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.

Food grinding is supposed to be influenced by multiple factors. However, how those factors affecting this behavior remain unclear. In this study, we investigated the effect of food restriction on food grinding in Brandt’s voles (Lasiopodomys brandtii), as well as the potential role of the gut microbiota in this process, through a comparison of the variations between voles with different food supplies. Food restriction reduced the relative amount of ground food to a greater extent than it lowered the relative food consumption, and altered the abundance of Staphylococcus, Aerococcus, Jeotgalicoccus, and Un--s-Clostridiaceae bacterium GM1. Fecal acetate content for the 7.5 g-food supply group was lower than that for the 15 g-food supply group. Our study indicated that food restriction could effectively inhibit food grinding. Further, Un--s-Clostridiaceae bacterium GM1 abundance, Aerococcus abundance, and acetate content were strongly related to food grinding. Variations in gut microbial abundance and short-chain fatty acid content induced by food restriction likely promote the inhibition of food grinding. These results could potentially provide guidance for reducing food waste during laboratory rodent maintenance.

Food grinding is an abnormal behavior in rodents and its influencing factors are unknown. Our study investigated the potential relationships between gut microbiota and food grinding in Brandt's voles ( Lasiopodomys brandtii (Radde, 1861)) by comparing the differences between groups with different degrees of food grinding. The strong food-grinding group showed more relative food ground, higher ratio of ground food to food consumption, and lower percentage of time spent in the central area. The structure of fecal microbiota community differed between the strong and weak food-grinding groups. Strong and weak food-grinding voles showed higher abundances of Alistipes and Aerococcus and Atopostipes, Paenalcaligenes, Un—s-Clostridiaceae bacterium GM1, and Streptococcus, respectively. Strong correlations between the food ground to consumption ratio and abundances of fecal microbiota were found in Streptococcus and Paenalcaligenes. Fecal acetate and isobutyrate contents were higher in strong food-grinding voles and positively correlated with relative ground food and food ground to consumption ratio. Our study suggests that gut microbiota and short-chain fatty acids may contribute to the regulation of food-grinding behavior.

Food-grinding occurs in rodents and is influenced by multiple-factors. However, the factors affecting this behavior remain unclear. In this study, we aimed to investigate the effect of food restriction on food grinding by Brandt’s voles (Lasiopodomys brandtii), as well as the potential role of the gut microbiota in this process, through a comparison of the variations between voles with different food supplies. Food restriction reduced the relative amount of ground food to a greater extent than it lowered the relative food consumption, and altered the abundance of Staphylococcus, Aerococcus, Jeotgalicoccus, and Un--s-Clostridiaceae bacterium GM1. Strong correlations between the ground-to-consumed food ratio and the abundance of fecal microbiota were found for Un--s-Clostridiaceae bacterium GM1 and Aerococcus. The content of fecal acetate and propionate for the 7.5 g-food supply group was lower than that for the 15 g-food supply group. Further, the relative amount of ground food and ground-to-consumed food ratio were both positively correlated with the acetate content. Our study indicated that food restriction can effectively inhibit food grinding. Further, Un--s-Clostridiaceae bacterium GM1 abundance, Aerococcus abundance, and acetate content were strongly related to food grinding. Variations in gut microbial abundance and metabolite short-chain fatty acid content induced by food restriction likely promote the inhibition of food grinding. These results could potentially provide guidance for reducing food waste during laboratory rodent maintenance.

Food waste is a common issue arising from grinding of food by experimental animals, leading to excessive food scraps falling into cages. In the wild, animals grind food by gnawing vegetation and seeds, potentially damaging the ecological environment. However, limited ecology studies have focused on food grinding behavior since the last century, with even fewer on rodent food grinding, particularly recently. Although food grinding’s function is partially understood, its biological purposes remain under-investigated and driving factors unclear. This review aims to explain potential causes of animal food grinding, identify influencing factors, and discuss contexts and limitations. Specifically, we emphasize recent progress on gut microbiota significance for food grinding. Moreover, we show abnormal food grinding is determined by degree of excess normal behavior, emphasizing food grinding is not meaningless. Findings from this review promote comprehensive research on the myriad factors, multifaceted roles, and intricate evolution underlying food grinding behavior, benefiting laboratory animal husbandry and ecological environment protection, and identifying potential physiological benefits yet undiscovered.