Increased de novo lipogenesis in liver contributes to the augmented fat deposition in dexamethasone exposed broiler chickens (Gallus gallus domesticus).

Effect of dexamethasone (DEX, a synthetic glucocorticoid) on lipid metabolism in broiler chickens (Gallus gallus domesticus) was investigated. Male Arbor Acres chickens (1 wk old, n=30) were injected with DEX or saline for 1 wk, and a pair-fed group was included. DEX administration resulted in enhanced lipid deposition in adipose tissues. Plasma insulin increased about 3.3 fold in DEX injected chickens as against the control and hepatic triglyceride was higher as compared with the pair-fed chickens. In DEX injected chickens, the hepatic activities of malic enzyme (ME) and fatty acid synthetase (FAS) were significantly increased, while the mRNA levels of acetyl CoA carboxylase (ACC), ME, and FAS were significantly up-regulated, compared with the control. Although the mRNA levels of lipoprotein lipase (LPL), peroxisome proliferator-activated receptor-gamma (PPARgamma) and adipose triglyceride lipase (ATGL) genes in adipose tissue were not affected by DEX injection, ME activity and mRNA levels in abdominal fat pad of chickens treated with DEX are higher than those of control chickens. The results indicated that the increased hepatic de novo lipogenesis and in turn, the increased circulating lipid flux contributes to the augmented fat deposition in adipose tissues and liver in DEX-challenged chickens. The results suggest that glucocorticoids together with the induced hyperinsulinemia should be responsible for the up-regulated hepatic lipogenesis.