Frontiers in microbiology · 2026
Alkaline mineral complex supplementation alters gut microbiota and metabolic profiles and supports colonic health in finishing cattle.
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Li Jia, Liu Xingyu, Gu Li, Liu Xiaowan, Wang Yixin, Guo Hongrui, Gou Liping, Qi Jiancheng, Zuo Zhicai
Аннотация
INTRODUCTION: The ruminant colon plays a critical role in intestinal homeostasis but is highly susceptible to dysfunction induced by high-concentrate diets during the finishing period. This study investigated the efficacy of alkaline mineral complex (AMC) against such colonic disturbances in finishing cattle.
METHODS: Fifty-four Simmental crossbred cattle were randomly allocated into the Ctrl group (n = 27) and AMC supplementation group (n = 27) over a 142-day feeding trial. Fecal consistency was recorded twice daily on 2 days per week in 10 randomly selected cattle per group, and on day 142, samples of blood, colonic tissue, mucosa, and contents were collected for serum biochemistry, histology, 16S rRNA gene sequencing, metabolomics, and proteomics.
RESULTS: AMC supplementation significantly improved fecal consistency, markedly reducing watery feces (P = 0.0082) while increasing normal feces (P = 0.0051). Serum biochemistry showed that AMC supplementation was associated with higher serum concentrations of Na+ (P = 0.0058), K+ (P = 0.0141), and total Ca (P = 0.0076), along with reduced diamine oxidase (DAO) activity (P < 0.0001) compared to the Ctrl group (n = 10 per group). Histological analysis showed that AMC supplementation reduced inflammation and increased goblet cells (P = 0.0013) (n = 3 per group). 16S rRNA gene sequencing demonstrated that AMC supplementation increased gut microbial α-diversity and reduced abundance of potentially pathogenic bacteria (n = 5 per group). Metabolomic analysis showed that AMC supplementation was associated with lower levels of Sph(d18:0) and ornithine, and with distinct alterations in sphingolipid metabolism and branched-chain amino acid (BCAA) degradation pathways (n = 5 per group). Proteomic profiling highlighted the enrichment of aldosterone-regulated sodium reabsorption and tight junction pathways (Ctrl, n = 4; AMC, n = 5). Using ELISA and spectrophotometric assays, we found that AMC supplementation significantly downregulated the levels of TNF-α (P = 0.0401) and IL-6 (P = 0.0104), while elevating GSH-Px activity (P = 0.0097) (n = 10 per group). The qPCR results indicated that AMC supplementation upregulated the mRNA expression of key intestinal barrier components MUC2 (P = 0.0186), ZO-1 (P = 0.0382), and transporters AQP3 (P = 0.0156), NBCe1 (P < 0.0001), and ATP1A1 (P < 0.0001) (n = 3 per group).
DISCUSSION: Collectively, AMC supplementation improved fecal consistency and markers of colonic health. These benefits were accompanied by coordinated shifts in the gut microbiota, metabolic, and proteome, reduced inflammation, and enhanced expression of barrier and transport genes, suggesting a potential interplay between the microbiota, metabolome, and host mucosa.
METHODS: Fifty-four Simmental crossbred cattle were randomly allocated into the Ctrl group (n = 27) and AMC supplementation group (n = 27) over a 142-day feeding trial. Fecal consistency was recorded twice daily on 2 days per week in 10 randomly selected cattle per group, and on day 142, samples of blood, colonic tissue, mucosa, and contents were collected for serum biochemistry, histology, 16S rRNA gene sequencing, metabolomics, and proteomics.
RESULTS: AMC supplementation significantly improved fecal consistency, markedly reducing watery feces (P = 0.0082) while increasing normal feces (P = 0.0051). Serum biochemistry showed that AMC supplementation was associated with higher serum concentrations of Na+ (P = 0.0058), K+ (P = 0.0141), and total Ca (P = 0.0076), along with reduced diamine oxidase (DAO) activity (P < 0.0001) compared to the Ctrl group (n = 10 per group). Histological analysis showed that AMC supplementation reduced inflammation and increased goblet cells (P = 0.0013) (n = 3 per group). 16S rRNA gene sequencing demonstrated that AMC supplementation increased gut microbial α-diversity and reduced abundance of potentially pathogenic bacteria (n = 5 per group). Metabolomic analysis showed that AMC supplementation was associated with lower levels of Sph(d18:0) and ornithine, and with distinct alterations in sphingolipid metabolism and branched-chain amino acid (BCAA) degradation pathways (n = 5 per group). Proteomic profiling highlighted the enrichment of aldosterone-regulated sodium reabsorption and tight junction pathways (Ctrl, n = 4; AMC, n = 5). Using ELISA and spectrophotometric assays, we found that AMC supplementation significantly downregulated the levels of TNF-α (P = 0.0401) and IL-6 (P = 0.0104), while elevating GSH-Px activity (P = 0.0097) (n = 10 per group). The qPCR results indicated that AMC supplementation upregulated the mRNA expression of key intestinal barrier components MUC2 (P = 0.0186), ZO-1 (P = 0.0382), and transporters AQP3 (P = 0.0156), NBCe1 (P < 0.0001), and ATP1A1 (P < 0.0001) (n = 3 per group).
DISCUSSION: Collectively, AMC supplementation improved fecal consistency and markers of colonic health. These benefits were accompanied by coordinated shifts in the gut microbiota, metabolic, and proteome, reduced inflammation, and enhanced expression of barrier and transport genes, suggesting a potential interplay between the microbiota, metabolome, and host mucosa.