Glucose and lipid metabolism disorders in the chickens with dexamethasone-induced oxidative stress.

ABSTRACT

The purpose of this study was to investigate the effects of long-term treatment with dexamethasone (DEX) on the antioxidation and nutrition metabolism in broiler chickens. Broilers were placed on a high-nutrient diet for 41 days, and half were given orally DEX-supplemented water at 20 mg/L every other day from 19 to 41 days of age. DEX treatment downregulated superoxide dismutase activity as well as the mRNA expression of CuZn-superoxide dismutase and glutathione peroxidase with a decrease in GSH/GSSG ratio and an increase in malondialdehyde level in the liver of broilers. DEX treatment aggravated oxidative damage in the liver and, therefore, increased the sensitivity of broilers to ascites syndrome with higher mortality and reduced growth performance. Serum metabolomics analysis showed that DEX treatment significantly increased the levels of glucose, intermediates in protein metabolism (valine, proline, serine, threonine and urea) and lipid metabolism-related products (palmitic acid, stearic acid and cholesterol) while decreasing the levels of ß-hydroxy butyric acid, succinic acid and malic acid, demonstrating that DEX treatment inhibited the Krebs cycle and the oxidation of fatty acids, and promoted the de novo synthesis of fatty acids as well as protein decomposition in the liver of broilers. Additionally, detection of metabolism-related enzymes revealed that DEX treatment inhibited glycolysis and promoted glycogen decomposition. In summary, DEX treatment resulted in oxidative stress and glucose and lipid metabolism disorders in the broilers.