Elucidating the pathogenesis of rumen abnormal adipose deposition in high-concentrate fed Hu sheep through...

Abnormal ruminal fat accumulation is a significant rumen health problem under high-concentration feeding regimes. However, the pathogenesis of abnormal ruminal fat accumulation remains poorly understood, the determinants of inter-individual variability are undetermined, and the incidence is relatively high.

This study assessed the incidence of abnormal ruminal adipose deposition in 326 fattening Hu lambs and conducted comparative analyses between lesion (LG) and normal (NG) groups. Production performance and feed intake were monitored over a 100-day trial. At slaughter (180 days), rumen samples were collected for histological evaluation using hematoxylin-eosin staining and ultrastructural analysis with transmission electron microscopy. Transcriptome sequencing was employed to identify differentially expressed genes associated with the condition.

The incidence of abnormal ruminal adipose deposition was 11.96%. Phenotypic analysis revealed that LG group showed significantly reduced growth performance (P < 0.05) and shorter ruminal papillae (P < 0.05) compared to NG group, accompanied by histopathological hallmarks including ectopic adipocyte infiltration in submucosal/muscular layers and localized inflammation. Ultrastructural examination identified desmosomal disruption, mitochondrial swelling, dilated rough endoplasmic reticulum, and cytoplasmic lipid droplet accumulation. Transcriptome sequencing identified 9,292 differentially expressed genes (DEGs). Key pathways included tumor-related signaling, cytokine-receptor interactions, and Hippo signaling. The aberrant upregulation of lipid regulatory factors such as LIPC and CLPSL2, coupled with the suppression of PNPLA3 and LIPG, establishes an interactive network.

Abnormal rumen adipose deposition in intensively fed sheep involves significant transcriptomic alterations affecting lipid metabolism and signaling pathways. These findings enhance understanding of ARAD pathogenesis and provide a foundation for developing targeted strategies to mitigate this underreported condition in intensive feeding systems.