
박테리아 유래 비타민 B12가 S-아데노실메티오닌(SAM) 및 인지질 합성 경로를 활성화시켜 인지질 수준을 높이고, 이를 통해 지방 생합성 유전자 fat-7의 발현을 억제하고 지방 구적 동역학을 조절함으로써 C. elegans의 지질 함량을 감소시킨다.


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Dietary factors play a pivotal role in regulating metabolism in both health and disease. Lipid metabolism is particularly important for organismal health and longevity. However, the mechanisms by which dietary factors influence lipid metabolism remain poorly understood. Here, using the nematode C. elegans as a model system, we investigated the influence of distinct bacterial diets on fat metabolism. We found that dietary vitamin B12 activates the S-adenosyl methionine (SAM) and phosphatidylcholine (PC) biosynthetic pathways. This activation leads to elevated levels of PC, which in turn suppresses the expression of the gene fat-7 and modulates lipid droplet dynamics through the regulatory proteins SBP-1/SREBP1 and SEIP-1/SEIPIN, respectively. Additionally, we identified a feedback loop involving SBP-1-mediated regulation of acid sphingomyelinase ASM-3, which enhances the production of phospho-choline and further stimulates PC synthesis. Our localization studies further suggest that ASM-3 may act as a signaling mediator between the intestine and coelomocytes, coordinating their roles in vitamin B12-mediated fat regulation. Overall, our findings shed new light on the complex interplay between diet and metabolic regulation, with a particular emphasis on the central role of phosphatidylcholine.

Highlights 

### Competing Interest Statement

The authors have declared no competing interest.

Dietary bacteria control C. elegans fat content through pathways converging at phosphatidylcholine

박테리아-식단이-c-elegans의-지질-대사를-인지질-합성-경로를-통해-조절한다


박테리아 식단이 C. elegans의 지질 대사를 인지질 합성 경로를 통해 조절한다
