Background
Amino acid-chelated zinc (Zn) can increase anabolism of animals. However, the underlying mechanisms are unclear. We aimed to examine how autophagy impact anabolism following a diet containing methionine-chelated Zn (ZnMet) compared with inorganic Zn (ZnSO4).
Conclusions
ZnMet increased anabolism through integrating mTOR signal and autophagy pathway in yellow catfish. The present study unravels a novel mechanism for amino acid-chelated minerals improving anabolism.
Methods
Yellow catfish (weight: 4.02 ± 0.08 g) were fed two diets containing ZnSO4 or ZnMet for 8 wk. The differences in transcriptional responses and corresponding biological profiles were compared between the livers of fish fed the two Zn sources of diets. Hepatocytes of yellow catfish were incubated for 48 h in medium containing ZnSO4 (10 μM ZnSO4) or ZnMet (10 μM ZnMet) after 2 h pretreated with or without pathway inhibitors. Intracellular Zn, TG and protein contents, lipid droplet and autophagic vesicles were detected. Ultrastructural observation, enzymatic activities, qPCR assays, western blot and immunofluorescence analysis were conducted.
Results
ZnMet up-regulated the expression of genes associated with anabolism and autophagy. The differentially expressed genes (DEG) analysis indicated that both mTOR and autophagy pathways were activated. ZnMet-induced activation of autophagy was mTOR-independent. In this process, forkhead box class O was deacetylated and activated, and induced autophagy, which provided substrates for energy generation. Conclusions: ZnMet increased anabolism through integrating mTOR signal and autophagy pathway in yellow catfish. The present study unravels a novel mechanism for amino acid-chelated minerals improving anabolism.