Pathophysiological Mechanisms of Emaciation Syndrome in Plectropomus leopardus : Insights From Histology and Transcriptomics

ABSTRACT

Emaciation syndrome presents a major challenge to aquaculture by reducing growth performance and survival in cultured fish. However, its underlying physiological and molecular mechanisms remain poorly understood. This study investigated the pathological characteristics and transcriptomic alterations associated with severe emaciation in the leopard coral grouper ( Plectropomus leopardus ). Histological examination revealed extensive intestinal villus atrophy, hepatic lipid depletion, and pronounced skeletal muscle fiber shrinkage in emaciated fish. RNA‐seq analysis across the intestine, liver, and muscle identified 3327, 4482, and 5496 differentially expressed genes (DEGs), respectively, between the emaciated and control groups. Functional enrichment analysis indicated that suppression of digestive enzyme genes (e.g.,  cela1 , cela3b , and cpa5 ) in the intestine, activation of lipid catabolism and gluconeogenic pathways (including pck1 ) in the liver, and upregulation of proteasome subunit genes ( psma1 , psmb1 , and psmc3 ) in the muscle were key molecular alterations associated with emaciation syndrome. Quantitative reverse transcription polymerase chain reaction (qRT‐PCR) and in situ hybridization (ISH) validated the tissue‐specific transcriptional patterns of these representative DEGs. Collectively, these findings suggest coordinated tissue‐specific alterations involving intestinal digestive and absorptive function, hepatic metabolic regulation, and muscle protein turnover in emaciated groupers. This integrative analysis provides new insights into the molecular responses of the intestine, liver, and muscle to emaciation and offers a useful molecular reference for future studies on early diagnosis and health‐management strategies in aquaculture.