingly, the present study aimed to evaluate the safety and efficacy of caloric restriction combined with chemotherapy in a Sarcoma-180 model, investigating its effects on immunological and hematological parameters, antioxidant activity, oxidative stress, and tumor and liver morphology, as well as DNA damage. Methods: Mice bearing Sarcoma-180 were randomly assigned to four groups: Ad Libitum (AL), Ad Libitum + Doxorubicin (ALDOX), Caloric Restriction (CR), and Caloric Restriction + Doxorubicin (CRDOX). Assessment included tumor weight and volume, food and caloric intake, hematotoxicity, lipid metabolism, oxidative stress and antioxidant markers, genotoxicity, morphological alterations in the tumor and liver, and overall survival. Results: The data obtained demonstrate that caloric restriction combined with doxorubicin is both safe and feasible, as it preserves body weight and does not induce metabolic disturbances. Importantly, this combined strategy produced a marked reduction in tumor volume and mass while also mitigating the hematotoxicity typically associated with doxorubicin. In peripheral blood, the regimen decreased chemotherapy-induced DNA damage, supporting a systemic protective effect. Consistently, the combination reduced oxidative stress markers (NOx and MDA) and enhanced antioxidant activity within the tumor. Histological analyses further confirmed these outcomes, showing tumor cell death with features compatible with apoptosis and reduced local invasion. Together, these data indicate that caloric restriction enhances the antitumor efficacy of doxorubicin while simultaneously improving treatment tolerance. Conclusions: This study demonstrates that caloric restriction, combined with doxorubicin, is safe, well-tolerated, and enhances the antitumor response in the Sarcoma-180 model.