Brandt’s vole (Lasiopodomys brandtii) is a small herbivorous mammal that feeds on plants rich in secondary metabolites (PSMs), including tannins. However, plant defense mechanisms against herbivory by Brandt’s voles are not clearly established. This study aimed to investigate the effects of dietary tannic acid (TA) on the growth performance, intestinal morphology, digestive enzyme activities, cecal fermentation, intestinal barrier function, and gut microbiota in Brandt’s voles. The results showed that TA significantly hindered body weight gain, reduced daily food intake, changed the intestinal morphology, reduced digestive enzyme activity, and increased the serum zonulin levels (p < 0.05). The number of intestinal goblet and mast cells and the levels of serum cytokines and immunoglobulins (IgA, IgG, TNF-α, IL-6, and duodenal SlgA) were all reduced by TA (p < 0.05). Moreover, TA altered β-diversity in the colonic microbial community (p < 0.05). In conclusion, the results indicate that TA could damage the intestinal function of Brandt’s voles by altering their intestinal morphology, decreasing digestive ability and intestinal barrier function, and altering microbiota composition. Our study investigated the effects of natural PSMs on the intestinal function of wildlife and improved our general understanding of plant–herbivore interactions and the ecological role of PSMs.

Predator cues have profound impacts on the behavior and physiology of prey animals. However, the mechanisms underlying stress responses induced by chronic exposure to predator cues in mammals, particularly the role of the gut microbiota, remain insufficiently understood. This study investigated how gut microbiota contributes to behavioral and physiological responses in Brandt's voles ( Lasiopodomys brandtii ) under chronic predator odor exposure. Adult voles were repeatedly exposed to cat feces odor (CO) for 18 days (1 h/day), followed by behavioral tests to assess anti‐predator and anxiety‐like behaviors, hormonal measurements to evaluate basal hypothalamic–pituitary–adrenal (HPA) axis activity, and 16S rRNA sequencing to analyze gut microbiota composition. The results showed that repeated CO exposure increased anxiety‐like behaviors and basal HPA axis activity in both sexes. However, anti‐predator behaviors exhibited sex‐specific responses: Males were habituated to repeated CO exposure by reducing freezing and alerting behaviors, whereas females consistently displayed concealing strategies, reflecting different adaptive strategies to prolonged predator threats. While CO exposure did not alter the α‐diversity of gut microbiota, it significantly affected the β‐diversity in females, including a reduction in the relative abundance of Treponema and Quinella . Cecal microbiota transplantation from female CO‐exposed voles to naive recipients increased anxiety‐like behaviors and basal HPA levels but did not alter anti‐predator behaviors in the recipients. In contrast, male recipients showed no significant behavioral or physiological changes. These findings suggest that gut microbiota is involved in regulating anxiety‐like behavior and HPA axis activity in female voles but has a limited regulating role in male voles.

Background: Sleep deprivation (SD), defined as the disruption or loss of normal sleep, negatively affects energy metabolism, immune function, and gut microbiota in both humans and animals. Although SD has detrimental effects, it is often unavoidable due to work or study demands. Exercise has been shown to improve sleep quality, regulate metabolism, and enhance immune function. However, whether exercise can mitigate the adverse effects of unavoidable SD remains unclear. Methods: To explore the protective effects of exercise against SD-induced gut microbiota and metabolic dysfunction, mice were randomly assigned to four groups: control (CTR), exercise (EXE), SD, and exercise + SD (EXE + SD). Inflammatory markers and gut microbiota composition were analyzed to assess the impacts of SD and exercise interventions. Results: The inflammatory levels and energy metabolism in SD mice were significantly increased compared to those in CTR mice. Compared with SD mice, EXE + SD mice had a more stable gut microbiota structure and higher butyrate levels. Meanwhile, the inflammatory response caused by SD was also inhibited by exercise preconditioning. Both lipopolysaccharide inhibitors injection and butyrate supplementation can partially alleviate the elevation of inflammatory response and energy metabolism caused by SD. Conclusion: The inflammation and energy metabolism disorders in mice caused by SD can be inhibited by exercise preconditioning through stabilizing the structure of gut microbiota. This protective effect is highly likely related to the increase in butyric acid levels caused by exercise.

Environmental stressors encountered during pregnancy can exert profound effects on fetal development and program long-term physiological outcomes in offspring. Among these, ecologically relevant stressors such as predation risk remain understudied despite their potential to disrupt maternal physiology and placental function. In this study, we investigated how prenatal exposure to predator odor influences placental glucocorticoid metabolism and fetal growth in Brandt's voles (Lasiopodomys brandtii). Pregnant voles were exposed to predator odor to simulate prenatal predator stress, allowing us to assess its effects on fetal growth, maternal and fetal corticosterone levels, and the expression of key enzymes and transport proteins involved in glucocorticoid regulation. The results revealed that prenatal exposure to predator odor significantly reduced fetal weight. While maternal and fetal serum corticosterone levels increased, placental corticosterone levels remained unchanged. Additionally, our study observed significant increases in the expression of placental P-glycoprotein and 11β-hydroxysteroid dehydrogenase 1, both of which are crucial for maintaining placental glucocorticoid metabolic homeostasis. However, 11β-hydroxysteroid dehydrogenase 2 levels were unaffected. In the fetal brain, corticotropin-releasing hormone expression in the hypothalamus showed a downward trend, whereas glucocorticoid receptor expression in the hippocampus remained unchanged, indicating a disruption in the development of the hypothalamic-pituitary-adrenal axis. These findings suggest that prenatal exposure to predator odor alters placental glucocorticoid metabolism, leading to increased fetal corticosterone exposure and potentially impairing fetal development.