Background/Objectives: High-fat diets (HFDs) are widely used to induce obesity, but cost-effective and reproducible formulations remain challenging. Moreover, the reversibility of metabolic and gut microbiota alterations following HFD withdrawal is not fully understood. This study evaluated a low-cost HFD model in mice and investigated metabolic, oxidative, and gut microbiota changes during a subsequent 12-week dietary normalization phase. Methods: Male C57BL/6 mice were fed a standard diet (CTN) or a lard-supplemented HFD for 12 weeks (Phase 1), followed by 12 weeks dietary normalization to a standard diet (Phase 2). Body weight, adiposity, blood glucose, biochemical parameters, and oxidative markers were assessed. Fecal samples were analyzed for short-chain fatty acids (SCFAs), microbiota composition (16S rRNA sequencing), and predicted functions using FAPROTAX and PICRUSt2. Results: The HFD significantly increased body weight, abdominal circumference, the Lee index, and adipose tissue mass compared to CTN. Following diet normalization, both groups exhibited weight loss, but the previously obese mice maintained a higher Lee index and distinct lipid and uric acid profiles. No hepatic oxidative stress was detected after normalization. SCFA profiles underwent a temporal shift: CTN showed higher fecal acetate, while HFD mice exhibited elevated butyrate. Functional prediction revealed one pathway associated with an unclassified Rickettsiales bacterium that was exclusively found in HFD mice. The CTN group exhibited a higher abundance of the thiamine diphosphate formation pathway (PWY-7357), suggesting enhanced oxidative metabolism. Conclusions: This low-cost HFD successfully induced obesity and dysbiosis. Dietary normalization resulted in a partial modulation of metabolic and microbial balance, thereby highlighting host–microbe metabolic plasticity.

Background: The study evaluated the effects of resistance exercise training and açaí supplementation on cardiac parameters in hypertensive animals. Methods: For this study, rats from the Wistar and SHR lines (spontaneously hypertensive rats) were used. The animals were divided into 5 groups: Wistar Control (C); Control Hypertensive (H); Trained Hypertensive (HT); Hypertensive and Supplemented with Açaí (HA); and Hypertensive Trained and Supplemented with Açaí (HAT). Resistance exercise training was carried out through climbing. The supplemented groups received 3 g of açaí/kg of body mass. The animals’ systolic blood pressure (SBP), body mass, and physical test were measured at the beginning and end of the intervention. At the end, an echocardiographic analysis was performed. Histological analysis and oxidative stress of the LV were performed. Results: It was found that hypertensive animals showed an increase in SBP, and the treatments reduced this parameter. The trained groups achieved higher values of maximum carrying load. Hypertension increased the dimension of the left ventricular free wall in diastole and reduced ejection and shortening fractions. The trained groups showed improvement in ejection and shortening fractions. The H group increased the proportion of extracellular matrix and reduced the proportion of cells, with the HAT group attenuating this change. Cell diameter was greater in group H, and all treatments reduced this parameter. Hypertension increased the concentration of malondialdehyde and decreased catalase activity in LV. The treatments managed to mitigate this damage. Conclusions: It is concluded that the treatments managed to generate positive cardiovascular adaptations, and their combination enhanced these effects.

Background: Recent studies indicate that maintaining a healthy gut microbiota balance positively influences brain function through the microbiota-gut-brain (MGB) axis. Intestinal inflammation disrupts gut microbial homeostasis, exacerbates inflammatory and oxidative processes, and reduces beneficial microbial metabolites essential for brain health. These alterations may impair MGB axis signaling and increase intestinal and blood-brain barrier (BBB) permeability, facilitating the translocation of inflammatory mediators and potentially contributing to neurological dysfunction. Kefir has emerged as a fermented food with potential psychobiotic properties due to its ability to modulate gut microbiota and its metabolites. However, its effects on brain-related outcomes during intestinal inflammation remain poorly understood.Aim: To investigate the association between milk kefir consumption and selected brain biomarkers in IL-10^-/^- mice.Methods: Male C57BL/6 mice were allocated into four groups (n = 5/group): wild-type mice receiving water (WWT), wild-type mice receiving milk kefir (KWT), IL-10^-/^- mice receiving water (WKO), and IL-10^-/^- mice receiving milk kefir (KKO). Brain analyses included cytokine levels, antioxidant activity, tight junction protein expression, and short-chain fatty acids (SCFAs), while histological evaluation focused on the small intestine.Results: Kefir consumption was associated with improved intestinal morphology in IL-10^-/^- mice (p < 0.03), increased brain SCFA levels (p < 0.001), reduced malondialdehyde concentrations, and higher occludin expression in brain tissue.Conclusion: Overall, these findings suggest that milk kefir intake may influence specific brain biomarkers in IL-10^-/^- mice. These observations provide preliminary insights and support the need for further studies to elucidate the potential psychobiotic role of kefir in intestinal inflammation.

This study aimed to evaluate the effects of milk kefir on parameters related to inflammatory bowel disease (IBD) in interleukin‐10 knockout (IL‐10 ^−/− ) mice. Sixteen C57BL/6J IL‐10 ^−/− male mice were divided into two experimental groups. The control group ( n = 8) received 0.4 mL of whole milk (UHT) and the kefir group ( n = 8) received 0.4 mL of a fermented beverage made from milk kefir grains (2.4 × 10 ⁸ colony‐forming units [CFU]), both administered via gavage for 4 weeks. Feces were collected and body weight was measured weekly. At the end of the study, the animals were anesthetized and euthanized, and the small intestine and cecum content were collected for analysis. Proximate composition of kefir and microbiological analysis were conducted. Histomorphometry measurements and quantification of short‐chain fatty acids (SCFAs) were conducted in small intestine. SFCAs were also evaluated in cecum content, and microbiota composition was evaluated in fecal samples. The kefir beverage improved histomorphometry characteristics of the small intestine, increased the number of goblet cells, reduced inflammatory infiltrates, increased Lactobacillus , and reduced Desulfovibrio , suggesting attenuation of the inflammatory process. Furthermore, the kefir beverage increased the concentration of butyrate, a short‐chain fatty acid with anti‐inflammatory properties, in the small intestine, which may also be associated with reduced inflammation in this group.