Curcumin supplementation regulates lipid metabolism in broiler chickens.

The purpose of this study was to investigate whether dietary curcumin affects lipid metabolism in the liver of broiler chickens. Four treatment groups were formed from 1200 1-day-old broiler chickens, including a base diet (control, supplemented with 0 mg/kg curcumin), 500 mg/kg, 1,000 mg/kg, and 2,000 mg/kg dietary curcumin, for 49 d. At the end of experiment, each group of 50 chickens were sampled and analyzed. Compared with the control group, the results have showed that body weight, average daily weight gain, absolute and relative liver weight significantly decreased in the 1,000 and 2,000 mg/kg curcumin groups (P < 0.05). The absolute and relative abdominal fat weight were significantly decreased in the 2,000 mg/kg curcumin group (P < 0.05). The concentrations of plasma low-density lipoprotein cholesterol (P < 0.05) and plasma and hepatic triglyceride concentrations (P < 0.01) were markedly decreased in the 2,000 mg/kg curcumin group. The hepatic nonesterified fatty acid concentration (P < 0.05) and the hepatic glycogen (P < 0.05) and liver hepatic lipase activities (P < 0.01) were significantly increased in the 1,000 and 2,000 mg/kg curcumin groups. The plasma-free triiodothyronine and thyroxine concentrations were significantly increased in the 2,000 mg/kg curcumin group (P < 0.05). The gene expression levels of fatty acid synthase (FAS) and sterol regulatory element binding protein-1c (SREBP-1c) were significantly decreased in all curcumin groups (P < 0.05), but the gene expression levels of acetyl CoA carboxylase (ACC) and ATP-citrate lyase (ACLY) were significantly decreased only in the 2,000 mg/kg curcumin group (P < 0.05). The expression levels of peroxisome proliferators-activated receptor α (PPARα) and carnitine palmitoyl transferase-I (CPT-I) were significantly increased in the 1,000 and 2,000 mg/kg curcumin groups (P < 0.05). These results indicated that curcumin plays an important role in reduction abdominal fat deposition by decreasing the hepatic and plasma lipid profile and affecting the expression levels of genes related to lipogenesis and lipolysis including ACC, FAS, SREBP-1c, ACLY, PPARα, and CPT-I.