Cholesterol deregulation induced by chronic corticosterone (CORT) stress in pectoralis major of broiler chickens

Chronic endogenous glucocorticoid (GC) excess in mammals is associated with metabolic dysfunction and dyslipidemia that are characterized by increased plasma triglyceride and total cholesterol (Tch) levels. However, the effects of chronic GC administration on cholesterol metabolism, particularly in muscle tissues of broiler chickens, are unknown. In this study, broiler chickens were treated chronically with vehicle (CON) or corticosterone (CORT) for 2 weeks. Chronic CORT treatment significantly increased Tch levels in pectoralis major muscle (PMC) (p < 0.001) as well as in leg muscle (p < 0.01), and CORT enhanced triglyceride levels in the PMC (p < 0.001). Real-time PCR results showed that HMGCR (p < 0.05) mRNA expression was up-regulated by CORT in PMC, and 11β-HSD1 gene transcription (p = 0.08) was not significantly downregulated, whereas glucocorticoid receptor (GR) mRNA expression, 11β-HSD2, CYP7A1, CYP27A1, ApoB and LDLR were unchanged by CORT (p > 0.05). Western blot results showed that the levels of total GR (p = 0.08) tended to be increased and nuclear GR protein (p < 0.05) was increased in PMC by CORT administration. Parallel to an increase in gene expression, HMGCR protein expression in PMC was significantly increased (p < 0.05) by CORT. Moreover, LDLR (p < 0.05), ApoA1 (p = 0.06) and 11β-HSD2 (p = 0.07) protein expression in PMC tended to be increased by CORT compared to control. These results indicate that chronic CORT administration causes cholesterol accumulation in PMC tissues of broiler chickens by increasing cholesterol synthesis and uptake.