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Valine enhances intramuscular fat deposition through activating autophagy and fatty acid metabolism pathways in C2C12 myoblasts

ABSTRACT: The branched-chain amino acids (BCAA) are essential to animal growth and intramuscular fat deposition, and also metabolic health (circulating level elevated in obesity and diabetes). However, the molecular role and effect of valine on muscle growth and fat deposition were less explored. Valine supplementation significantly affected mouse muscle growth, increasing the abdominal fat but decreasing the back fat. In the leg muscle, the expression levels of genes related to autophagy and fat deposition were significantly disturbed. Furthermore, valine promotes lipid deposition in myoblasts in a dose-dependent manner, and co-treatment of valine and palmitic acid can act in concert to enhance lipid deposition in myoblast. Moreover, transcriptome sequencing on myoblasts revealed that the signaling pathways such as mTOR, PI3K-AKT and fatty acid metabolism were activated after valine treatment, and palmitic acid additionally stimulated signaling pathways related to lipid metabolism in myoblasts. Therefore, valine could independently activate the autophagy pathway, and the fatty acid metabolism pathway to enhance intramuscular fat deposition

ORGANISM(S): Mus musculus

PROVIDER: GSE217813 | GEO | 2022/11/18

REPOSITORIES: GEO

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Project description:Background: Marketing products with added-value characteristics is a current trend in livestock production systems. Regarding meat, selection for intramuscular fat and muscular fatty acid composition is a way to improve the palatability and juiciness of meat while assuring a healthy fat content. This represents selecting animal with a different muscular metabolic profile with respect to the extended selection of lean animals. Results: The present study has analysed the muscular gene expression profiles of 68 commercial Duroc pigs belonging to two groups with extreme phenotypes for traits strongly related with lipid deposition and composition. This has allowed us to compare the physiological and metabolic implications of selecting for each of these extreme groups. Rather than upregulation of a single pathway, the main differences lied on the transcriptional levels of genes related with lipogenesis and lipolysis, revealing the existence of a cycle where triacylglycerols are continuously synthesized and degraded. Most strikingly, several genes which enhanced fatty acid Î²-oxidation and favoured insulin signalling and glucose uptake were upregulated in the fattest animals, indicating that the events leading to peripheral insulin resistance in humans with increased levels of intramuscular fat and obesity do not take place in these pigs. Moreover, neither was detected the well-characterised low-grade inflammatory state observed in overweighed humans. Conclusion: As a whole, our data suggest that selection for increasing intramuscular fat content in pigs would lead to a shift but not a disruption of the metabolic homeostasis of muscle cells. Future studies on the post-translational changes affecting protein activity or expression as well as information about protein location within the cell would be needed to fully understand how lipid deposition affects muscle physiology in pigs. 68 gluteus medius samples form 68 animals belonging to two groups of 34 animals each: HIGH group had higher carcass, plasma and muscle fat content; LOW group had lower carcass, plasma and muscle fat content

Project description:CPT1B, as the major rate-limiting enzyme for fatty acid β-oxidation, involved in the regulation of adipose tissue lipid deposition, but its role in the regulation of goat intramuscular fat (IMF) remains unclear. Here, we conducted knockdown experiments targeting the CPT1B gene in goat intramuscular preadipocytes, resulting in a significant increase in intracellular triglyceride (TAG) content and lipid droplet accumulation. Conversely, the overexpression of CPT1B led to a significant decrease in intracellular TAG content and lipid droplet accumulation. Mechanistically, through RNA-seq analysis of CPT1B knockdown samples, we identified 285 differentially expressed genes (DEGs), including 71 up-regulated and 214 down-regulated genes. Notably, these DEGs were significantly enriched in various KEGG signaling pathways, such as fatty acid metabolism, focal adhesion, FoxO signaling, PI3K-Akt signaling, and MAPK signaling pathways. Gene Set Enrichment Analysis (GSEA) further confirmed the upregulation of the MAPK signaling pathway upon CPT1B knockdown in adipocytes. In rescue experiments, we demonstrated that the addition of a p38MAPK inhibitor (PD169316) to CPT1B-knockdown adipocytes counteracted the increase in lipid deposition caused by the loss of CPT1B function. These findings suggest that CPT1B inhibits lipid deposition in goat intramuscular preadipocytes via the p38MAPK signaling pathway. In addition, we observed a potential interaction between CPT1B and CPT1A through Protein-Protein Interaction Networks (PPIs). Interestingly, CPT1A exhibited a similar regulatory function to CPT1B, and they both were able to partially restore the changes in lipid deposition induced by each other. This observation supports the hypothesis of synergistic effects between CPT1B and CPT1A. Collectively, our results elucidate the role of CPT1B in the regulation of lipid deposition in goat intramuscular adipocytes through the p38MAPK signaling pathway, providing valuable insights for enhancing the quality of goat intramuscular fat.

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Valine enhances intramuscular fat deposition through activating autophagy and fatty acid metabolism pathways in C2C12 myoblasts

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