Abstract: To investigate the ameliorative effects of Weizmannia coagulans (W. coagulans) CGMCC 9951 on the damage induced by a high-sucrose diet in Caenorhabditis elegans (C. elegans) and to elucidate the target pathways involved in the regulation of lipid metabolism. Methods: A high-sucrose diet model of C. elegans was established by supplementing the culture medium with 100 mmol/L sucrose. The effects of W. coagulans CGMCC 9951 on the body length, body width, locomotor activity, and egg production of C. elegans were assessed, along with changes in oxidative stress and lipid accumulation. Results: The lifespan of C. elegans on a high-sucrose diet was extended by up to 27.36% (P<0.05) by CGMCC 9951. Head thrashing frequency was significantly increased by 64.01%, and body bending frequency by 101.91% (P<0.05). Egg production was increased by up to 77.14% (P<0.05). Body width was significantly reduced (P<0.05), but no significant changes were observed in body length (P>0.05). Catalase activity and glutathione levels were enhanced by up to 123.34% and 55.63%, respectively (P<0.05), while malondialdehyde accumulation was reduced by up to 74.88% (P<0.05) by CGMCC 9951. Additionally, triglyceride levels were decreased by up to 56.25% (P<0.05) by CGMCC 9951, and a significant reduction in lipid accumulation was revealed by Oil Red O staining. Real-time quantitative PCR showed that the expression of genes related to the SREBP signaling pathway was significantly downregulated (P<0.05) by CGMCC 9951, while the genes related to the NHR-49 and 5-HT signaling pathways were upregulated (P<0.05). Moreover, in the insulin signaling pathway, daf-2 expression was downregulated, and daf-16 expression was upregulated (P<0.05). Compared to daf-16, a pivotal role in the regulation of lipid accumulation in C. elegans on a high-sucrose diet was played by daf-2 under the treatment of CGMCC 9951. Finally, the nuclear translocation of DAF-16 was reduced by CGMCC 9951. Conclusion: High-sucrose diet-induced damage in C. elegans can be mitigated and lipid accumulation reduced through modulation of lipid metabolism pathways by W. coagulans CGMCC 9951.