Inflammatory bowel diseases (IBD) affect the gastrointestinal tract, and the imbalance of intestinal immune homeostasis can trigger them. Pequi oil (PO), a monounsaturated (MUFA) and carotenoid-rich food with nutraceutical potential, could help reshape the intestinal immune response, ameliorating IBD outcomes. This study investigates the effects of a 28 days intake of PO on elements of the intestinal immune response of mice with DSS-induced ulcerative colitis (disease activity index, colonic damage, inflammatory cells and markers). PO reduces body weight, colonic crypt and goblet cell losses and ameliorates diarrhea. In the colon, it increases T cells and secretory-IgA and decreases CD8+T cells. In lymphoid organs, it reduces CD8+T cells. Moreover, it also reduces the IL-17 and CRP in plasma. PO oil promotes a less cytotoxic response that may protect mice from immunological injuries caused by an IBD in the intestinal mucosa, improving the disease prognosis. Practical applications: This study demonstrates that the intake of pequi oil contributes to the regulation of immune response and improves clinical and histological signs of DSS-induced ulcerative colitis in mice. Its effects in cytotoxic cell reduction and other inflammatory markers and stimulation of regulatory cells, and preservation of mucus-producing cells, provide news insights about the importance of the regular intake of this food to better prognosis of ulcerative colitis acute episodes. In addition, these findings encourage further studies with foods with a protective potential for the intestinal mucosa.

Background Caryocar brasiliense (pequi) oil is high in monounsaturated fat acids (MUFA), especially oleic, and in carotenoids, which have been associated with protection against cardiovascular disease. However, this food is poorly studied in this context, especially in the cardiac function. Therefore, we investigated the effects of a long-term intake of pequi oil in systemic cardiovascular risk factors and in the ex vivo cardiac function of rats.MethodsPreviously, we determined fatty acids and carotenoids in pequi oil. Next, male rats were divided in C – control group feed a standard diet, and PO – pequi oil group fed the same diet added pequi oil (+2.25 g.100 g−1). After 15 weeks, plasma lipids, glucose, insulin, blood pressure, heart rate, hepatic lipids were accessed and visceral fat pads were harvested. Hearts were used for the ex vivo cardiac function, histologic assays, SERCA2a and phospholanban (PLB) determinations.ResultsIn agreement with scientific data, pequi oil had expressive amounts MUFA, especially oleic acid, and carotenoids. Hepatic triglycerides (TG) were reduced by pequi oil intake (p < 0.05). All others cardiovascular risk factors were not changed. The intrinsic heart rate was lower in PO group (p < 0.05). SERCA2a content was higher in this group (p < 0.05), without affecting PLB. Also, SERCA2a/PLB ratio increased in PO group (p < 0.05).Conclusion Pequi oil intake improved cardiac function ex vivo, despite no significant changes in systemic cardiovascular risk factors. The higher lipid offer in pequi oil diet, its composition in oleic acid and carotenoids could be related to those effects.

Caryocar brasiliense (pequi) is an exotic fruit, high in monounsaturated fat acids (MUFA) and bioactive compounds, which have beneficial effects on cardiometabolic risk factors. However, this fruit is poorly studied in this context. In this study, the effects of pequi pulp intake on cardiometabolic risk factors of rats were evaluated. Therefore, 16 male weaned rats were divided into two groups: Control group and Pequi group. Control group was feed a standard diet and pequi group, the same diet added pequi pulp (3.26 g.100 -1 ) for 15 weeks. At the end, plasma lipids, glucose, insulin, Homeostasis Model Assessment of Insulin Resistance index (HOMA-IR), blood pressure, heart rate, hepatic and fecal lipids and intestinal histomorphometric parameters were accessed. Liver and heart samples were harvested for redox status assays. There were no differences between experimental groups for blood pressure, heart rate, glucose, insulin, HOMA-IR, triglycerides, cholesterol, HDL-cholesterol, and liver and heart redox status (p<0.05). Pequi group had lowered lipid hepatic deposition and increased fecal output (p<0.05), increased intestinal villus height and crypt depth. Thus, pequi pulp intake minimized liver fat deposition by increasing its intestinal output and improved intestinal structure of rats, which can contribute for reducing cardiometabolic risk factors. MUFA, carotenoids and fibres can be associated, at last in part, with these effects.

Ultra-processed foods (UP) are frequently associated with poor diet quality and lack many nutrients necessary for skeletal muscle health, which could contribute to developing sarcopenia. However, investigations about possible associations between the intake of UP and sarcopenia are missing. This study aimed to describe the magnitude of the exposition to UP (eating frequency) and compare it in older adults with and without sarcopenia. It also described associations between the magnitude of exposition of UP with body composition markers of sarcopenia in all subjects. It was a cross-sectional study with a sample of 118 community-dwelling older adults. Body composition was accessed by Dual-energy X-ray absorptiometry (DXA) and UP intake by a food frequency questionnaire (FFQ). All foods in the FFQ were categorized into two groups: (1) non-UP and (2) UP. SCORE I (mean score for food group 1) and SCORE II (mean score for food group 2) were calculated. The eating frequency of UP was near 3 to 4x/week and higher for sarcopenic subjects (p<0.05). Subjects consuming UP more than 1-2x/week were more likely to be sarcopenic than those consuming less than 1-2x/week. Therefore, sarcopenic subjects were more exposed to UP. In addition, even at a low exposition, the intake of UP increases the chances of developing sarcopenia in older adults.

Caloric restriction (CR) reduces body weight and systemic inflammation, but effects on adipose tissue under dietary lipid overload are controversial. We evaluated the effects of CR-induced weight loss with a high-fat diet (HF) on adipose tissue inflammation of obese mice. Male mice were assigned into LF (low-fat diet) and HF. After 8-wk, HF was reassigned for another 7-wk into HF – kept at HF; LFAL - switched from HF to LF ad libitum; RHF - fed HF calorie-restricted to reach LFAL body weight. Serum markers, adipocytokines, morphology, and inflammatory infiltrates in retroperitoneal adipose tissue (RAT) were accessed. LFAL and RHF reduced body weights, equaling to LF. LFAL restored almost all inflammatory markers as LF, except tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and adiponectin. Compared to HF, RHF lowered visceral adiposity, retroperitoneal adipocyte sizes, RAT inflammatory cell infiltration as well as TNF-α, interleukin-6, hepatic and serum C-reactive protein, which were higher than LFAL; adiponectin and MCP-1 did not change. CR with high-fat diet reduced body weight and attenuated visceral adiposity, but did not fully recover visceral tissue inflammation. Novelty bullets • Caloric restriction in a high-fat diet ameliorated visceral adiposity. • Caloric restriction in a high-fat diet did not recover visceral adipose tissue inflammation.