C. cochlearium 2316 Ameliorates High-Fat Diet-Induced Obesity and Metabolic Syndrome Risk Factors via Enhanced Energy Expenditure and Glucose Homeostasis

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Abstract

Objectives: This study investigated the potential beneficial effects of a probiotic candidate, Clostridium cochlearium 2316, in modulating physiological and metabolic markers in mice with high-fat diet-induced obesity (DIO). Methods: C57BL/6 DIO mice were assigned to three groups (ad libitum): standard low-fat control (LF, 10% fat), high-fat diet (HF, 60% fat), and high-fat diet supplemented with approximately one billion CFU/day of CC2316 via daily oral gavage for 16 weeks. Results: After 16 weeks, the CC group exhibited 17.3% lower body weight gain (p < 0.001) and significant fat mass decrease (p < 0.0001) compared to HF mice. Serum biochemistry showed that CC2316 supplementation resulted in a 27.7% reduction in fasting blood glucose (p < 0.05), a 58.4% reduction in fasting insulin (p < 0.01), and an 89.4% improvement in HOMA-IR score (p < 0.05). Furthermore, serum total cholesterol level decreased dramatically by 40.2% in the CC group (p < 0.001). Despite a higher caloric absorption rate (p < 0.001), CC mice demonstrated a significant beneficial shift in energy expenditure, characterized by an increased basal metabolic rate (p < 0.05), higher energy expenditure (p < 0.05), and an elevated respiratory quotient (RER) (p < 0.05), alongside increased physical activity (p < 0.05). Conclusions: This investigation strongly suggests that CC2316 supplementation mitigates the adverse effects of HFD-induced obesity by modulating whole-body energy metabolism, positioning it as a potential aid to lower risk factors associated with metabolic syndrome. The precise mechanisms linking the gut microbiome to altered energy substrate utilization are discussed and suggested for further investigation.

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APA

Zhu, W., Edirisuriya, P., Ai, Q., Yang, F., Tang, J., Nie, K., … Zhou, K. (2025). C. cochlearium 2316 Ameliorates High-Fat Diet-Induced Obesity and Metabolic Syndrome Risk Factors via Enhanced Energy Expenditure and Glucose Homeostasis. Nutrients , 17(24). https://doi.org/10.3390/nu17243848

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