Abstract
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).
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.
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).
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.
| Original language | English |
|---|---|
| Journal | Journal of Trace Elements in Medicine and Biology |
| Publication status | Accepted/In press - 8 Feb 2021 |
Keywords
- Methionine
- chelated zinc
- autophagy
- mTOR
- Molecular Nutrition
- nutrition