Dexamethasone and prednisolone treatment in beef cattle: influence on glycogen deposition and gene expression in the liver.

The illegal administration of glucocorticoids in livestock is problematic and identification of pathways in which these hormones are involved is critically important, and new direct or indirect biomarkers should be identified. In this work, glucocorticoid transcriptional effects on some genes involved in the glucose metabolism were studied in the bovine liver. This study was conducted on adult Charolais male cattle treated with long-term low dose dexamethasone or prednisolone. Gene expression analysis was conducted in the liver by qPCR, and the geNorm algorithm was applied to select optimal reference genes. In line with the literature, a significant overexpression of genes involved in the gluconeogenic pathway and glycogen synthesis was detected in the liver of dexamethasone-treated animals, but histological and biochemical examination showed hepatocyte glycogen depletion particularly in dexamethasone-treated animals. It possible to hypothesize that glucocorticoids or adrenal insufficiency due to glucocorticoids withdrawal inhibit the enzymatic activity of glycogen synthase and/or induce glycogen autophagy in bovine liver. In fact, markers of glycophagy as starch-binding domain-containing protein 1 and γ-aminobutyric acid receptor-associated protein-like 1 mRNAs were upregulated in the liver by glucocorticoids treatment. Furthermore, glycogen synthase kinase-3 beta gene was significantly overexpressed in dexamethasone-treated animals, and this protein is also implicated in liver autophagy modulation and glycogen synthesis inhibition. These results showed that glucocorticoids likley have dual roles in hepatic glycogen metabolism of cattle, and investigation of these pathways could help find treatment biomarkers.

Satellite cell-mediated breast muscle regeneration decreases with broiler size.

Satellite cells (SCs) reside between the sarcolemma and basal lamina of muscle fibers and are the primary contributor of DNA for post-hatch muscle growth and repair. Alterations in SC content or properties by intrinsic and extrinsic factors can have detrimental effects on muscle health and function, and ultimately meat quality. We hypothesized that disrupted SC homeostasis may account in part for the increased breast myopathies observed in growing broilers. To test this hypothesis, we selected broilers with different body weights at comparable ages and studied SC characteristics in vitro and in vivo. Data shows that SC numbers in the breast muscles decrease (P < 0.001) and their inherent abilities to proliferate and differentiate diminish (P < 0.001) with age and size. Further, when breast muscle is presented with an insult, muscle of larger broilers regenerates more slowly than their smaller, age-matched counterparts arguing that SC quality changes with size and age. Together, our studies show that birds with greater muscle hypertrophy have less SCs with diminished ability to function, and suggest that aggressive selection for breast growth in broilers may exhaust SC pools when birds are grown to heavier processing weights. These findings provide new insights into a possible mechanism leading to breast myopathies in the poultry industry and provide targets for mitigating adverse fresh breast quality.