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Mast cell-driven adipocyte lipolysis promotes post-expansive VAT atrophy and ectopic hepatic steatosis

Wang, J.; Zhang, L.; Liu, W.-Y.; Jin, X.-Z.; Yin, H.; Cai, H.; Yuan, H.-Y.; Yang, W.; Bao, B.; Zheng, M.-h.; Wang, H.; Shi, G.-P.; Zhang, X.; Liu, J.

2026-01-08 cell biology
10.64898/2026.01.07.698076 bioRxiv
Show abstract

Excessive visceral fat is an essential risk factor of metabolic dysfunction-associated steatotic liver disease (MASLD). Yet, the cellular and molecular mechanisms implicated in the correlation between visceral fat metabolism and hepatic steatosis remain poorly understood. Here we report post-expansive epididymal adipose tissue (EAT) atrophy and hepatic steatosis in mice fed a high-fat diet (HFD) primarily due to elevated adipocyte lipolysis in EAT. Mast cell (MC) accumulation in EAT represents a lipolysis-associated feature. Pharmacological stabilization of MCs suppresses EAT adipocyte lipolysis, and improves EAT atrophy and hepatic steatosis. MC-derived serotonin (5-HT) correlates with visceral adipose tissue (VAT) lipolysis in HFD-fed mice as well as in MASLD patients. Conditional deletion of 5-HT from MCs or its receptor HTR2b on adipocytes demonstrates that MC-derived 5-HT promotes adipocyte lipolysis, EAT atrophy, and hepatic steatosis by binding on adipocyte HTR2b. These results suggest that MCs and MC-derived 5-HT are potential therapeutic targets for obesity-associated MASLD.

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