Resveratrol attenuated fatty acid synthesis through MAPK-PPAR pathway in red tilapia.
Comp Biochem Physiol C Toxicol Pharmacol
; 268: 109598, 2023 Jun.
Article
in En
| MEDLINE
| ID: mdl-36898469
ABSTRACT
High-fat (HF) diets have been shown to cause hepatic impairment in fish species, but the mode of action, especially the pathways involved, has not yet been determined. In this study, the effects of resveratrol (RES) supplementation on the hepatic structure and fat metabolism of red tilapia (Oreochromis niloticus) were determined. Based on transcriptome and proteomics results, RES was found to promote fatty acid ß-oxidation in the blood, liver, and liver cells associated with apoptosis and the MAPK/PPAR signaling pathway. RES supplementation was found to alter the expression of genes related to apoptosis and fatty acid pathways like blood itga6a and armc5 which were upregulated and downregulated respectively by high-fat feeding while ggh and ensonig00000008711 increased and decreased, respectively, with RES addition. Relative to the PPAR signaling pathway, fabp10a and acbd7 showed a reverse U-shaped tendency, both in different treatments and at different times. Proteomics results demonstrated that MAPK/PPAR, carbon/glyoxylate, dicarboxylate/glycine serine, and threonine/drug-other enzymes/beta-alanine metabolism pathways in the RES group were significantly affected, and Fasn and Acox1 decreased and increased, respectively, with RES addition. Seven subgroups were obtained using scRNA-seq, and enrichment analysis showed that the PPAR signaling pathway was upregulated with RES supplementation. RES significantly increased the expression of the marked genes (pck1) ensonig00000037711, fbp10a, granulin, hbe1, and zgc136461, which are liver cell-specific genes. In conclusion, RES resulted in significantly enriched DGEs associated with fat metabolism and synthesis via the MAPK-PPAR signaling pathway.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Tilapia
Limits:
Animals
Language:
En
Journal:
Comp Biochem Physiol C Toxicol Pharmacol
Year:
2023
Document type:
Article