Feed restriction significantly alters lipogenic gene expression in broiler breeder chickens.
Broiler breeder pullets were divided into two groups at 21 wk of age. One group was given free access to feed (ad libitum) and the other fed a limited amount of feed (restricted). At 22 wk, all birds were photostimulated and maintained throughout an egg-laying cycle ending at 36 wk. Samples of liver and abdominal fat pad were collected just before photostimulation (prelight), after photostimulation at first egg and at peak egg production (plateau). Hepatic expression of sterol regulatory element binding protein-1, ATP-citrate lyase, fatty acid synthase, malic enzyme, acetyl-CoA carboxylase and stearoyl-CoA (Delta9) desaturase 1 genes in ad libitum birds declined from their highest levels just before photostimulation as the birds came into and maintained egg production. In contrast, the restricted birds had significant (P < 0.05) increases in the expression of these genes after photostimulation at first egg with a subsequent decline as they reached peak egg production. Hepatic expression of fatty acid binding protein, VLDL apolipoprotein (apoVLDL-II) and apoB genes increased significantly (P < 0.05) in both ad libitum and restricted breeders after photostimulation, whereas apoA1 gene expression declined during this time. Abdominal fat pad weights were significantly (P < 0.05) higher in the ad libitum compared with restricted birds after photostimulation. Lipoprotein lipase in this tissue showed a pattern of expression similar to that observed for the hepatic lipogenic enzyme genes. In conclusion, feed restriction during the pullet-to-breeder transition period significantly (P < 0.05) altered hepatic lipogenic gene expression in broiler breeders.
Richards
Mark P
MP
U.S. Department of Agriculture, ARS, Growth Biology Laboratory, Beltsville, MD 20705-2350, USA. richards@anri.barc.usda.gov
Poch
Stephen M
SM
Coon
Craig N
CN
Rosebrough
Robert W
RW
Ashwell
Christopher M
CM
McMurtry
John P
JP
D001275:ATP Citrate (pro-S)-Lyase / Q000235:genetics; D000005:Abdomen; D000103:Acetyl-CoA Carboxylase / Q000235:genetics; D000273:Adipose Tissue / Q000737:chemistry; D000818:Animals; D016632:Apolipoprotein A-I / Q000235:genetics; D001053:Apolipoproteins / Q000235:genetics; D001055:Apolipoproteins B / Q000235:genetics; D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics; D002352:Carrier Proteins / Q000235:genetics; D002645:Chickens / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000235:genetics; D004958:Estradiol / Q000097:blood; D064429:Fatty Acid Synthases / Q000235:genetics; D050556:Fatty Acid-Binding Proteins; D005508:Food Deprivation; D015870:Gene Expression; D008027:Light; D008055:Lipids / Q000096:biosynthesis* / Q000235:genetics*; D008079:Lipoproteins, VLDL / Q000235:genetics; D008099:Liver / Q000737:chemistry; D008291:Malate Dehydrogenase / Q000235:genetics; D009363:Neoplasm Proteins; D010058:Oviposition; D012333:RNA, Messenger / Q000032:analysis; D013230:Stearoyl-CoA Desaturase / Q000235:genetics; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors
D016632:Apolipoprotein A-I; D001053:Apolipoproteins; D001055:Apolipoproteins B; D022762:CCAAT-Enhancer-Binding Proteins; D002352:Carrier Proteins; D004268:DNA-Binding Proteins; D050556:Fatty Acid-Binding Proteins; D008055:Lipids; D008079:Lipoproteins, VLDL; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors; C027610:apolipoprotein VLDL II; D004958:Estradiol; D008291:Malate Dehydrogenase; D013230:Stearoyl-CoA Desaturase; D064429:Fatty Acid Synthases; D001275:ATP Citrate (pro-S)-Lyase; D000103:Acetyl-CoA Carboxylase