Effect of early feed restriction on hepatic lipid metabolism and expression of lipogenic genes in broiler chickens.
The study was conducted to investigate the effect of early feed restriction (ER) on lipid metabolism and mitochondrial function in the liver of broiler chickens. Newly hatched broiler chickens were randomly allocated into control and ER group which was subjected to feed restriction with feed provided on alternate days from hatch to 14 days of age (14 d), followed by ad libitum feeding until the end of the experiment on 63 d. ER group exhibited significantly lower body weight throughout the experiment. Serum concentrations of total cholesterol (TC) and high density lipoprotein cholesterol (HDLC) were significantly higher in ER group at 14 d (P<0.05), and the higher serum TC level in ER group was also observed at 63 d. In contrast, the contents of triglyceride (TG), TC and lipoprotein lipase (LPL) activity in liver were significantly lower in ER group at 14 d (P<0.05). At 14 d no significant difference was detected for the mRNA expression of the acetyl-CoA carboxylase-α (ACC-α), carnitine palmitoyltransferase I (CPT-I), sterol regulatory element binding protein-1c (SREBP-1c) or peroxisome proliferator-activated receptors α (PPAR-α) between control and ER group. At 63 d ACC-α mRNA expression was significantly down-regulated accompanied with a significantly up-regulated CPT-ImRNA and a decreased tendency of SREBP-1c mRNA expression in ER group (P=0.09). Swollen mitochondria with fragmented and reduced cristae were observed in liver of ER group at 14 d. Meanwhile the inner mitochondria membrane viscidity increased and hepatic mitochondrial superoxide dismutase (SOD) activity decreased at 14 d. The results suggest that feed restriction at early postnatal stage may produce long-term effect on lipid metabolism of broiler chicken, probably through, at least in part, alterations in mitochondria morphology and function.
Yang
Xiaojing
X
Key Laboratory of Animal Physiology and Biochemistry, Nanjing Agricultural University, Nanjing 210095, PR China.
Zhuang
Junying
J
Rao
Kaiqing
K
Li
Xiao
X
Zhao
Ruqian
R
D000101:Acetyl-CoA C-Acetyltransferase / Q000378:metabolism; D000818:Animals; D002334:Carnitine O-Palmitoyltransferase / Q000378:metabolism; D002645:Chickens / Q000378:metabolism* / Q000502:physiology; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D005508:Food Deprivation / Q000502:physiology*; D005786:Gene Expression Regulation / Q000502:physiology*; D050356:Lipid Metabolism / Q000502:physiology*; D008071:Lipoprotein Lipase / Q000378:metabolism; D008560:Membrane Fluidity; D008930:Mitochondria, Liver / Q000378:metabolism / Q000502:physiology; D051336:Mitochondrial Membranes / Q000378:metabolism; D047493:PPAR alpha / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D051780:Sterol Regulatory Element Binding Protein 1 / Q000097:blood; D013482:Superoxide Dismutase / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
D008076:Cholesterol, HDL; D047493:PPAR alpha; D012333:RNA, Messenger; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; D002784:Cholesterol; D013482:Superoxide Dismutase; D002334:Carnitine O-Palmitoyltransferase; D000101:Acetyl-CoA C-Acetyltransferase; D008071:Lipoprotein Lipase