Camu-camu (Myrciaria dubia) attenuates intestinal alterations induced by a high-fat, high-fructose diet in C57BL/6 mice

Metabolic alterations induced by excessive consumption of sugars and fats are frequently associated with intestinal imbalance, oxidative stress, and impaired gastrointestinal homeostasis. In this context, foods rich in bioactive compounds, such as camu-camu (Myrciaria dubia), have been investigated due to their potential modulatory effects on intestinal parameters. This study aimed to evaluate the effects of camu-camu on gastrointestinal alterations induced by a high-fat, high-fructose (HFHF) diet in C57BL/6 mice. The animals were divided into three groups (n = 9): AIN-93M, HFHF, and HFHF with camu-camu (HFCC). Fecal parameters, including color, moisture, pH, and stool consistency according to the Bristol Stool Scale, were evaluated, in addition to the quantification of short-chain fatty acids (acetate, propionate, butyrate) by high-performance liquid chromatography (HPLC). Markers related to oxidative balance were quantified using spectrophotometric assays, including catalase (CAT), glutathione S-transferase (GST), superoxide dismutase (SOD), protein carbonyls (PCN), malondialdehyde (MDA), nitric oxide (NO), and ferric reducing antioxidant power (FRAP). Statistical analyses were performed using GraphPad Prism software, and data normality was assessed using the Shapiro-Wilk test. Intergroup differences were analyzed by one-way analysis of variance (ANOVA), followed by Tukey’s post hoc test. This project was approved by CEUA/UFV (10/2023). Animals in the HFHF group showed a higher frequency of discolored stools and predominance of type 2 stools on the Bristol Stool Scale, indicating impaired intestinal transit. In contrast, the HFCC group predominantly exhibited type 3 stools, suggesting improved intestinal function. No significant differences were observed in fecal pH among the groups (p > 0.05), whereas the HFCC group showed lower fecal moisture values compared to the AIN-93M (p < 0.05). In addition, significant reductions in acetate, propionate, and butyrate concentrations were observed in the HFHF group compared to the AIN-93M (p < 0.05), while camu-camu treatment promoted recovery of these metabolites, especially butyric acid (p < 0.05). Regarding oxidative parameters, the HFHF group exhibited lower CAT and NO levels, associated with increased GST and SOD activities compared to the AIN-93M (p < 0.05), indicating redox imbalance. Camu-camu supplementation significantly increased CAT and NO levels, in addition to reducing PCN levels compared to the HFHF group (p < 0.05), suggesting reduced oxidative protein damage. No significant differences were observed for MDA and FRAP (p > 0.05). These results demonstrate that the HFHF diet promotes important metabolic and intestinal alterations, including reduced short-chain fatty acids, fecal changes, and oxidative imbalance. In contrast, camu-camu supplementation exerted a modulatory effect on these parameters, contributing to improved intestinal function, increased beneficial metabolites, and reduced oxidative damage. In conclusion, camu-camu improved intestinal and oxidative parameters in C57BL/6 mice fed an HFHF diet, supporting its role in maintaining intestinal homeostasis under metabolic stress. Acknowledgments: CAPES (001) and FAPEMIG (APQ-01202-24).