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.

在家畜中非法给予糖皮质激素是有问题的，鉴定涉及这些激素的途径至关重要，应确定新的直接或间接生物标志物。在这项工作中，在牛肝中研究了糖皮质激素对涉及葡萄糖代谢的某些基因的转录作用。这项研究是在长期长期服用低剂量地塞米松或泼尼松龙的成年夏洛来牛雄性牛上进行的。通过qPCR在肝脏中进行基因表达分析，并应用geNorm算法选择最佳参考基因。与文献一致的是，在地塞米松治疗的动物的肝脏中发现了糖原异生途径和糖原合成相关基因的显着过表达，但组织学和生化检查显示肝细胞糖原耗竭，尤其是在地塞米松治疗的动物中。可以推测，由于糖皮质激素的戒断引起的糖皮质激素或肾上腺功能不全会抑制糖原合酶的酶活性和/或诱导牛肝中糖原的自噬。实际上，通过糖皮质激素处理，肝脏中糖基化的标志物为含淀粉结合域的蛋白质1和与γ-氨基丁酸受体相关的蛋白质样1 mRNAs。此外，糖原合酶激酶3β基因在地塞米松治疗的动物中显着过表达，该蛋白也与肝脏自噬调节和糖原合成抑制有关。