The growth inhibition of yellow catfish (Pelteobagrus fulvidraco) under long-term low-concentration ammonia stress is regulated by the GH/IGF-1/IGFBP network

This experiment aimed to investigate the mechanisms behind growth inhibition in Pelteobagrus fulvidraco exposed to long-term low levels of ammonia in their environment. Fish (1.86 ± 0.05 g) were exposed to three ammonia levels (0 mg/L, 2.5 mg/L, 25 mg/L) for 84 d. The findings indicated that ammonia stress led to growth inhibition (decreased weight growth rate (WGR), specific growth rate (SGR), body condition factor (CF) and feed intake (FI)), blood deterioration (serum ammonia (SA), triglycerides (TG), cortisol, total cholesterol (TCHO), glucose (GLU), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and low-density lipoprotein cholesterol (LDL-C) elevated), digestive enzyme activity decreased (lipase, α-amylase, and pepsin), GH/IGF-1 axis suppression (decreased liver growth hormone (GH) and muscle insulin-like growth factor (IGF-1)1 levels), muscle fiber proliferation suppressed (muscle fiber density, and frequency of muscle fiber diameter < 20 μm decreased), and the mRNA expression of growth genes ( ghr , igf-1 , igfbp-1 , myod , myog , myf5 , mek , erk , mtor , pi3k , and akt ) down-regulation. This study reveals that under ammonia stress conditions, the expression of muscle igfbp-1 is significantly upregulated, leading to a decrease in muscle IGF-1 content. The reduction in IGF-1 content may inhibit the MEK/ERK and PI3K/AKT/mTOR signaling pathways, thereby suppressing the process of muscle fiber proliferation. The synergistic effects of these related mechanisms are closely associated with the observed growth retardation in yellow catfish. • Ammonia stress inhibits growth and reduces intestinal digestive enzyme activity. • Ammonia stress leads to deteriorated serum biochemical indicators. • Ammonia stress leads to the suppression of the GH/IGF-1/IGFBP network. • Ammonia stress inhibits muscle growth.